Become a Health and Happiness Addict

Overwriting self-demoting neurosignatures

Posted Jun 17, 2014

The brain uses complex patterns of nerve cell firings and chemical releases to represent sensory experiences, thoughts, feelings, attitudes, beliefs, memories and imagination called neurosignatures.1,2 Every human life-event is associated with its unique and distinct neurosignature.1 Understanding how neurosignatures work is key in understanding the challenges compulsive and emotional eaters face. 

There are two types of neurosignatures: top-down and bottom-up.1 In bottom-up neurosignatures, your five senses cause various ligands (think of them as specific keys), to insert themselves (chemo taxis) into specific matching locks on the surface of the cell (receptor sites).3 Biochemists call this binding. Thus, binding-status describes which keys are in which locks at a given time. Binding-status initiates the processes that send signals from sensory receptors to the brain, where they blend with accumulative thought, memory and feeling.1,2,4,5  This process causes a unique and distinct pattern of nerve cell firing and chemical release, which creates a distinct and unique neurosignature. Neuroscientists call this type of neurosignature creation bottom-up because external cues travels from the body up to the brain.1 Top-down is the second way we create neurosignatures. This occurs when one imagines or recalls an event. Neuroscientists call these top-down neurosignatures because they travel from the brain down to the human body. Top-down neurosignatures cause the release of chemical messenger molecules and nerve cell firing patterns that change the binding status of ligands and receptors on the surface of the cell.3 Thus, metaphorically speaking, the brain reaches down and puts different keys in different locks.

Good News and Bad News

Creating a neurosignature is similar to drawing a line on a piece of paper in ink. Thus, you cannot erase a neurosignature.1 However, you can overwrite one in the same manner one might change an upper case cursive “D” into a “B.”  Furthermore, once your brain creates a neurosignature for an event, every time it experiences another event that is similar or reminiscent of the original event, it creates a new distinct neurosignature.1 Not only that, it evokes the original neurosignature as well, making it more robust. Now think in terms of the ink lines on the paper. If the ink line on the paper is a negative behavior or traumatic event, the more robust it becomes, the harder it becomes to overwrite. Hence, eventually, it may become impossible to turn that “D” into a “B.”

In addition, research has found that the human body cannot tell the difference between a real event and a vividly imagined event.6-9 Thus, whether the neurosignature is top-down or bottom-up, the pattern of nerve cell firing and chemical release is similar. Dr. Kosslyn and colleagues found that there were no differences between regional brain activation of subjects in response to actual or vividly imagined events in a Positron Emission Tomography (PET) study.6 This demonstrates how powerful neurosignatures are in dictating how the human mind and body influence each other. 

This is potentially good and/or bad. On a positive note, you can use mindfulness to overwrite negative neurosignatures, by continuously re-creating positive top-down neurosignatures. On the bad side, people with self-demoting behaviors are more likely to strengthen negative neurosignatures more so than overwrite them.10-13

For example, compulsive overeaters report more early life trauma than normal eaters do.11,14-16 Every time a person experiences an event that is identical, similar or reminiscent of his or her early life trauma, he or she relives that early life trauma exponentially in the creation of a new neurosignature and the thickening of older ones. We know the brain prefers familiarity. For example, abused children often choose abusive adult situations because the change-resistant brain is more comfortable with a familiar abusive environment than an unfamiliar healthy one.17 Likewise, the underlying behaviors that drive compulsive eating are more desirable to our brains because they are familiar. What is the solution?

Seemingly, the solution is proactive creation of healthy top-down neurosignatures. Intuitively, this would begin as goal-directed behaviors projected from the pre-frontal cortex (your thoughts), to the dorsal striatum (part of the reward circuitry) and repetition would result in healthier stimulus-response behaviors in dorsal striatum. Regrettably, compulsive overeaters seldom think their way out of self-demoting behaviors.18,19 However, we may be able to party our way out. Say what?

Unlike the prefrontal cortex, when the ventral striatum generates goal-directed behavior, dopamine releases, making the dorsal striatum more likely to repeat the action in the future.20-23 This is because both the ventral and dorsal striatum love dopamine (the brain’s happy dance drug).24-26 However, in the dorsal striatum, dopamine initiates action, but in the ventral striatum, it signals reward.21,27 That is because the nucleus accumbens, the capital of the brain’s reward system lies in the ventral striatum. The nucleus accumbens is addiction’s hometown.28-32

Incentive salience, your brain’s reward utility, is the key component of addiction.33-35 It works by using sensory cues, associated with memory or imagination, to motivate you to want to do something based on anticipating the reward of doing it. For example, imagining the reward of food, makes you want to eat, and thereby signals the impending reward of eating, causing dopamine release and structural and functional brain alterations. 36-42

Changing the brain by overwriting negative neurosignatures is the goal. Thus, the solution is difficultly simple. The simple part is appealing to the dorsal striatum via the ventral striatum as opposed to via your prefrontal cortex. 

