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Psychology
2011.
Vol.2, No.4, 382-387
Copyright © 2011 SciRes. DOI:10.4236/psych.2011.24060
Romantic Breakups, Heartbreak and Bereavement
*
—Romantic Breakups
Tiffany Field
1,2
1
Touch Research Institute, School of Medicine, University of Miami, Miami, USA;
2
Fielding Graduate University, Santa Barbara, USA.
Email: tfield@med.miami.edu
Received March 26
th
, 2011; revised May 11
th
, 2011; accepted May 20
th
, 2011.
This literature review suggests that romantic breakups may lead to bereavement symptoms including intrusive
thoughts and attempts to suppress them and insomnia as well as morbidity factors including broken heart syn-
drome and immune dysfunction. Although the broken heart syndrome has mimicked real heart attacks, an-
giograms revealed no clogged arteries or permanent heart damage. Compromised immune function may result
from reduced vagal activity and increased cortisol and catecholamines leading to increased inflammatory cyto-
kines and decreased natural killer cell activity. The model proposed here is that romantic breakups result in the
loss of a person as a regulator of stimulation and arousal modulation that can then lead to these physiological
and biochemical effects. These data highlight the complexity of romantic breakups, heartbreak and bereavement
and the need for multi-variable research on these systems both before and after the breakups occur.
Keywords: Romantic Breakups, Heartbreak, Bereavement, Social Regulators
Romantic breakups can be followed by symptoms of heart-
break and bereavement (Prigerson & Jacobs, 2001; Raphael,
Minkov, & Dobson, 2001; Davis, Shaver, & Vernon, 2003),
typically, these symptoms have been associated with a loss
from death, although they can also occur following other losses
like divorce and romantic breakups (Prigerson & Jacobs, 2001;
Davis et al., 2003).
This review of research from these different literatures sug-
gests that romantic breakups, like the losses following death or
divorce, can lead to bereavement symptoms including intrusive
thoughts, difficulty controlling intrusive thoughts and insomnia
as well as heartbreak syndrome and compromised immune
function. Studies on bereavement symptoms, heartbreak syn-
drome and immune dysfunction are followed by a summary of
research on romantic breakups and their symptoms. A potential
underlying mechanism model is then presented, suggesting that
it is the loss of the person as a regulator of stimulation and
arousal modulation that can result in physiological and bio-
chemical dysregulation including reduced vagal activity, in-
creased cortisol and catecholamines and compromised immune
function. Limitations of this literature are then suggested as
well as future research including multi-variable studies that
could assess these systems both before and after the breakups
occur.
Bereavement Symptoms
Bereavement symptoms have varied cross-culturally, with
more symptoms reported for non-Western cultures (Kleinman
& Good, 1985), and the symptoms have differed even within
religions. For example, Egyptian Muslims show intense grief,
while Muslims in Bali do not (Wikan, 1988). Contradictory
data include an international study that reported very similar
symptoms across diverse cultures (Simon, VonKorff, Piccinelli,
Fullerton, & Ormei, 1999). In that large sample study, sleep
disturbances were among the most frequently reported symp-
toms across cultures (Simon et al., 1999).
Sleep Disturbances
Sleep disturbances have been reported by as many as 43% of
bereaved subjects in one sample (Bisconti, Bergeman, & Boker,
2004), and poor sleep has been noted in bereavement-related
depression (McDermott, Prigerson, Reynolds, Houck, Dew,
Hall et al., 1997; Hardison, Neimeyer, & Lichstein, 2005). In a
study on college students, for example, insomnia was greater in
bereaved versus non-bereaved groups (22% versus 17%) (Har-
dison et al., 2005), with sleep onset insomnia being related to
nighttime ruminations about the loss, and sleep maintenance
insomnia being related to dreaming about the lost person. Ele-
vated cortisol has also contributed to poor sleep including more
REM sleep and less delta wave activity (Reynolds, Hoch,
Buysse, Houck, Schlernitzauer, Pasternak et al., 1992), al-
though it is not clear whether those EEG sleep changes pre-
ceded or followed the depression.
