I am familiar with desensitization. For example, if you are afraid of driving, driving every day will eventually reduce your fear, desensitizing you.

But today I came across another concept, that of sensitization. I looked up the wiki article on Sensitization, which says at the end,

Sensitization may also contribute to psychological disorders such as post-traumatic stress disorder, panic anxiety and mood disorders.

So which is it then? What determines whether repeated exposure to something sensitizes someone or desensitizes them? With the example of PTSD, for instance, should not repeated exposure to war actually desensitize people?

I searched google scholar but could not find a paper that discusses both sensitization and desensitization. Mostly discuss the latter, in terms of reducing fears.

Appreciate any references or books that might help me understand this.

Thanks you.

  • 1
    $\begingroup$ Welcome and kudos for this great question. I stumbled upon exactly this question yesterday when reading about a related topic. $\endgroup$ – AliceD Sep 17 '18 at 7:00

The terminology in this area can be a source of confusion because sensitization is not usually meant as the opposite of desensitization but of habituation. E.g., Blumstein (2016)

People have written about habituation, a process that leads to decreased responsiveness to a stimulus, as well as its counterpart, sensitization, or an increased responsiveness to a stimulus, for over 2000 years.

So what's desensitization then? Well...

Systematic desensitization is basically an extinction procedure for (assumed) previously conditioned stimuli:

Behavior therapy employs interventions based on classical and operant conditioning. An early example is Wolpe’s (1954) systematic desensitization in which patients are taught progressive relaxation techniques and then are systematically exposed to stimuli that elicit fear while in a relaxed state. Because the relaxation response is incompatible with anxiety, it weakens the learned association between a stimulus and an anxiety response.

And desensitization is often taken to mean the roughly the same as the systematic one, e.g. Clay (2007):

Desensitization is generally described as a process by which the active pairing of a positive reinforcer with a negative event causes the negative event to slowly lose its ability to adversely influence behavior (Chance, P., 2003). This active process is also called counter-conditioning. Systematic desensitization has been used successfully to treat human phobias, such as fear of flying, fear of public speaking, and fear of spiders, and has also been used to reduce the intensity of Post-Traumatic Stress Disorder in veterans of the Vietnam War (Chance, P., 2003). For animals, a similarly competing response could be eating. Using competing responses to interfere with a fearful response is an integral part of the systematic desensitization process as defined by Wolpe (1958, as cited by Callen, E.J., & Boyd, T.L., 1990).

To add to this confusion, some mean by sensitization only the conditioned version, e.g.

Sensitization occurs when a reaction to a stimulus causes an increased reaction to a second stimulus. It is essentially an exaggerated startle response and is often seen in trauma survivors.

But this is actually not that wrong, because unlike for habituation, it's hard to come up with many examples of unconditioned sensitization, e.g. what does Blumstein give (for both)?

Habituation is a process that leads to decreased responsiveness to a stimulus with repeated presentation and is often adaptive in that it makes it less likely that individuals will respond to harmless stimuli. Found throughout the animal kingdom, some plants have also been shown to habituate (Jensen, Dill, & Cahill, 2011). However, habituation may also have consequences. Aesop recognized the consequences of habitation 2500 years ago when he noted that the boy who cried wolf would ultimately be ignored when he needed help to fend off a real wolf.

Habituation's counterpart is sensitization--the increased responsiveness to a stimulus with repeated presentation. Sensitization may be adaptive if it helps animals avoid potentially risky or costly situations. Being sensitized to the sound of bees may help elephants avoid getting their sensitive trunks stung (sensu King, Douglas-Hamilton, & Vollrath, 2007), and may help allergic humans avoid an anaphylactic reaction. But it too may be costly. For instance, while drug addiction is usually thought to involve some degree of tolerance to drugs, indeed, it also involves sensitized responses that can be used diagnostically because greater salience is attached to the drugs and drug-associated cues (Steketee & Kalivas, 2011). Living without risk is impossible (Sagarin et al., 2010), and the public may become sensitized to real or manufactured threats repeated by the press (e.g. consider the U.S. government assertions that Iraq had weapons of mass destruction, or the American response to Ebola cases being treated in the United States in September--November 2014). Over-reacting to risk can lead to costly foreign policy mis-steps and costly public health responses.

