Depression - How to Overcome Using the Outer Child Program

How to Overcome Depression Using Outer Child Tools

The outer child program explained in Taming Your Outer Child shows you how to propel your life out of depression.   Indeed, Outer Child can get stuck in depression, clogging up the works, making it hard to work your way through.   The key to recovery is to nourish your Adult Self – the part of you that needs to get strong enough to overtake your depression. 

Negative Thoughts -- Spooling

Negative thoughts may be spooling in your head (obsessively perhaps).  This represents your Outer Child’s futile, unconscious attempt to search (in all the wrong places) for its lost happiness.  It’s trying to “think” your way out of the depression.  Your Adult Self knows better.  Your Adult knows that trying to “think” your way out of the depression won’t work.  You have to DO your way out. 

Bulleted List of Facts about Depression

Below is a helpful DOING task which is not included in the book, a list of information and questions designed to redirect your brain-search away from self-obsession and toward exploring helpful information about depression.  So much has been discovered about depression, enough to fill volumes.  But when you’re depressed and having difficulty concentrating (perhaps), rather than trying to read walls of words, you may find it easier to scan random items on a list.  You don’t need to digest or even understand all of the tidbits presented below, but they can give your spooling brain something to feast on, namely the inroads science has been making about depression and treatment approaches that may be coming down the pike. 

I’ve collected this bulleted list of random miscellany to inspire your interest.  No need to read all of these items at once; portion off a few at a time.  The idea is to redirect your spooling mind to a more constructive task that can strengthen your cognitive mind and lift you out of pointless obsession. 

Please write to me with any new information you’ve got so I can add it to the bulleted list. 

The Science and Psychology of depression

  • 5% to 10% of Americans suffer clinical depression in any given year, %15 over a life time. 
  • 100% of people have depressing periods of life.
  • When it comes to anxiety and depression, there are old theories, newer theories and newest theories.   
  • One of the older theories sees the brain as a bowl of soup. To treat depression, you add a chemical and stir[1].

Q. If antidepressants improve my mood with chemicals, does this mean my depression was caused by a chemical imbalance? 

Q. Which came first, the chemical imbalance or the depression?

  • Serotonin[2] is associated with wellbeing, reward, pleasure, motivation. 
  • Antidepressants like Prozac, Paxil, Zoloft, etc. enhance serotonin and are called SSRIs which stand for Selective Serotonin Reuptake Inhibiters. 
  • Most people think antidepressants provide the brain with serotonin, but they do not. Instead they block the re-uptake of your own supply of serotonin. 
  • By altering brain mechanics in this way, antidepressants cause your own internal supply of serotonin to hang out longer in the synapses (between your neurons) where it reportedly increases its bombardment on the neuron’s receptor cites. 
  • One of the older theories (still popular) holds that this serotonin bombardment is what accounts for antidepressants’ benefit. 

Did you know that…

  • 95 of serotonin is in the gut.
  • As of the writing of this book, blood tests are still unreliable in testing brain serotonin levels because the total amount of serotonin in the blood does not reflect how serotonin is being utilized in the brain (there is a blood/ brain barrier).
  • Sadness and anxiety have their own separate neural pathways[3].

A newer theory…

  • A newer theory sees depression and anxiety a reversible neurodegenerative disorder which involves atrophy of certain brain areas.
  • According to this perspective, antidepressant therapies (including electroshock therapy) would work by repairing atrophied neurons, sprouting new neurons in key brain regions[4] and promoting growth in dendrites – connective branches protruding at the end of branches[5]
  • Antidepressants, for example, are known to increase dendrite receptors for serotonin.
  • In this sense, antidepressants take advantage of the brain’s plasticity. 
  • Depression can result from having a defect in neural development of the prefrontal cortex – the initial abnormality in depression that leads to cascade of changes in other systems[6]

Newer ways of looking at depression also say…

  • Depression can be seen as a reduction in overall brain functioning which leads to deficits in learning, memory, sleeping, sex drive, weight control, the ability to experience pleasure, and the senses of smell and taste. 
  • In other words, “Depression is syndromal – characterized by a reliable cluster of disabilities…[7]” Sadness just happens to be its most notable system.   
  • The concept of depression as a disorder specific to sadness was created by drug companies with a product to sell, namely, antidepressants[8]
  • The proposition that antidepressant therapies work because they are neuro-regenerative (rather than because they enhance serotonin) resolves a number of inconsistencies. 
  • It explains the lag time in taking an antidepressant – why it usually takes weeks for depression to lift even though serotonin levels increase within hours.  Several weeks are about how long it would take for neural growth and repair to make an impact. 
  •  It would explain why reducing serotonin is known to neither worsen nor create depression.   
  • It would explain why tianeptine, a chemical which dampens serotonin, actually helps with depression[9]
  • It would explain why antidepressants are good for ‘lazy eye,’ helping to repair weakened, damaged cells in the visual cortex.  