Intrusive Thoughts and Attempts to Control Intrusive
Thoughts
Intrusive images and attempts to control them are thought to
contribute to the insomnia associated with bereavement. In-
somnia, based on actigraphic recordings, for example, has re-
sulted from unpleasant images (Nelson & Harvey, 2002). And,
unpleasant images have been correlated with sleep onset la-
*
This research was supported by a merit Award (MH46586), NIH grants
(AT00370 and HD056036) and Senior Research Scientist Awards (MH0033
and AT0011585) and a March of Dimes Grant (12-FY03-48) to Tiffany
Field and funding from Johnson and Johnson Pediatric Institute to the Touch
Research Institute.
T. FIELD
383
tency, with more of those images related to intimate relation-
ships. Pre-sleep images have also been rated as less controllable
than pre-sleep verbal thoughts, although more disengagement
has been noted from images than verbal thoughts (Nelson &
Harvey, 2003). Negative images have also been associated with
higher heart rate, which is surprising given that negative verbal
thoughts typically elicit greater cardiovascular responses than
negative verbal images (Vrana, Cuthbert, & Lang, 1986).
Attempts to suppress the images and thoughts often lead to
dreams. In one study, participants were asked to think about a
romantic “crush” or a “non-crush” (Wegner, Wenzlaff, & Ko-
zak, 2004). Although there was no greater dreaming about the
romantic “crush,” suppression enhanced eroticism of the
“crush”. Thus, the increased accessibility of intrusive thoughts
resulting from thought suppression transferred even to dreams.
Potential Morbidity Factors
Morbidity factors have also been associated with bereave-
ment. And, romantic breakups may be a risk factor for the more
serious complications associated with bereavement including
broken heart syndrome (Wittstein, Thiemann, Lima, Baughman,
Schulman, Gerstenblith et al., 2005) and endocrine and immune
dysfunction (Frazier, Strauss, & Steinhauer, 2004).
“Broken Heart” Syndrome
The “broken heart” or heartbreak syndrome has been de-
scribed as physical pain in the heart or chest after losing some-
one. Although the heartache mimics symptoms of a real heart
attack, those with broken heart syndrome typically recover
faster (Wittstein et al., 2005). This condition has also been
called stress cardiomyopathy or “takotsubo cardiomyopathy,”
takotsubo being a fishing pot with a narrow neck and a wide
base that is used to trap octopus in Japan, a shape that is similar
to that of the left ventricle. Cardiac contractile abnormalities
and heart failure have been recorded by several investigators,
although angiograms have revealed no clogged arteries in
heartbreak, unlike real heart attacks (Kawai, Suzuki, Yamagu-
chi et al., 2000; Kurisu, Sato, Kawagoe, Masaharu, Yuji, Kenji
et al., 2002; Villareal, Achari, Wilansky, & Wilson, 2001).
Norepinephrine and epinephrine levels have also been ele-
vated (7 - 34 times the normal levels) in individuals with bro-
ken heart syndrome, but cardiac enzymes typically released
from damaged heart muscle during real heart attacks were not
noted (Wittstein et al., 2005). Echocardiograms suggested that
although the left ventricle was contracting normally, there ap-
peared to be a weakened contraction in the middle and upper
portions of the heart muscle, and inverted T waves and pro-
longed Q-T intervals which are often associated with stress
were noted. Magnetic resonance imaging scans suggested that
none of the broken heart syndrome patients suffered irreversible
heart damage, and their recovery rates were faster (typically
two months) than after real heart attacks (Akashi, Nakazawa,
Sakakibara, Miyake, Koike, & Sasaka, 2003; Nyui, Yamanaka,
Nakayama, Sawano, & Kawai, 2000).
