Some behavioral problems seem to plague compulsive overeaters and substance abusers more than other groups. Excess attention seeking appears to be one of them. All humans require attention. Without getting and giving attention, you could not have a social species. Getting attention is necessary for life’s vital enterprises and can be the difference between life and death in a crisis. Therefore, not getting adequate attention can threaten the quality and sustainability of life.  Thus, getting functional social attention is understandable. However, extreme attention seekers go to unhealthy lengths that are driven by emotional desperation.
Excessive attention seeking is not a character flaw. It is a brain wiring response to early developmental trauma caused by neglect. The developing brain observes its environment and wires itself accordingly to survive in that world that it presumes will be like those experiences. Newborns are extremely dependent on getting their mother’s attention for survival. The more their needs are neglected during early development the more the child equates getting attention with survival and safety. In turn, the more he or she develops the belief system that it is necessary to go to whatever lengths to get attention.
How excessive attention seeking evolves in adults
Brains wired to equate lack of attention as dangerous, naturally respond to it as threat in the amygdala, a subcortical structure, where thinking does not occur. [6-11] Now the anterior cingulate cortex (ACC), which is like a micromanaging mother, “don’t do this, do that, stop that, go here, don’t go there” can intervene in this, if given the opportunity.[12-16] But as my friend Greg says, “If a dog had wings, he wouldn’t be a dog.” The ACC is in the cortical thinking part of the brain, which disengages when the amygdala swings into action.[12, 17-21] In addition, the ACC needs serotonin to do its micromanaging. There are a number of conceivable problems with that: people who have these types of core issues are often over stressed. Sustained excess stress limits serotonin availability.[22-25] In addition, hypothalamic remodeling is one of the consequences of neglect.[23, 26-31] This often means that your hypothalamus is smaller, and has fewer receptors for serotonin and other neurochemicals. Thus, even if your ACC has troopers to dispatch, they may not have anywhere to land and do their work.
How This Partners With Drama Addiction
The obvious answer is drama gets attention. However, it is more than that. Drama causes the pituitary gland and hypothalamus to secrete endorphins, which are the pain-suppressing and pleasure-inducing compounds, which heroin and other opiates mimic.[32-40] Hence, drama eases the anxiety of wanting more attention than you are getting. Naturally, since drama uses the same mechanisms in the brain as opiates, people can easily become addicted to drama.[41-45] Like any addiction, you build up a tolerance that continuously requires more to get the same neurochemical affect.[46-49] In the case of drama, then means you need more and more crises to get the same thrill.
There is also another factor. Using drama as a drug feels good so it is rewarding. Reward uses dopamine, the brain’s happy dance drug.[50-52] Dopamine works by releasing more dopamine on anticipating getting the reward (the way evolution gets you to want to do what you need to do).[52-54] Like all addiction, this begins as a goal-directed behavior in the ventral striatum [55-58](I’m turning on the light because I walked into a dark room and want light), which becomes a stimulus response behavior in the dorsal striatum (I am flipping the light switch because every time I walk into a dark room I automatically flip the light switch). Once this train leaves the station, you have your classic attention seeking drama queen.
Is it fixable?
No, it is not fixable in the sense that you cannot change your brain’s basic hardwiring.[4, 27, 29, 59] Nor can you completely erase the residual effects of early life trauma.[4, 23, 27] However, it is manageable. One begins by accepting who they are, and loving what they have more than what they do not have. This means even if what they have is a challenge and difficult to manage. In additon, find a person who is honest, and cares enough about you to tell you the truth, even when you do not want to hear it. You can ask this person if your emotional interpretation of a situation is over the top. Use creative outlets to lessen your baseline stress level. Meditate. Do yoga. Act as if you are not a drama queen and a compulsive attention seeker. The more you do that the more efficiently those neurons will fire. Hence, the easier that behavior will become.
I suspect the reason compulsive overeaters, alcoholics and substance abusers are more prone to excess attention seeking and drama addiction is because those populations are more likely to have endured developmental trauma. The important thing to realize here is that not all neglect is evidence of a lack of love. Sometimes, people only have so much they can give; sometimes that is not enough. There is healing in accepting that your parents did not give you as much attention as you required. Forgiving them for being who they were is getting to higher ground. Sometimes, you have to give yourself the attention you needed from parents. However, most importantly, at all times, remain fabulous and phenomenal.
Sidebar: Recently Psychology Today was named the Top Website for Psychology and I was named one of the “30 Most Influential Neuroscientists Alive.” Thank you very much. I am truly honored, and very grateful to be included on that list with such great scientists.
Images created by Dr. Gordon from Shutterstock images purchased by UCLA CNS for use and alteration by Dr. Gordon
1. Stockley, P. and J. Bro-Jorgensen, Female competition and its evolutionary consequences in mammals. Biol Rev Camb Philos Soc, 2011. 86(2): p. 341-66.