Q. Does this mean that antidepressants’ main benefit isn’t about increasing availability of serotonin in the brain after all?

Q. Does this mean antidepressants would be good for other types of mind/body dysfunctions? 

  • Depression is seen as a physical disorder misinterpreted by brain.  Sickness is read as sadness.  The low mood is a secondary response.  The withdrawing is the body’s way of conserving energy and minimizing risk – an evolved pattern of behavior mediated by the immune system[10]
  • Feelings are the brain’s representation of what’s going on in the body[11]
  • William James called depression ‘psychical neuralgia.’ 


  • About half of the people who benefited from antidepressant drug trials were actually taking placebo.  What’s up with placebo?  It must be pretty powerful stuff.
  • Placebo is the brain’s own pharmacy of powerful internal mood-stabilizers, pleasure enhancers, pain killers, healers, and cell-progenitors.
  • Placebo seems to be mediated by automatic brain processes, since it is produced when the cognitive mind is ‘tricked’ rather than by conscious will. 
  • The outer child program is designed to enhance benefits of this internal pharmacopeia by integrating primal emotion, visualization, with motoric action. 


  • According to research, aerobic exercise like walking or running (minimum of three times a day for 20 minutes) is as effective as individual psychotherapy, group psychotherapy, and cognitive therapy for many psychiatric conditions including depression and anxiety disorders[12].


  • You can have medication ‘poop-out’ where your antidepressant loses its effectiveness (after about three months or longer)[13].
  • Most people don’t experience ‘poop out’ but there are many exceptions requiring changes in doses or medication. 

Stress hormones and depression

Stress and stress hormones

  • People with early trauma have elevated stress hormones[14]
  • The stress hormone cortisol in high enough doses damage the brain. 
  • Stress hormones permanently sensitize neurons and receptors so they perpetually over respond to stress.
  • The stress hormone CRF acts on various brain sites to create depression[15]
  • Stress in early life primes people for later depression.
  • Stress hormones are highest with major depression. 
  • Sex abuse in girls before puberty creates hyperactivity of stress hormone system[16], priming them for depression as adults[17]
  • Other types of stressors include: being a subordinate within a group, being physically restrained, social isolation, deprivation of maternal care[18], abandonment feelings (fear of). 
  • Stress both shrinks the hippocampus – a critical site for memory – and decreases a nerve growth and repair factor[19] -- BDNF, leaving the brain vulnerable. 
  • Even a small degree of later stress provokes an outpouring of stress hormones, producing depression’s vegetative state, sleep disturbances, cognitive dullness, and loss of pleasure. 
  • The amygdala, seat of emotions like fear, goes into overdrive, hurling out negative emotions that promote anxiety states. 
  • Stress hormones destabilize glutamate – a brain chemical involved in cognition and learning.  When glutamate over-stimulates neurons, it causes dendrite collapse. 
  • Peter Kramer offers a poetic metaphor noting how depressed people look just like their brains, describing the depressed brains’ retreating neurons and withering dendrites, their fragility, brittleness, lack of resilience – just like the patients themselves.   
  • He also compares overwrought people to their stress-impaired neurons, noting how neurons in the hippocampus shed branches for incoming messages and outgoing messages, losing communication with neighboring cells, becoming isolated[20] and shutting down. 
  • Depression with its elevated cortisol (stress hormone) robs the skeleton of calcium, leading to osteoporosis[21]
  • Depressed women have lower bone density.   
  • Depression causes blood platelets (that help blood clot) to be sticker. They aggregate when they should be flowing. 
  • Depression makes heart attacks more deadly[22]
  • Depression and stress cause shrinkage of the hippocampus, an important memory site, which explains the cognitive impairments seen in depressives. 
  • Antidepressants prevent shrinkage in the hippocampus[23].”
  • Major depression is considered a risk factor for Alzheimer’s[24] -- a progressive hippocampal illness. 

What about shrinkage?