Potential underlying mechanisms offered for these effects in-
clude: 1) increased catecholamines causing spasms in the coro-
nary arteries (Wittstein et al., 2005); 2) multiple simultaneous
spasms of the coronary arteries that would cause enough loss of
blood flow to lead to the transient stunning of the heart (Kurisu
et al., 2002); and 3) a failure of the arteries to provide adequate
oxygen to the heart (Kawai et al., 2000). Most of these re-
searchers have suggested, however, that all of these factors may
be operating.
Unfortunately, many of these studies were based on small
samples, and although there are strong associations between
increased heart rate and the release of catecholamines and the
resultant cardiomyopathy, the relationships are only suggestive.
The elevated catecholamines may simply be an epiphenomenon
or a secondary response in the patients with the stress cardio-
myopathy rather than an original cause. Nonetheless, elevated
catechalomines are typically indicative of elevated stress and
when prolonged can lead to endocrine and immune dysfunc-
tion.
Endocrine and Immune Dysfunction
Decreased vagal activity and increased skin conductance
have been associated with elevated stress (Frazier et al., 2004),
and increased heart rate and blood pressure have been accom-
panied by increased cortisol and norepinephrine levels, which
when prolonged can have negative effects on the immune sys-
tem (Uchino, Kiecolt-Glaser, & Glaser, 2000). This initial
“fight-or-flight” mechanism is adaptive in mobilizing energy
stores leading to increased inflammatory cytokines which ulti-
mately mobilize antibodies as a defense against infection
(Black, 2002). In this way, immune activity is initially en-
hanced, but, over time, elevated stress hormones and cytokine
activity can result in impaired immune function (Kiecolt-Glaser,
McGuire, Robles, & Glaser, 2002). Compromised immune
function occurs via the necrotic effects of stress hormones on
the immune organs. Examples have been given of elevated
inflammatory cytokines (IL-1, IL-2, IL-6 and PNF-alpha) ac-
companying the depressed state (Leonard, 2006), as well as
higher antibody titres to the Epstein-Barr virus and lower than
normal natural killer cell activity (noted to kill bacterial, viral
and cancer cells) following divorce (Powell, Lovallo, Matthews,
Meyer, Midgley, Baum et al., 2002).
Bereaved individuals have had profiles of high anxiety and
depression scores, elevated cortisol and decreased natural killer
cell activity which in some individuals lasted for as long as six
months (Gerra, Monti, Panerai, Sacerdote, Anderlini, &
Avanzini, 2003). These physiological and biochemical changes
may contribute to the greater incidence of physical illnesses
(following “betrayal”) (Freyd, Klest, & Allard, 2005) and heart
disease (related to “broken hearts”) (Johnson & Grippo, 2006)
in bereaved individuals.
Romantic Breakups
Although most adults are resilient following romantic
breakups, some experience symptoms similar to those of be-
reavement including intrusive thoughts, insomnia and depres-
sion. In a study conducted by our group, university students
who experienced romantic breakups had elevated scores on
intrusive thoughts, difficulty controlling intrusive thoughts and
insomnia scales (Field, Diego, Pelaez, Deeds, & Delgado, 2009)
(see Table 1). In a regression on these data, scores on these
scales contributed to 34% of the variance on breakup distress
which was experienced by 58% of the students following ro-
mantic breakups (see Table 2).
Similarly, in a survey of more than 5000 internet respon-
T. FIELD
384
Table 1.
Means for high and low Breakup Distress Scale scores groups (Standard deviations in parentheses).
Primary Variables Low High F p
Intrusive Thoughts 2.88 (2.94) 5.63 (2.84) 15.27 .000
Controlling Int. Thoughts 15.73 (10.61) 26.05 (8.18) 27.20 .000
Sleep Disturbances 4.00 (2.39) 5.35 (2.97) 9.07 .003
Depression (CES-D) 13.56 (9.30) 20.88 (11.22) 8.15 .005
Anxiety (STAI) 38.36 (11.34) 45.69 (10.55) 9.05 .003
Table 2.
Stepwise regression on breakup distress.