Meaning, find healthy things you do not have to think you should do, but rather cannot wait to do because you enjoy them, subsequently making them a party. This will cause dopamine release in the ventral and dorsal striatum and you will become addicted to that behavior because that is how the neurobiology of addiction unfolds in the brain.43-48 You get more dopamine from wanting to do something than actually doing it, so you are always wanting to do it, and of course subsequently doing it. For example, if you do not like the gym, maybe you like to dance. Then forget the gym and go boogie. The difficult part is finding your healthy party behaviors. However, they are there, but only you can find them. Of course, that means paying more attention to yourself and your truths than to other people and society’s truths. Remain fabulous and phenomenal. 

Click here to like Obesely Speaking on Facebook

Click here to visit me on The Huffington Post

Click here to visti Just Billi on Dr. Gordon on line

Click here for the Billi Club (Billi Gordon Fan Page)

Click here to receive notices of new post via email

Click here to follow me on Twitter

Click here and find something surprising

Click here for Google Plus


1. Salt W. Irritable Bowel Syndrome and The Mind Body Connection.  Columbus, OH: Parkview Publsihing 2002

2. Pert CB. Molecules of Emotion. New York: Scribner Book company; 1999.

3. Pert CB, Ruff MR, Weber RJ, Herkenham M. Neuropeptides and their receptors: a psychosomatic network. J Immunol. 1985 Aug;135(2 Suppl):820s-6s.

4. Pert CB. Type 1 and type 2 opiate receptor distribution in brain--what does it tell us? Adv Biochem Psychopharmacol. 1981;28:117-31.

5. Pert CB. The wisdom of the receptors: neuropeptides, the emotions, and bodymind. 1986. Adv Mind Body Med. 2002 Fall;18(1):30-5.

6. Kosslyn SM, Thompson WL, Sukel KE, Alpert NM. Two types of image generation: evidence from PET. Cogn Affect Behav Neurosci. 2005 Mar;5(1):41-53.

7. Brown HD, Kosslyn SM, Breiter HC, Baer L, Jenike MA. Can patients with obsessive-compulsive disorder discriminate between percepts and mental images? A signal detection analysis. J Abnorm Psychol. 1994 Aug;103(3):445-54.

8. Kosslyn SM. Understanding the mind's eye...and nose. Nat Neurosci. 2003 Nov;6(11):1124-5.

9. Kosslyn SM, Behrmann M, Jeannerod M. The cognitive neuroscience of mental imagery. Neuropsychologia. 1995 Nov;33(11):1335-44.

10. McEwen BS. Protective and damaging effects of stress mediators: Central role of the brain. In: Mayer EA, Saper CB (eds). The Biological Basis for Mind Body Interactions. Amsterdam: Elsevier, 2000:25-34.

11. McEwen BS. The End Of Stress As We Know It. Washington, D.C.: Joseph Henry Press; 2002.

12. McEwen BS. Protective and damaging effects of stress mediators: central role of the brain. Dialogues Clin Neurosci. 2006;8(4):367-81.

13. McEwen BS. Stress, adaptation, and disease. Allostasis and allostatic load. Ann N Y Acad Sci. 1998 May 1;840:33-44.

14. Eiland L, McEwen BS. Early life stress followed by subsequent adult chronic stress potentiates anxiety and blunts hippocampal structural remodeling. Hippocampus. Jan;22(1):82-91.

15. McEwen BS. Brain on stress: how the social environment gets under the skin. Proc Natl Acad Sci U S A.  Oct 16;109 Suppl 2:17180-5.

16. McEwen BS. Effects of stress on the developing brain. Cerebrum.  Sep;2011:14.

17. McEwen BS. Physiology and neurobiology of stress and adaptation: central role of the brain. Physiol Rev. 2007 Jul;87(3):873-904.

18. Harris MB, Waschull S, Walters L. Feeling fat: motivations, knowledge, and attitudes of overweight women and men. Psychol Rep. 1990 Dec;67(3 Pt 2):1191-202.

19. Roefs A, Jansen A. Implicit and explicit attitudes toward high-fat foods in obesity. J Abnorm Psychol. 2002 Aug;111(3):517-21.

20. Ahn S, Phillips AG. Dopamine efflux in the nucleus accumbens during within-session extinction, outcome-dependent, and habit-based instrumental responding for food reward. Psychopharmacology (Berl). 2007 Apr;191(3):641-51.

21. Haber SN, Kim KS, Mailly P, Calzavara R. Reward-related cortical inputs define a large striatal region in primates that interface with associative cortical connections, providing a substrate for incentive-based learning. J Neurosci. 2006 Aug 9;26(32):8368-76.

22. Kienast T, Heinz A. Dopamine and the diseased brain. CNS Neurol Disord Drug Targets. 2006 Feb;5(1):109-31.

23. Mele A, Wozniak KM, Hall FS, Pert A. The role of striatal dopaminergic mechanisms in rotational behavior induced by phencyclidine and phencyclidine-like drugs. Psychopharmacology (Berl). 1998 Jan;135(2):107-18.

24. Oswald LM, Wong DF, McCaul M, et al. Relationships among ventral striatal dopamine release, cortisol secretion, and subjective responses to amphetamine. Neuropsychopharmacology. 2005 Apr;30(4):821-32.