  • People with depression have reduced volume in an area in the brain associated with reward, fear, and stress[25].
  • Hippocampus – an important site for memory – is smaller in adults (on autopsy) who spent time in orphanages as children.    
  • Prefrontal cortex is smaller in depressed people[26].
  • Area 25’s “Ventral subgenual cingulated cortex is 40% smaller in depressed[27].
  • Q. Does depression cause shrinkage or does shrinkage cause depression?
  • In people with family history of depression, the shrinkage has to do with the glia, not neuron loss. 

The Glia?

  • The glia promote the development of serotonin receptors[28].
  • The glia perform housekeeping tasks like cell growth and repair, unlike neurons which process information and generate action. 
  •  The Glia stabilize glutamate – a neurotransmitter that allows the brain to fire so that cognitive processes like learning can occur.  Too much glutamate causes collapse of dendrites (the connective sprouts of branches at the end of the neuron). 
  • Depressed alcoholics show worst glial loss, “…the liquor [having supplied] toxic damage to the depressive’s vulnerable brain[29].” This may be what alcoholics’ ‘wet brain’ is all about – their neurons don’t fire properly.
  • The good news is that antidepressants compensate for the loss of glial cells by promoting new cell and dendrite growth. 
  • Antidepressants also reduce sensitivity to glutamate, so there is less damage to brain[30]

Do you wonder…

Q. If depression is such a pervasive, destructive illness, why is it possible to have a complete recovery just because you might meet Mr. Right or your life circumstances greatly improve? 

Did you know that…

  • Even some of your happier past experiences are remembered as negative when seen through the prism of depression. 
  • Q. Does this mean that depression is retroactive? 
  • Thoughts about the future are likewise distorted by depression’s malaise. You feel hopeless about ever feeling happy and motivated again. 
  • Remember, depression is reversible.

What is Kindling?

  • Thanks to a process called ‘kindling,’ the more episodes of depression you have, the worse they get – and the less stress it takes to trigger them[31].
  • Epilepsy is considered a kindled illness.  The more seizures you have, the worse they get – and the less it takes to trigger them.
  • At first stress can affect the brain without causing depression, but each event acts like kindling wood for a fire.  Eventually the impact of stress leads to ‘an open blaze’ of depression[32]
  • A Peter Kramer comment: “The more often you’ve been depressed, the more often you contribute to your own misery[33].”
  • If major depression is similar to seizure, it would seem imperative to intervene quickly to prevent brain damage[34].

The brain can regenerate!

  • It’s always worth repeating:  Depression is reversible.  The brain undergoes neurogenesis.  It is plastic, moldable, and regenerative.
  • The brain adapts by sprouting new branches from nerve cells. 
  • This sprouting allows us to learn and remember and change behavior. It’s what we are doing through the Outer Child program – creating new neural topiaries in the brain[35]

BDNF – a brain growth factor

  • BDNF is a nerve growth factor involved in sprouting new dendrites.[36]
  • BDNF enhances growth of neurons that respond, for instance, to serotonin[37]
  • Depressed people have deficit in BDNF.
  • Stress and depression suppress BDNF[38]
  • BDNF is a trophic factor for brain health. Suppressing BDNF is like depriving a plant of sunlight. Your brain shuts down, neurons stop growing, and stops creating new cells. 
  • BDNF is opposite of stress hormone[39].  Whereas stress hormones damage key areas in the brain, BDNF repairs them. 
  • A flawed gene involved in BDNF creates biological vulnerability for developing major depression[40].

Did you know that …

  • Scanning the brain (with fMRI) shows a certain brain site called Area 25[41] to be overactive in depressed patients. 
  • Quieting Area 25 immediately reduces depression. 
  • Area 25 lights up (in fMRI) in depressed people, or even in non-depressed people instructed to think depressed thoughts.
  • By implanting electrodes in the brain (a procedure called Deep Brain Stimulation (DBS)), Area 25 can be turned off, and depressed feelings immediately go away[42].
  • Bi-polar, uni-polar, and major depression light up different sites in the area[43]


  • People with long versus short version of a certain gene called SERT scan differently on the fMRI in Area 25[44]
  • The SERT gene is involved in serotonin transport. It is shorter in people with depression.
  •  A study showed that if you had two long 5HTT genes, stress did not cause depression.  Even if you were a victim of early child abuse or had high stressors in adulthood, the stress did not lead to depression.  You could get depressed if you had two long 5HTT genes, but it would be a non-stress-induced depression. 
  • With two short 5HHT genes, you were more prone to depression; one long one short less prone. 