Step R R square R
2
change F for change P
1 .46 .21 .21 57.19 .000
2 .56 .32 .11 34.06 .000
3 .58 .34 .02 7.33 .007
Predictors in order of their entry, 1) Sleep disturbance scale; 2) Intrusive thoughts
scale; 3) Controlling intrusive thoughts scale.
dents, romantic breakups were associated with more extreme
physical and emotional distress including exaggerated attempts
to re-establish the relationship, angry and vengeful behavior,
drugs and alcohol use (Taylor & Bryant, 2007). Laboratory
studies have also been conducted to assess physiological and
biochemical changes associated with bereavement and romantic
breakups including regional brain and neurotransmitter activity.
Regional Brain Activity
Bereavement and romantic breakups have been assessed for
regional brain activity by positron emission tomography (PET)
and functional magnetic resonance imaging (fMRI). In a paper
entitled “Craving love? Enduring grief activates brain reward
center”, PET showed reduced cerebral blood flow to the hippo-
campus in individuals with bereavement symptoms (O’Connor,
Wellisch, Stanton, Eisenberger, Irwin, & Lieberman, 2008).
The more severe the symptoms, the less blood flow to this re-
gion. In contrast, increased blood flow has been noted for the
cingulate cortex in fMRI studies. This was shown in bereaved
women, for example, in a paradigm in which grief was elicited
by photographs of the lost person (Gündel, O’Connor, Littrell,
Fort, & Lane, 2003), and in women who were grieving the loss
of a romantic relationship (Najib, Lorberbaum, Kose, Bohning,
& George, 2004). Involvement of the cingulate cortex is con-
sistent with brain activity associated with rejection and the
mixed emotional state of sadness, anger and anxiety, suggesting
that rejection may be a key factor in romantic breakups (Eisen-
berger, Lieberman, & Williams, 2003).
fMRIs of Rejected Love are Similar to Those of
Romantic Love
Paradoxically, the same brain areas that light up in those ex-
periencing romantic breakups also light up in individuals in
long-term love relationships. In a recent study, women who
were still very much in love but had been rejected by their ro-
mantic partner alternately viewed a photograph of their aban-
doning loved one and a photograph of a familiar individual
(Fisher, Aron, & Brown, 2006). These researchers then com-
pared their data on rejected lovers with the results from a study
on happily-in-love individuals (Aron, Fisher, Mashek, Strong,
Li, & Brown, 2005).The data showed that activity in regions
associated with physical pain increased during both love and
rejection.
The PET and fMRI data are difficult to interpret, and it is not
clear that they would lead to any implications for treatment,
especially since similar areas appear to be activated both during
romantic relationships and after romantic breakups. However,
these findings are noteworthy inasmuch as they are consistent
with data showing that biochemical profiles are also similar for
both romantic love and romantic rejection.
Romantic Breakups and Romantic Love Also Have
Similar Biochemical Profiles
The brain also releases similar chemicals for both romantic
breakups and romantic love including pheromones, dopamine,
norepinephrine, epinephrine and serotonin. As dopamine and
norepinephrine levels increased, serotonin levels decreased, and
these changes were associated with increased heartrate, trem-
bling, flushing, pupil dilation, sleeplessness and loss of appetite
(Fisher, 2006). These data are understandable given that these
physiological and biochemical responses have generally been
noted during stressful situations (Luciana, Collins, & Depue,
1998; Griffin & Taylor, 1995).
Potential Mechanisms Underlying Romantic
Breakups, Heartbreak and Bereavement
Potential underlying mechanisms have been explored for
romantic breakups, heartbreak and bereavement. These include
loss of regulation models labeled “relationships as social regu-
lators” and “psychobiological attunement”.
Relationships as Social Regulators
In the social regulators model of bereavement, the loss of a
significant other represents the loss of major social time cues
((Ehlers, Frank, & Kupfer, 1988). In seminal papers on “Rela-
tionships as Regulators”, Hofer outlined a model for the loss of
a relationship as being the loss of a regulator (Hofer, 1984,
1996). He suggested that losing an attachment figure means
“losing regulatory control of stable daily patterns, of tasks,
attention, concentration, sleep, food intake and mood, such that
they become fragmented, and the individual has a sense of in-
T. FIELD
385
ternal disorganization”.