Somewhat more interesting examples are given by Çevik (2014)

The signal value of a stimulus is correlated with its potential to support responsiveness, which for a given set of physical parameters depends largely on the history of non-associative learning, i.e., habituation and sensitization for the stimulus. Habituation refers to the reduction in the probability or amplitude of responding that is observed upon inconsequential stimulus repetition. For example, repeated delivery of an odor at constant inter-stimulus-intervals (ISI) would eventually lead to the habituation of the response that is initially triggered by the odor. I say eventually, because depending on the parameters of the stimulation protocol (e.g., odor concentration, frequency of odor presentation), a temporary increment in responsiveness might initially be observed. If, however, an appetitive gustatory stimulus (e.g., sugar) is repeated with the same ISI, depending again on the concentration of sugar, frequency of stimulation, and the physiological state of the organism, this protocol is likely to result in an increment in the probability of responding, i.e., sensitization. Finally if odor and sugar are paired instead of being presented separately, the standard paradigm for Pavlovian conditioning would ensue, where the two stimuli would now be termed conditioned (CS) and unconditioned stimuli (US), respectively. Hence, associative learning can be suggested to entail an evasion from habituation for the CS as it signals the arrival of a sensitizing event, the US, and a conditioned response (CR) would then be triggered during the CS in anticipation of the US.

And he actually proposes some general rules:

habituation might be the default fate for most stimuli in the absence of top-down modulation (although see Horn and Hinde, 1970 for examples of non-habituating reflexes). [...]

the likelihood of habituation, i.e., the inability of a perceivable stimulus to control behavior is higher for distal stimuli, whereas the likelihood of sensitization is higher for stimuli that come into direct contact with the body to activate gustatory and/or mechanoreceptors.

Although his rules are derived from research on flies.

The wiki sensitization page you mention doesn't talk of PTSD as far as I can tell.

From what I know of PTSD research in this area, it involves conditioned stimuli, e.g. a fairly cited paper in this line, Orr et al.:

Differential conditioning was assessed in 15 medication-free individuals meeting Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994) criteria for chronic posttraumatic stress disorder (PTSD) and 18 trauma-exposed individuals who never developed PTSD (non-PTSD). Conditioned stimuli (CSs) were colored circles, and the unconditioned stimulus was a "highly annoying" electrical stimulus. Individuals with PTSD had higher resting heart rate (HR) and skin conductance (SC) levels and produced larger SC orienting responses. During conditioning, the PTSD group showed larger differential SC, HR, and electromyogram responses to the reinforced vs. nonreinforced stimuli (CS+ vs. CS-) compared with the non-PTSD group. Only PTSD participants continued to show differential SC responses to CS+ vs. CS- during extinction trials. Results suggest that individuals with PTSD have higher sympathetic nervous system arousal at the time of conditioning and are more conditionable than trauma-exposed individuals without PTSD.

In that paper, PTSD patients were harder to de-condition or "desensitize" to use your terminology (see the sentence about extinction in the abstract I quoted above); PTSD patients also showed increased responses (compared to controls) to conditioned stimuli after conditioning took place, although as far as I can tell they were not easier to "sensitize"/condition, at least in that experiment.