What about the frontal lobes?

  • The prefrontal Cortex, located just behind your forehead, is a key depression site. 
  • Depressed people have power failure in the left side (left frontal lobe) – it doesn’t activate the machinery to process positive emotions or respond to positive stimuli. 
  • Left frontal lobe is crucial for positive feelings[45] whereas the right side is associated with negative feelings[46]
  • People with active left frontal lobes have lower cortisol, the stress hormone that can damage the brain. 
  • The left frontal lobe also inhibits negative emotions emanating from the amygdala, seat of emotions like fear. 
  • Blood flow is greater in the amygdala of depressed people causing them to be overwhelmed with dread, fear, sadness, etc.[47]  
  • When the left frontal lobe is activated, it dampens the amygdala’s flow of negative emotions, alleviating the distress[48]
  • Imbalances between left and right frontal lobe activation are set by the time you reach puberty. 


  • Interferon is known to cause depression.  Interferon, a medication taken for serious illnesses like multiple sclerosis (MS) and hepatitis C., is a synthetic form of cytokine – a substance produced in white blood cells for protection against infection. High levels of cytokines impact receptors in the brain, promote stress response, and induce depression.  Certain cancers produce high levels of cytokines and lead to depression[49].  
  • Carpet bombing entire brain rather than targeting depression’s central mechanism. 

Oscillating brain 

  • The brain is like an orchestra. Rather than each musician (each neuron) communicating with its neighbor, whole sections communicate with each other –aggregate rather than single cell[50]
  • Depression is mediated in primitive areas like the limbic system, as well as newer areas involved in memory, reward, and motivation – the areas I discuss in Taming Your Outer Child in the debt-gambling and hoarding-cluttering chapters. 
  • OSCILLATING Thalamus – a decoupling of two brain regions – thalamus and 6th layer of cerebral cortex which is directly connected to thalamus. The thalamus is an older brain structure which serves as a relay station. All information from outside world and from lower brain regions go through thalamus before being passed to cortex.  Cells in thalamus oscillate together at different frequencies [check Goleman].  And they oscillate, they cause adjacent cells in layer six of the cortex to oscillate at same frequency, allowing for actions, perceptions, movements, and consciousness.  When oscillating at a high enough frequency, the brain is awake.  When its frequency is low enough, the brain becomes unconscious and falls asleep.   In depressed patients, certain regions of thalamus oscillate at abnormally low frequencies which decouples it from corresponding areas in the cortex.  These areas in your cortex become overly excited because they’re no longer being properly regulated and symptoms of dysfunction emerge.  In one area, you get tremors as seen in Parkinson’s disease, in another you get Parkinson’s rigidity, in still another you get tinnitus, and another OCD, and another, depression. 

More about SSRI’s?

  • SSRI’s (i.e. Prozac, Paxil, Zoloft, etc.) affect “down stream” the impact causes greater depression further down the line (where the person needs more and more of the drug), and this impact can be either temporary or permanent. 
  • Another speculation is that the increased bombardment may make the receptors more sensitive – may damage them. 
  • It is thought that at the end of the cascade, the extra bombardment of serotonin may ultimately signal the brain to produce less serotonin (creating “down regulation”) causing a net loss to the system. 
  • Most drugs and psychotherapies ease rather than cure depression.
  • SSRI’s don’t affect the brain at the “end product” (as they would if they in fact contained serotonin).  Instead, they affect an earlier part in the whole cascade of neuro-chemical events within the brain.  The “down stream” affect of the SSRI’s upon the “end product” is entirely up to chance and differs from brain to brain.
  • Endogenous depressions had the same course as exogenous depressions. 
  • Once they are underway, all depressions lose their differences.  “All Roads Lead to Depression: Clinically Homogeneous, Etiologically Heterogeneous.”
  • A persistent low-grade depression known as chronic dysthymia is common, debilitating, and often untreated. 
  • Studies show best results combined antidepressants with talk therapy. 


[1] David Dobs quoting Helen Mayberg.  Also Lozano, Meyer, Lindenberg.

[2] Along with dopamine and NE (nor-epinephrine)

[3] Anxiety is associated with specific activations in ventral insula, orbitofrontal and anterior temporal lobes.  Sadness and anxiety have segregated corticolimbic pathways where selective dorsal cortical deactivations during sadness and ventral cortical deactivations in anxiety.  Liotti, Mayberg, Brannan, McGinnis, Jerabek, Fox, Biological Psychiatry 2000.