Relationships can help maintain psychological and physio-
logical equilibrium, as each person is associated with a state of
psychological security and physiological calm for the other and
serves to up- or down-regulate the partner’s psychophysiologi-
cal arousal (Hofer, 1984, 1996; Depue & Morrone-Strupinsky,
2005; Sbarra & Hazan, 2009). This co-regulation is considered
a property of the relationship (not a property of either individ-
ual alone), and, it can occur through several senses (e.g. touch,
smell, eye contact) and is thought to regulate and synchronize
body rhythms. In the absence of the “co-regulator,” the psy-
chological and physiological rhythms can become dysregulated,
leading to dysphoria, restlessness/agitation, sleep disturbances,
changes in appetite and decreased vagal tone (Sbarra & Hazan,
2008).
Dysregulation can happen when a partner is absent, for ex-
ample, during business trips and military deployments, as sleep
disturbances have been noted during the travel period, and the
individuals then return to a regulated state following reunion
(Diamond, Hicks, & Otter-Henderson, 2008). It can also hap-
pen during threat conditions that can be alleviated by holding
the hand of one’s partner versus the hand of a stranger (Coan,
Schaefer, & Davidson, 2006). The authors of the handholding
study suggested that the threatened person “borrowed emo-
tional and physiological stability from the partner”. Some have
noted that even mental representations of one’s partner can be
dysregulating following a breakup or loss, leading to intrusive
thoughts and disturbing dreams (Uvnäs-Moberg, 1998).
Most of the examples given have involved the partner de-
creasing arousal levels rather than helping find a balance be-
tween under- and over-arousal. Under-arousal could be equally
disturbing as, for example, the sensory deprivation experienced
by individuals who are in military combat and confined to light
and sound-proof chambers (Hofer, 1984).
Loss of Psychobiological Attunement
A model called “psychobiological attunement” or “being on
the same wavelength”, accommodates both the need for optimal
stimulation and for arousal modulation (Field, 1985, 1996). In
this model, each partner provides meaningful stimulation for
the other and has a modulating influence on the other’s arousal
level. Both over-stimulation and under-stimulation are aversive,
and stimulation that brings or keeps an individual within an
optimal arousal zone is considered reinforcing. Thus, the loss of
a significant other means the loss of both activating and calm-
ing stimulation. The individual experiencing the loss would be
expected to fluctuate between one end of the continuum of
under-stimulation and the other end of over-stimulation and not
be able to modulate these levels to experience optimal arousal
levels.
Other terms used to describe this phenomenon were syn-
chrony and sharing rhythms (Field, 1985, 1996). Synchrony is a
term that is usually applied to the matching of physiological or
physical activity rhythms by individuals in a close relationship.
Examples of this can be seen in partners who are extremely
close tending to coordinate their physical movements and ex-
pressions while talking, as well as their cortisol cycles tending
to be synchronized on weekends when they are together (Field,
1985, 1996). Thus, attunement or “being on the same wave-
length” happens for both behavioral and physiological rhythms
in adults who have a close relationship. Seemingly, the only
way this could happen is if each partner of the dyad is sensitive
and responsive to each other’s stimulation and arousal-modu-
lation needs, as in a feedback loop, and each accordingly ad-
justs his or her behavior to facilitate the behavioral and physio-
logical synchrony of the couple.
If and when the partner is not there to meet the needs for dif-
ferent types and degrees of stimulation, dysregulation may
occur including physiological disorganization such as decreased
vagal activity (Frazier et al., 2004; Diego, Field, & Hernan-
dez-Reif, 2007), and in some cases changes in immune function
such as increased inflammatory cytokines (Leonard, 2006) and
decreased natural killer cell activity (Powell et al., 2002). In our
model, the loss of a loved one may result in this dysregulation
simply because the source of stimulation and arousal modula-
tion is no longer present (Field, 1985, 1996).