The interaction between conditioned and unconditioned exposures to a stressful stimulus is fairly complex (even in animal [models]) and assumed to be of importance in PTSD. It's been known for a long time (Rescorla, 1974) that giving stronger unconditioned footshocks to rats increases their conditioned response to moderate footshock. So this is a kind of sensitization when conditional and unconditional effects interact. A more recent line of work on this interaction:

Rats presented with a single session of repeated painful footshocks normally express a robust and persistent associative fear of the training context (Gale et al., 2004; Poulos et al., 2009), whereas subsequent new fear learning to a single footshock of the same intensity becomes sensitized to a newly trained context or a tone (Rau et al., 2005). We call this phenomenon stress-enhanced fear learning (SEFL). Pharmacologically induced (NMDA antagonism) and naturally occurring (preweaned pups) amnesia of the repeated footshock context fail to disrupt this sensitized fear learning (Rau et al., 2005; Long & Fanselow, 2012; Poulos et al., 2013). These results suggest that prior exposure to a repeated footshock stress, independent of a contextual fear memory, enhances subsequent fear learning when footshock intensity is held constant. Further evidence that stress influences future learning and does not produce its effect by generalization between the stress and conditioning contexts is that SEFL only occurs when the stress occurs prior to the one-trial fear conditioning (Rau et al., 2005). [...]

SEFL would be a particularly problematic component of posttrauma behavior if intense stress results in substantial fear conditioning under conditions that would not normally support conditioning. Therefore, we determined if SEFL occurred when the conditioning shock was substantially milder than the SEFL-inducing shock. The results indicate that exposure to a sensitizing regimen of shock can convert a mild footshock that normally does not support measurable levels of fear conditioning into one that causes substantial learned fear. Moreover, as the intensity of single footshock increases, so does the capacity of the prior stressor to contribute to the sensitization of fear responses.

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Introduction to my answer

The subject of PTSD and its triggers is huge, and this answer is not an alternative, but an addition to @Fizz's good answer to this question.

The causes of PTSD @Fizz talked about are through prolonged timeframes of trauma (sensitisation through fear conditioning coming into play over a long period of time). This can involve soldiers who have been in combat situations whereby they have constantly witnessed attrocities, but not necessarily.

PTSD can also occur with hypersensitisation caused by a single instance of an initial sensitising event (ISE), again such as a particular event in combat, or through other physical violence with perceived or actual threat to life or physical wellbeing.

Desensitisation will be the process involved to resolve the hypersensitisation effects caused by the ISE and subsequent neurological and biological reactions to the ISE.

So to your question in summary

What determines whether repeated exposure to something sensitizes someone or desensitizes them?

Sensitisation doesn't just involve trauma leading to fear, but it can involve an ISE, or prolonged exposure to situations which leads to any irrational emotion. Disgust is one other example.

Desensitisation is the complete opposite. Desensitisation is where an event, or series of events, lowers inhibition towards something which would normally raise feelings of fear, disgust etc.

More detail on what I am talking about

Examples of single instances of ISE

Take a soldier in combat who is under constant heavy gunfire and "hell is raining down on everyone around them". Fellow soldiers in their troops are killed in the process, and maybe they have come close themselves. Maybe they have lost a limb from a mortar bomb explosion. This can be one ISE which on its own causes PTSD.

Take a man/woman who is threatened with their life and raped at knife/gunpoint. Again, this ISE alone can cause PTSD.

Initial Sensitising Events (ISEs)

The science behind ISEs is as follows

As a therapist I consider not only the how the memory (or gestalt) was encoded during a Initial Sensitizing Event (ISE), but what effect that the event had and has on the person both physiologically and mentally. If the event is traumatic enough to cause stress, the fight and flight defense mechanism will lead to increased cortisol flow, IL-6 fluctuations, and eventual adrenal fatigue. Mentally/Neurologically, dominant "brain maps" may be created, which perpetuate an overactive anterior cingulate (ACG), result in a continual looping (such as in PSTD) and create further mental dysfunction as the ACG will compete for energy resources (hemoglobin and oxygen, specifically).

Let's have a breakdown of what was said in the quote

The fight and flight mechanism

A more in depth rundown on this (what I call the 5F response — fright/flight/fight/freeze/fawn) can be found in my answer to Understanding fear as a response in classical conditioning, but in short, the 5F response is an unconscious reflex to perceived threats, initiated from Threat → Brain Receiving Signals → Brain Reacts (Fright) → Cortisol and Adrenaline is released → Physical Reactions occur from the release of hormones → Bodily response (Fight, Flight, Freeze or Fawn)

Fight Flight Response
(Source: Wikipedia)

Adrenaline and Cortisol Release

As you can see within the infographic above, the brain initially processes the threat signal in the amygdala and then the hypothalamus and the pituitary gland secretes adrenocortictropic hormone (ACTH) which leads to cortisol and adrenaline release to enable a speedy escape if chosen.

