Programs! Get your programs! In this article, we’re going to take a look at the default mode network (DMN), also known as the default state network.
The DMN is a specific set of brain regions that engage when we’re left to think for ourselves in peace and quiet or “resting state” [1-3]. There are other occasions, however, when this network springs to life, such as when we contemplate past and future events as well as when we consider the thoughts and feelings of other people [1,4].
It is a set of interconnecting hubs and systems that govern the so-called "internal mentation" (i.e., the periods of spontaneous and deliberate introspection we all engage in on a daily basis… thousands and thousands of times on average!) . Oh my, the stories and programs that dictate most of our behavior (like >95% for most people)!
But newsflash, folks… you are not your thoughts and not beholden to your programs if you are aware of them, oh mindful one (see more below)!
In this article, we will examine how our knowledge of the DMN has progressed, its structure, function, and role in health and disease. We will also assess the influence of behavior as well as pharmacological and psychedelic compounds on the DMN.
A Brief History of the Default Mode Network
The discovery of the DMN was completely accidental, and arose from evidence collected when researchers first measured brain activity in humans during undirected mental states . Although these early studies were not designed with this goal in mind, a resting-state measurement was (and still is) often collected as an experimental control.
The Swedish brain physiologist David Ingvar noted the importance of consistent, regionally-specific brain activity patterns during rest task states back in the 1970s and 1980s . His work established that the brain is not merely idle (like a television in standby mode) when left undirected. Instead, brain activity persists, and this increased resting activity is localized to specific regions, such as the prefrontal cortex (PFC).
Ingvar’s work built on early notions from the late 1800s through to the mid-1950s, proposing that cerebral metabolism would change when going from a quiet resting state to performing difficult arithmetic, due to the cognitive effort involved. Surprisingly, cerebral metabolism did not change, as revealed by Louis Sokoloff and colleagues, suggesting that resting-state activity can be as vigorous as that seen during demanding cognitive tasks.
By the early 21st century, the DMN was recognized as a research area in its own right, and began to garner significantly more attention from the academic community. The advent of new and innovative techniques, such as positron emission tomography (or PET) scans in the 1990s, enabled a more sophisticated assessment of brain activity in this context. Work from Marcus E. Raichle’s lab in the early 2000s corroborated earlier research suggesting that the brain is constantly active, even at rest, with comparable brain energy consumption between rest and focused cognitive tasks [6,7].
Anatomy and Function of the Default Mode Network
The DMN is generally thought to be the neurological basis for the sense of self or your ego due to its role in memories and recollections of events and facts about oneself, other traits and qualities of the self, and reflecting on one’s own emotional state at a given point in time . The anatomical regions responsible for this function include the posterior cingulate cortex (PCC), medial prefrontal cortex (mPFC), and angular gyrus , which are otherwise called "functional hubs."
When thinking about others, the DMN helps us interpret others' thoughts, understand their emotional state, empathize with them, and underpins our moral reasoning and ability to perceive one’s lack of social interaction [5,8]. Anatomically, the functional hubs are also involved here alongside the dorsal medial prefrontal cortex (dmPFC), temporoparietal junction (TPJ), lateral temporal cortex, and anterior temporal pole .
Lastly, the DMN is involved in remembering the past, envisioning the future, and comprehending narratives (i.e., stories and tales) [5,9]. The regions underpinning this aspect of the DMN are the functional hubs (i.e., PCC, mPFC, and angular gyrus) as well as the hippocampus, parahippocampus, retrosplenial cortex, and the posterior inferior parietal lobe .
Disruption of the DMN in Disease States
Evidence suggests that the connection between the different linking "hubs" within the DMN are disrupted in a disease-specific way in people with Alzheimer’s disease, autism spectrum disorder, schizophrenia, chronic pain, depression (see the next section for more), post-traumatic stress disorder, and many others [1,10,11]. Medication seems to help, and targeting a more functionally integrated DMN has been proposed as a therapeutic intervention within the context of such psychiatric orders.
The activity of the DMN, as measured by functional magnetic resonance imaging or MRI (a type of test that detects brain activity by measuring changes in blood flow), has also been used to distinguish Alzheimer’s disease from healthy aging . Reduced resting-state activity was shown in the posterior cingulate and hippocampus in mild Alzheimer’s disease patients, suggesting that disruption of these regions could underpin the disease. DMN activity could also be a vital biomarker in the diagnosis of this challenging condition .
The DMN in Depression
The DMN has been noted as a key player in major depressive disorder (MDD), specifically its overactivity . In MDD patients, increased levels of DMN dominance were associated with higher levels of depressive rumination (obsessive thoughts), and lower levels of adaptive and reflective rumination. A separate study found that people with depression fail to reduce activity in DMN regions after exposure to negative images, yet importantly had a much greater increase in activity in other specific areas of the DMN (amygdala, parahippocampus, and hippocampus) than controls .