2. Angstman, K.B. and N.H. Rasmussen, Personality disorders: review and clinical application in daily practice. Am Fam Physician, 2011. 84(11): p. 1253-60.
3. Goenjian, A.K., et al., Prospective study of posttraumatic stress, anxiety, and depressive reactions after earthquake and political violence. Am J Psychiatry, 2000. 157(6): p. 911-6.
4. McEwen, B.S., Brain on stress: how the social environment gets under the skin. Proc Natl Acad Sci U S A, 2012. 109 Suppl 2: p. 17180-5.
5. Wolff, P.H., Organization of behavior in the first three months of life. Res Publ Assoc Res Nerv Ment Dis, 1973. 51: p. 132-53.
6. Williams, L.M., et al., Arousal dissociates amygdala and hippocampal fear responses: evidence from simultaneous fMRI and skin conductance recording. Neuroimage, 2001. 14(5): p. 1070-9.
7. Tupak, S.V., et al., Implicit emotion regulation in the presence of threat: neural and autonomic correlates. Neuroimage, 2014. 85 Pt 1: p. 372-9.
8. Terburg, D., et al., Hypervigilance for fear after basolateral amygdala damage in humans. Transl Psychiatry, 2012. 2: p. e115.
9. Sripada, C.S., et al., Effects of alcohol on brain responses to social signals of threat in humans. Neuroimage, 2011. 55(1): p. 371-80.
10. Pouga, L., et al., Individual differences in socioaffective skills influence the neural bases of fear processing: the case of alexithymia. Hum Brain Mapp, 2010. 31(10): p. 1469-81.
11. Novembre, G., M. Zanon, and G. Silani, Empathy for social exclusion involves the sensory-discriminative component of pain: a within-subject fMRI study. Soc Cogn Affect Neurosci, 2014.
12. Zhang, G., et al., Functional alteration of the DMN by learned regulation of the PCC using real-time fMRI. IEEE Trans Neural Syst Rehabil Eng, 2013. 21(4): p. 595-606.
13. Yanagisawa, K., et al., Does higher general trust serve as a psychosocial buffer against social pain? An NIRS study of social exclusion. Soc Neurosci, 2011. 6(2): p. 190-7.
14. Williams, L.M., et al., Trauma modulates amygdala and medial prefrontal responses to consciously attended fear. Neuroimage, 2006. 29(2): p. 347-57.
16. Turner, B.M., et al., The cerebellum and emotional experience. Neuropsychologia, 2007. 45(6): p. 1331-41.
17. Strauss, M.M., et al., fMRI of sensitization to angry faces. Neuroimage, 2005. 26(2): p. 389-413.
18. Radua, J., et al., Common and specific brain responses to scenic emotional stimuli. Brain Struct Funct, 2014. 219(4): p. 1463-72.
20. Guhn, A., et al., Medial prefrontal cortex stimulation modulates the processing of conditioned fear. Front Behav Neurosci, 2014. 8: p. 44.
21. Gasic, G.P., et al., BDNF, relative preference, and reward circuitry responses to emotional communication. Am J Med Genet B Neuropsychiatr Genet, 2009. 150B(6): p. 762-81.
22. Tannenbaum, B., et al., Neurochemical and behavioral alterations elicited by a chronic intermittent stressor regimen: implications for allostatic load. Brain Res, 2002. 953(1-2): p. 82-92.
23. McEwen, B.S., Early life influences on life-long patterns of behavior and health. Ment Retard Dev Disabil Res Rev, 2003. 9(3): p. 149-54.
24. Jones, T. and M.D. Moller, Implications of hypothalamic-pituitary-adrenal axis functioning in posttraumatic stress disorder. J Am Psychiatr Nurses Assoc, 2011. 17(6): p. 393-403.
25. Beauchaine, T.P., et al., The effects of allostatic load on neural systems subserving motivation, mood regulation, and social affiliation. Dev Psychopathol, 2011. 23(4): p. 975-99.
26. McEwen, B.S. and P.J. Gianaros, Stress- and allostasis-induced brain plasticity. Annu Rev Med, 2011. 62: p. 431-45.
27. McEwen, B.S. and P.J. Gianaros, Central role of the brain in stress and adaptation: links to socioeconomic status, health, and disease. Ann N Y Acad Sci, 2010. 1186: p. 190-222.
28. McEwen, B.S., Commentary: the ever-changing brain. Neuropsychopharmacology, 2001. 25(6): p. 797-8.
29. McEwen, B.S., Stress and hippocampal plasticity. Annu Rev Neurosci, 1999. 22: p. 105-22.
30. McEwen, B.S., Hormones and the plasticity of neurons. Clin Neuropharmacol, 1992. 15 Suppl 1 Pt A: p. 582A-583A.
31. McEwen, B.S., Physiology and neurobiology of stress and adaptation: central role of the brain. Physiol Rev, 2007. 87(3): p. 873-904.