Physical intimacy can enhance attunement (Fisher, 2004).
Via touching, individuals can learn each other’s stimulation and
arousal modulation needs. Although it is possible to self-regu-
late in the absence of an intimate partner, it may not be as easy
or effective. When a partner is no longer there and touch
stimulation, for example, is missing, it may become necessary
to find that type of stimulation from other activities until a new
partner is found. Massage, yoga, and other forms of exercise,
for example, may help avoid the physiological dysregulation
and immune problems that can result from touch deprivation
(Field, 2009).
Limitations of This Research and Future
Directions
The intent of this review was to summarize the limited lit-
erature on romantic breakup symptoms that are similar to those
of the bereavement syndrome including intrusive thoughts,
attempting to control intrusive thoughts and insomnia and more
serious complications including heartbreak syndrome and im-
mune dysfunction. Much of the discussion regarding romantic
breakups, however, is mere speculation based on the bereave-
ment and heartbreak syndrome literature. And, the bereavement
and heartbreak syndrome literature has the problem that the
data are derived primarily from loss related to death and di-
vorce. These likely have commonalities with romantic breakups,
but also major differences, as in divorce not only involving
betrayal and rejection but also having to continue the relation-
ship for family reasons and death involving a permanent loss.
Even within the loss by divorce and the loss by death literatures,
comparisons across studies are problematic given the different
measures, the different intervals from the time of loss to the
time of assessment, and the different age, ethnic and cultural
groups assessed (among other potentially confounding vari-
ables).
Other nuisance factors are the small sample sizes and the
measurement of only one or two variables. This is particularly
problematic when the results appear paradoxical such as the
fMRI data showing that the same region of the brain is acti-
vated by romantic breakup and by romantic love and the same
biochemical profile emerging (albeit from different studies).
Without converging variables such as behavioral data, these
findings are difficult to interpret. And, as already mentioned,
they are not perhaps useful for informing potential treatment
T. FIELD
386
options. In brief, in any of these research areas, multi-variable
studies would be more informative. Combining self-report,
behavioral, physiological and biochemical measures in the
same sample of individuals experiencing loss from the same
cause would be optimal.
Perhaps the greatest weakness of these literatures is that it is
not clear what is happening in relationships that are then miss-
ing when the loss occurs, whether by death, divorce or romantic
breakups. Reviewing the “social regulators” and the “psychobi-
ological attunement” models in this paper was meant to high-
light how little we know about what changes occur from before
to after the loss or what was critical about the relationship that
was then missing after the loss occurred. This, of course, is
always difficult given the longitudinal nature of the problem.
However, convenience samples could be researched such as
university students whose relationships tend to be short-lived,
affording the opportunity to collect behavioral, physiological
and biochemical data during the relationship and after the
breakups. To address these questions, we are currently design-
ing research to videotape interactions of university student cou-
ples during their relationships and after their break-ups as well
as recording their heartrate and assaying saliva samples for
cortisol levels. Relationships between older couples, for exam-
ple couples in assisted living, could also provide the opportu-
nity for studies of long-term relationships that are “snuffed out”
by the death of one partner. These are potential challenges for
the very important problem of determining how to alleviate the
significant social pain of loss, be it by death, divorce or roman-
tic breakups. In a sense, each of these, no matter the cause, are
romantic breakups that can be chronically painful and therapeu-
tically costly.
Summary
In summary, romantic breakups, heartbreak syndrome and
bereavement are complex behavioral, physiological and bio-
chemical phenomena. Romantic breakups may be at risk for the
symptom profile of bereavement including intrusive thoughts
and attempts to suppress them as well as insomnia and more
serious complications including broken heart syndrome and
immune dysfunction. Although the broken heart syndrome
mimics a real heart attack, it has been differentiated from heart
attacks by angiograms revealing unclogged arteries and no
permanent heart damage. Reduced vagal activity and increased
cortisol and catecholamines are thought to lead to the associ-
ated immune dysfunction including increased inflammatory
cytokines and reduced natural killer cell activity. Potential un-
derlying mechanisms for romantic breakups, heartbreak and
bereavement effects include the loss of social regulators who
provide optimal stimulation and arousal modulation. These data
highlight the complexity of romantic breakups, heartbreak and
bereavement and the need for further multi-variable research
that is conducted both before and after the breakups.