[4] A neuroscientist Grigori Enikolopov at Cold Spring Harbor Labs near my home, discovered (2006) that Prozac increases number of neurons in the dentate gyrus.  Neurogenesis coverts unspecialized stem cells into specialized neurons.  Prozac promotes the second step in this process by stimulating ‘amplifying neural progenitors’ to divide and generate more neural cells.

[5] Bruce McEwen. Increasing number of serotonin receptors and BDNF factors.

[6] Drevets.

[7] Kramer, Against Depression, 2005.

[8] Cited in Kramer 2005.

[9] Tianeptine initially developed as an ant anxiety agent, protects neurons from affect of stress. Rats treated with tianeptine had growth in the hippocampus (memory site).  It promoted neuro-genesis – new cells and sprouting of connections between cells.  Kramer 2005 referencing Duman. 

[10] Bruce Charlton.

[11] Antonio Demasio.

[12] Tkachuk, Gregg, Martin, Garry, Exercise Therapy for Patients with Psychiatric Disorders: Research and Clinical Implications, Professional Psychology: Research and Practice, June 1999 Vol. 30, No. 3, 275-282.

[13] SSRI Possible explanations:  Speculation has it that increased serotonin-bombardment on the receptor sites, may cause the brain to create additional receptor sites in order to accommodate these additional “rounds of serotonin” – thus ramping up the brain’s need for serotonin. 

[14] Stress: Early experience shapes wiring patterns and sets sensitivity levels of brain’s neuro-molecular machinery, Kramer 2005.  

[15] Stress response works like this:  When threat is detected, hypothalamus produces CRF (corticotrophin-releasing factor), inducing the pituitary gland to secrete ACTH (adreno-corticotropin hormone), which in turn instructs adrenals to pour out cortisol. 

[16] In hippocampus.

[17] Was it morano article??????

[18] Ibid.

[19] McEwen.

[20] Kramer 2005.

[21] David Michaelson.

[22] Alexander Glassman. 

[23] Sheline YI, Gado MH, Kraemer HC, Untreated Depression and Hippoampal Volume Loss.  American Journal of Psychiatry, vol. 160:6, pp. 1515-1518, August 1 2003

[24] Ibid.

[25] Area 25 is the subgenual cingulate cortex which has connections to nucleus accumbens, amygdala, hypothalamus, and orbitofrontal cortex (OFC).

[26] Wayne Drevets: Ventral subgenual cingulate cortex 2 ½ inches behind the nose is 40% smaller in the depressed. 

[27] Depression is subgenual. H. Johansen-berg, Gutman, Behrens, Matthews, Rushworth, Katz, Lozano, and Mayberg., Anatomical Connectivity of the Subgenual Cingulate Region Targeted with Deep Brain Stimulation for Treatment-Resistant Depression, 2007.

[28] Glia are not neurons.

[29] Kramer referencing Grazyna Rajkowska. 

[30] for instance, in the hippocampus.

[31] Kramer referencing Kendler.  Kendler says that depression is a kindled illness.  Each episode makes subsequent epos ides more likely.  Later episodes can occur spontaneously in absence of inciting events,  tend to be more severe, less responsive to treatment. 

[32] Kramer referencing Kendler.

[33] Kramer 2005.

[34] A point made by Kramer.

[35] Term offered by Clive Clayton.

[36] Strengthening synaptic connections in the hippocampus, Ronald Duman.

[37] Ibid.

[38] Duman

[39] Kramer 2005.

[40] The flawed BDNF gene works opportunistically – awaiting an early stressful experience such as child neglect or abuse to set it in motion. 

[41] This area is subgenual anterior cingulated which connects to hypothalamus and instigates stress response.   H. Johansen-berg, Gutman, Behrens, Matthews, Rushworth, Katz, Lozano, and Mayberg., Anatomical Connectivity of the Subgenual Cingulate Region Targeted with Deep Brain Stimulation for Treatment-Resistant Depression, 2007.

[42] Mayberg. Deep brain stimulation (DBS) – sending electrodes into the thalamus breaks abnormal oscillation patterns. 

[43] Representing different types of depression, with implications for developing different types of treatments.

[44] Article Morano, meyerberg?????

[45] And pre-goal eagerness…

[46] Richard Davidson.

[47] Drevets, Davidson.

[48] Drevets.

[49] Kramer 2005.

[50] A Depression Switch? David Dobbs, NYT April 2 2006.