32. Spulber, S., T. Bartfai, and M. Schultzberg, IL-1/IL-1ra balance in the brain revisited - evidence from transgenic mouse models. Brain Behav Immun, 2009. 23(5): p. 573-9.
33. Fonseca-Pedrero, E., et al., Cluster B maladaptive personality traits in Spanish adolescents. Rev Psiquiatr Salud Ment, 2013. 6(3): p. 129-38.
34. Brinon, J.G., et al., Bilateral olfactory deprivation reveals a selective noradrenergic regulatory input to the olfactory bulb. Neuroscience, 2001. 102(1): p. 1-10.
35. Zhang, T.A., et al., Synergistic effects of the peptide fragment D-NAPVSIPQ on ethanol inhibition of synaptic plasticity and NMDA receptors in rat hippocampus. Neuroscience, 2005. 134(2): p. 583-93.
36. Yau, Y.H. and M.N. Potenza, Stress and eating behaviors. Minerva Endocrinol, 2013. 38(3): p. 255-67.
37. Xu, W., et al., L-isocorypalmine reduces behavioral sensitization and rewarding effects of cocaine in mice by acting on dopamine receptors. Drug Alcohol Depend, 2013. 133(2): p. 693-703.
38. Wolf, M.E., The role of excitatory amino acids in behavioral sensitization to psychomotor stimulants. Prog Neurobiol, 1998. 54(6): p. 679-720.
39. Volkow, N.D. and R.D. Baler, Addiction science: Uncovering neurobiological complexity. Neuropharmacology, 2014. 76 Pt B: p. 235-49.
40. Van Ree, J.M., Endorphins and experimental addiction. Alcohol, 1996. 13(1): p. 25-30.
42. Peregud, D.I., et al., Changes in anxiety in abstinence correlate with the state of the nigrostriatal system in the rat hippocampus. Neurosci Behav Physiol, 2008. 38(5): p. 443-8.
43. Mao, L., et al., Group III metabotropic glutamate receptors and drug addiction. Front Med, 2013. 7(4): p. 445-51.
44. Garcia-Fuster, M.J., et al., Regulation of the extrinsic and intrinsic apoptotic pathways in the prefrontal cortex of short- and long-term human opiate abusers. Neuroscience, 2008. 157(1): p. 105-19.
45. Dejean, C., T. Boraud, and C. Le Moine, Opiate dependence induces network state shifts in the limbic system. Neurobiol Dis, 2013. 59: p. 220-9.
46. Tops, M., et al., Why social attachment and oxytocin protect against addiction and stress: Insights from the dynamics between ventral and dorsal corticostriatal systems. Pharmacol Biochem Behav, 2014. 119: p. 39-48.
47. Rothwell, P.E., S. Kourrich, and M.J. Thomas, Environmental novelty causes stress-like adaptations at nucleus accumbens synapses: implications for studying addiction-related plasticity. Neuropharmacology, 2011. 61(7): p. 1152-9.
48. Lloyd, D.R., et al., Habituation of reinforcer effectiveness. Front Integr Neurosci, 2014. 7: p. 107.
49. De Luca, M.A., Habituation of the responsiveness of mesolimbic and mesocortical dopamine transmission to taste stimuli. Front Integr Neurosci, 2014. 8: p. 21.
50. Yin, H.H., S.B. Ostlund, and B.W. Balleine, Reward-guided learning beyond dopamine in the nucleus accumbens: the integrative functions of cortico-basal ganglia networks. Eur J Neurosci, 2008. 28(8): p. 1437-48.
51. Wise, R.A. and P.P. Rompre, Brain dopamine and reward. Annu Rev Psychol, 1989. 40: p. 191-225.
52. Wise, R.A. and M.A. Bozarth, Brain reward circuitry: four circuit elements "wired" in apparent series. Brain Res Bull, 1984. 12(2): p. 203-8.
53. Wise, R.A., Dual roles of dopamine in food and drug seeking: the drive-reward paradox. Biol Psychiatry, 2013. 73(9): p. 819-26.
54. Wise, R.A., Brain reward circuitry: insights from unsensed incentives. Neuron, 2002. 36(2): p. 229-40.
55. Root, D.H., et al., Absence of cue-evoked firing in rat dorsolateral striatum neurons. Behav Brain Res, 2010. 211(1): p. 23-32.
56. Packard, M.G., et al., Task-dependent role for dorsal striatum metabotropic glutamate receptors in memory. Learn Mem, 2001. 8(2): p. 96-103.
58. Michaelides, M., et al., Translational neuroimaging in drug addiction and obesity. ILAR J, 2012. 53(1): p. 59-68.
59. McEwen, B.S., Hormones as regulators of brain development: life-long effects related to health and disease. Acta Paediatr Suppl, 1997. 422: p. 41-4.