25. Pine A, Shiner T, Seymour B, Dolan RJ. Dopamine, time, and impulsivity in humans. J Neurosci.  Jun 30;30(26):8888-96.

26. Wickens JR, Budd CS, Hyland BI, Arbuthnott GW. Striatal contributions to reward and decision making: making sense of regional variations in a reiterated processing matrix. Ann N Y Acad Sci. 2007 May;1104:192-212.

27. Tomasi D, Volkow ND. Striatocortical pathway dysfunction in addiction and obesity: differences and similarities. Crit Rev Biochem Mol Biol.  Jan-Feb;48(1):1-19.

28. Adinoff B. Neurobiologic processes in drug reward and addiction. Harv Rev Psychiatry. 2004 Nov-Dec;12(6):305-20.

29. Fattore L, Fadda P, Spano MS, Pistis M, Fratta W. Neurobiological mechanisms of cannabinoid addiction. Mol Cell Endocrinol. 2008 Apr 16;286(1-2 Suppl 1):S97-S107.

30. Filbey FM, Schacht JP, Myers US, Chavez RS, Hutchison KE. Marijuana craving in the brain. Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):13016-21.

31. Motzkin JC, Baskin-Sommers A, Newman JP, Kiehl KA, Koenigs M. Neural correlates of substance abuse: Reduced functional connectivity between areas underlying reward and cognitive control. Hum Brain Mapp.  Feb 7.

32. Redish AD, Johnson A. A computational model of craving and obsession. Ann N Y Acad Sci. 2007 May;1104:324-39.

33. Beckmann JS, Marusich JA, Gipson CD, Bardo MT. Novelty seeking, incentive salience and acquisition of cocaine self-administration in the rat. Behav Brain Res.  Jan 1;216(1):159-65.

34. Berridge KC. The debate over dopamine's role in reward: the case for incentive salience. Psychopharmacology (Berl). 2007 Apr;191(3):391-431.

35. Zhang J, Berridge KC, Tindell AJ, Smith KS, Aldridge JW. A neural computational model of incentive salience. PLoS Comput Biol. 2009 Jul;5(7):e1000437.

36. Berthoud HR, Lenard NR, Shin AC. Food reward, hyperphagia, and obesity. Am J Physiol Regul Integr Comp Physiol. Jun;300(6):R1266-77.

37. Bolstad I, Andreassen OA, Reckless GE, Sigvartsen NP, Server A, Jensen J. Aversive event anticipation affects connectivity between the ventral striatum and the orbitofrontal cortex in an fMRI avoidance task. PLoS One.8(6):e68494.

38. Flagel SB, Akil H, Robinson TE. Individual differences in the attribution of incentive salience to reward-related cues: Implications for addiction. Neuropharmacology. 2009;56 Suppl 1:139-48.

39. Ivlieva N. [Neurobiology of addictive behavior]. Zh Vyssh Nerv Deiat Im I P Pavlova.  Mar-Apr;61(2):133-50.

40. Lovic V, Saunders BT, Yager LM, Robinson TE. Rats prone to attribute incentive salience to reward cues are also prone to impulsive action. Behav Brain Res.  Oct 1;223(2):255-61.

41. Newton TF, De La Garza R, 2nd, Kalechstein AD, Tziortzis D, Jacobsen CA. Theories of addiction: methamphetamine users' explanations for continuing drug use and relapse. Am J Addict. 2009 Jul-Aug;18(4):294-300.

42. Robinson TE, Berridge KC. The psychology and neurobiology of addiction: an incentive-sensitization view. Addiction. 2000 Aug;95 Suppl 2:S91-117.

43. Caravaggio F, Raitsin S, Gerretsen P, Nakajima S, Wilson A, Graff-Guerrero A. Ventral Striatum Binding of a Dopamine D Receptor Agonist But Not Antagonist Predicts Normal Body Mass Index. Biol Psychiatry.  Mar 27.

44. Chinta SJ, Andersen JK. Dopaminergic neurons. Int J Biochem Cell Biol. 2005 May;37(5):942-6.

45. Di Chiara G. Role of dopamine in the behavioural actions of nicotine related to addiction. Eur J Pharmacol. 2000 Mar 30;393(1-3):295-314.

46. Di Chiara G. A motivational learning hypothesis of the role of mesolimbic dopamine in compulsive drug use. J Psychopharmacol. 1998;12(1):54-67.

47. Franken IH, Booij J, van den Brink W. The role of dopamine in human addiction: from reward to motivated attention. Eur J Pharmacol. 2005 Dec 5;526(1-3):199-206.

48. Gamberino WC, Gold MS. Neurobiology of tobacco smoking and other addictive disorders. Psychiatr Clin North Am. 1999 Jun;22(2):301-12.

 <a href=""" rel="nofollow" target="_blank">">Google</a> 

About the Author

Billi Gordon, Ph.D., is a co-investigator in the Ingestive Behaviors & Obesity Program, Center for the Neurobiology of Stress, David Geffen School of Medicine at UCLA.

More Posts