The DMN seems to underpin, or drive, the representation of negative thoughts that are a hallmark of MDD  and is associated with symptom severity in this condition. There is no clear indication that DMN dysfunction causes MDD or vice versa, but the correlation is strong in many studies. This is likely why both non-pharmacologic and pharmacologic interventions that decrease DMN activity also improve depressive symptoms.
Non-Pharmacologic Manipulation of the DMN
Do you meditate? The practice of meditation has significant mental health benefits and is known to reduce activity in the DMN. Monitoring the activity of the DMN may also serve as a useful biomarker for assessing the impact of meditation practices [15,16]. There are many ways to meditate. Dr. Ted’s favorite (and easy way to start) is to find a quiet place, close your eyes, and observe your thoughts arise and pass. Try it for 30 seconds, and then a minute, and then 10.
Do you flow? The DMN is also implicated in "flow states" – the mental state when we are in full task engagement. During flow states, there are low levels of self-referential thinking , and activity in regions of the DMN is reduced (mFC and amygdala) when compared to conditions of boredom or overload .
Do you exercise? Exercise also decreases DMN activity. Maybe that’s why many studies have shown that exercise works just as well as antidepressant medications for many people!
The Influence of Psychedelics on the DMN
Research has shown that psilocybin (the psychedelic compound found in "magic mushrooms") brings about profound changes in consciousness in humans . Using functional MRI, scientists have noted decreased blood flow, and therefore brain activity, in hub regions including the thalamus as well as anterior and posterior cingulate cortex. The magnitude of the decreased activity was related to the intensity of the subjective effects of psilocybin, suggesting that the decreased activity and connectivity in the DMN brings about a state of unconstrained cognition .
Other psychedelics have also been investigated within the context of the DMN. Lysergic acid diethylamide (LSD or "acid") administration decreased connectivity between the parahippocampus and retrosplenial cortex, which was associated with ratings of "ego-dissolution" and "altered meaning," suggesting that this circuit is responsible in part for the maintenance of "self" or "ego" , as detailed above.
Here at Troscriptions, we define enlightenment as freedom from the illusion of the self. And we mean "the self" as a verb and not a noun… in that you are “selfing” all the time (stories, programs, thoughts, feelings, emotions). And the seat of all this “selfing” is happening in the DMN!
So what we do is provide enlightenment cheat codes (i.e., buccal troches) that drop you into flow (Blue Cannatine), relieve stress/tension/anxiousness (Tro Calm), and energize your mitochondria (Just Blue).
And we have more on the way!
 R.L. Buckner, J.R. Andrews-Hanna, D.L. Schacter, The brain’s default network: anatomy, function, and relevance to disease, Ann N Y Acad Sci. 1124 (2008) 1–38. https://doi.org/10.1196/annals.1440.011.
 J.R. Andrews-Hanna, J. Smallwood, R.N. Spreng, The default network and self-generated thought: component processes, dynamic control, and clinical relevance, Ann N Y Acad Sci. 1316 (2014) 29–52. https://doi.org/10.1111/nyas.12360.
 Y. Yeshurun, M. Nguyen, U. Hasson, The default mode network: where the idiosyncratic self meets the shared social world, Nat Rev Neurosci. 22 (2021) 181–192. https://doi.org/10.1038/s41583-020-00420-w.
 R.L. Buckner, D.C. Carroll, Self-projection and the brain, Trends Cogn Sci. 11 (2007) 49–57. https://doi.org/10.1016/j.tics.2006.11.004.
 J.R. Andrews-Hanna, The brain’s default network and its adaptive role in internal mentation, Neuroscientist. 18 (2012) 251–270. https://doi.org/10.1177/1073858411403316.
 V. Kiviniemi, J.-H. Kantola, J. Jauhiainen, A. Hyvärinen, O. Tervonen, Independent component analysis of nondeterministic fMRI signal sources, Neuroimage. 19 (2003) 253–260. https://doi.org/10.1016/s1053-8119(03)00097-1.
 M.E. Raichle, The brain’s dark energy, Sci Am. 302 (2010) 44–49. https://doi.org/10.1038/scientificamerican0310-44.
 R.N. Spreng, E. Dimas, L. Mwilambwe-Tshilobo, A. Dagher, P. Koellinger, G. Nave, A. Ong, J.M. Kernbach, T.V. Wiecki, T. Ge, Y. Li, A.J. Holmes, B.T.T. Yeo, G.R. Turner, R.I.M. Dunbar, D. Bzdok, The default network of the human brain is associated with perceived social isolation, Nat Commun. 11 (2020) 6393. https://doi.org/10.1038/s41467-020-20039-w.