IL-6 (Interleukin 6) fluctuations

Based on the Wikipedia link I provided, the epigenetic effects of IL-6 have been implicated in the pathology of depression. The effects of IL-6 on depression are mediated through the repression of brain-derived neurotrophic factor (BDNF) expression in the brain; DNMT1 (DNA (cytosine-5)-methyltransferase 1) hypermethylates the BDNF promoter and reduces BDNF levels (Sharma, et al. 2008). Altered BDNF function has been implicated in depression (Hwang, et al. 2006), which is likely due to epigenetic modification following IL-6 upregulation (Sharma, et al. 2008).

The Anterior Cingulate Cortex (ACG)

The ACG is responsible for detecting incongruences between expectation and perceived experience (Somerville, et al. 2006). Altered connectivity of the anterior cingulate cortex in depression, therefore, may cause altered emotions following certain experiences, leading to depressive reactions (Somerville, et al. 2006). This altered connectivity is mediated by IL-6 and its effect on epigenetic regulation of BDNF (Sharma, et al. 2008).


This will be a slow process. As @Fizz quoted,

Desensitization is generally described as a process by which the active pairing of a positive reinforcer with a negative event causes the negative event to slowly lose its ability to adversely influence behavior (Chance, P., 2003).

also called counter-conditioning.

Desensitisation for PTSD whether caused through trauma over prolonged timeframes or one single instance of ISE, can be obtained through therapy of many different types. Therapy may also be supported through medication to alleviate symptoms such as anxiety and depression.

CBT has been the go-to form of therapy within services linked to the program called Improving Access to Psychological Therapies (IAPT), but it does have its limitations. Whatever method of therapy is employed (CBT, REBT, Person Centred Therapy...), the therapy at some point will have to enable the person who is suffering from PTSD to re-evaluate their perceptions of what constitutes a threat to their personal safety.

Initially, they will have to look at what startles them (what are their triggers), evaluate where those triggers came from and look at how they can form rational thought patterns when they arise again.

Take for example, a veteran of war. When carying out routine patrols of hostile areas, they will have had to have a constant awareness of their surroundings, assessing who or what could consitute a threat. Once they are suffering the severe effects of war, they could have a hightened sense of alertness which carries forward into civilian life at home outside of war. If there is a sound of a car backfiring, in extreme cases, this can lead to a sudden reaction which can leave that person feeling very vulnerable.

This war veteran will need to be able to immediately determine that they are not in a hostile situation and in fact the loud bang was just a car backfiring (desensitising against loud bangs to a safe and rational level). It is likely that these situations (loud bangs) will not be the only trigger, and the others will need identifying and resolving.


Chance, P. (2003). Learning and behavior, Fifth Edition. CA:Wadsworth Publishing.

Hwang, J. P., Tsai, S. J., Hong, C. J., Yang, C. H., Lirng, J. F., & Yang, Y. M. (2006). The Val66Met polymorphism of the brain-derived neurotrophic-factor gene is associated with geriatric depression. Neurobiology of aging, 27(12), 1834-1837. doi: 10.1016/j.neurobiolaging.2005.10.013

Sharma, R. P., Tun, N., & Grayson, D. R. (2008). Depolarization induces downregulation of DNMT1 and DNMT3 in primary cortical cultures. Epigenetics, 3(2), 74-80. doi: 10.4161/epi.3.2.6103

Somerville, L. H., Heatherton, T. F., & Kelley, W. M. (2006). Anterior cingulate cortex responds differentially to expectancy violation and social rejection. Nature neuroscience, 9(8), 1007. doi: 10.1038/nn1728

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