 C. Higgins, Y. Liu, D. Vidaurre, Z. Kurth-Nelson, R. Dolan, T. Behrens, M. Woolrich, Replay bursts in humans coincide with activation of the default mode and parietal alpha networks, Neuron. 109 (2021) 882-893.e7. https://doi.org/10.1016/j.neuron.2020.12.007.
 T.J. Akiki, C.L. Averill, K.M. Wrocklage, J.C. Scott, L.A. Averill, B. Schweinsburg, A. Alexander-Bloch, B. Martini, S.M. Southwick, J.H. Krystal, C.G. Abdallah, Default mode network abnormalities in posttraumatic stress disorder: A novel network-restricted topology approach, Neuroimage. 176 (2018) 489–498. https://doi.org/10.1016/j.neuroimage.2018.05.005.
 G.E. Doucet, D. Janiri, R. Howard, M. O’Brien, J.R. Andrews-Hanna, S. Frangou, Transdiagnostic and disease-specific abnormalities in the default-mode network hubs in psychiatric disorders: A meta-analysis of resting-state functional imaging studies, Eur. Psychiatr. 63 (2020) e57. https://doi.org/10.1192/j.eurpsy.2020.57.
 M.D. Greicius, G. Srivastava, A.L. Reiss, V. Menon, Default-mode network activity distinguishes Alzheimer’s disease from healthy aging: Evidence from functional MRI, Proc. Natl. Acad. Sci. U.S.A. 101 (2004) 4637–4642. https://doi.org/10.1073/pnas.0308627101.
 J.P. Hamilton, D.J. Furman, C. Chang, M.E. Thomason, E. Dennis, I.H. Gotlib, Default-Mode and Task-Positive Network Activity in Major Depressive Disorder: Implications for Adaptive and Maladaptive Rumination, Biological Psychiatry. 70 (2011) 327–333. https://doi.org/10.1016/j.biopsych.2011.02.003.
 Y.I. Sheline, D.M. Barch, J.L. Price, M.M. Rundle, S.N. Vaishnavi, A.Z. Snyder, M.A. Mintun, S. Wang, R.S. Coalson, M.E. Raichle, The default mode network and self-referential processes in depression, Proc. Natl. Acad. Sci. U.S.A. 106 (2009) 1942–1947. https://doi.org/10.1073/pnas.0812686106.
 R. Simon, M. Engstrom, The default mode network as a biomarker for monitoring the therapeutic effects of meditation, Front. Psychol. 06 (2015). https://doi.org/10.3389/fpsyg.2015.00776.
 K.A. Garrison, T.A. Zeffiro, D. Scheinost, R.T. Constable, J.A. Brewer, Meditation leads to reduced default mode network activity beyond an active task, Cogn Affect Behav Neurosci. 15 (2015) 712–720. https://doi.org/10.3758/s13415-015-0358-3.
 D. van der Linden, M. Tops, A.B. Bakker, The Neuroscience of the Flow State: Involvement of the Locus Coeruleus Norepinephrine System, Front. Psychol. 12 (2021) 645498. https://doi.org/10.3389/fpsyg.2021.645498.
 M. Ulrich, J. Keller, K. Hoenig, C. Waller, G. Grön, Neural correlates of experimentally induced flow experiences, NeuroImage. 86 (2014) 194–202. https://doi.org/10.1016/j.neuroimage.2013.08.019.
 R.L. Carhart-Harris, D. Erritzoe, T. Williams, J.M. Stone, L.J. Reed, A. Colasanti, R.J. Tyacke, R. Leech, A.L. Malizia, K. Murphy, P. Hobden, J. Evans, A. Feilding, R.G. Wise, D.J. Nutt, Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin, Proc Natl Acad Sci U S A. 109 (2012) 2138–2143. https://doi.org/10.1073/pnas.1119598109.
 R.L. Carhart-Harris, S. Muthukumaraswamy, L. Roseman, M. Kaelen, W. Droog, K. Murphy, E. Tagliazucchi, E.E. Schenberg, T. Nest, C. Orban, R. Leech, L.T. Williams, T.M. Williams, M. Bolstridge, B. Sessa, J. McGonigle, M.I. Sereno, D. Nichols, P.J. Hellyer, P. Hobden, J. Evans, K.D. Singh, R.G. Wise, H.V. Curran, A. Feilding, D.J. Nutt, Neural correlates of the LSD experience revealed by multimodal neuroimaging, Proc Natl Acad Sci U S A. 113 (2016) 4853–4858. https://doi.org/10.1073/pnas.1518377113.