References
Akashi, Y. J., Nakazawa, K., Sakakibara, M., Miyake, F., Koike, H., &
Sasaka, K. (2003). The clinical features of takotsubo cardiomyopathy.
Quarterly Journal of Medicine, 96, 563-573.
Aron, A., Fisher, H., Mashek, D. J., Strong, G., Li, H., & Brown, L. L.
(2005). Reward, motivation, and emotion systems associated with
early-stage intense romantic love. Journal of Neurophysiology, 94,
327-337.
doi:10.1152/jn.00838.2004
Bisconti, T. L., Bergeman, C. S., & Boker, S. M. (2004). Emotional
well-being in recently bereaved widows: A dynamical systems ap-
proach. Journals of Gerontology Series B: Psychological Sciences
and Social Sciences, 59, 158-167.
doi:10.1093/geronb/59.4.P158
Black, P. H. (2002). Stress and the inflammatory response: A review of
neurogenic inflammation. Brain, Behavior, and Immunity, 16,
622-635. doi:10.1016/S0889-1591(02)00021-1
Coan, J. A., Schaefer, H. S., & Davidson, R. J. (2006). Lending a hand:
Social regulation of the neural response to threat. Psychological Sci-
ence, 17, 1032-1039.
doi:10.1111/j.1467-9280.2006.01832.x
Davis, D., Shaver, P. R., & Vernon, M. L. (2003). Physical, emotional
and behavioral reactions to breaking up: The roles of gender, age,
emotional involvement, and attachment style. Personality and Social
Psychology Bulletin, 29, 871-884.
doi:10.1177/0146167203029007006
Depue, R. A., & Morrone-Strupinksy, J. V. (2005). A neurobehavioral
model of affiliative bonding: Implications for conceptualizing a hu-
man trait of affiliation. Behavioral and Brain Sciences, 28, 313-395.
doi:10.1017/S0140525X05000063
Diamond, L. M., Hicks, A. M., & Otter-Henderson, K. (2008). Every
time you go away: Changes in affect, behavior, and physiology asso-
ciated with travel-related separations from romantic partners. Journal
of Personality and Social Psychology, 95, 385-403.
doi:10.1037/0022-3514.95.2.385
Diego, M., Field, T., & Hernandez-Reif, M. (2007). Preterm infant
massage consistently increases vagal activity and gastric motility.
Acta Paediatrica, 96, 1588-1591.
doi:10.1111/j.1651-2227.2007.00476.x
Ehlers, C. L., Frank, E., & Kupfer, D. J. (1988). Social zeitgebers and
biological rhythms: A unified approach to understanding the etiology
of depression. Archives of General Psychiatry, 45, 948-952.
Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does
rejection hurt? An fMRI study of social exclusion. Science, 302,
290-292.
doi:10.1126/science.1089134
Faschingbauer, T., Zisook, S., & DeVaul, R. (1987). The Texas revised
inventory of grief. In S. Zisook, (Ed.), Biopsychosocial aspects of
bereavement (pp. 111-124). Washington, DC: American Psychiatric
Press, Inc.
Field, T. (1985). Attachment as psychobiological attunement: Being on
the same wavelength. In M. Reite and T. Field (Eds.), Psychobiology
of attachment. New York: Academic Press.
Field, T. (1996). The effects of mother’s physical and emotional un-
availability on emotion regulation. The Development of Emotion
Regulation: Biological and Behavioral Considerations, 59, 208-227.
Field, T. (2009). Complementary and alternative therapies research.
Washington, DC: American Psychological Association.
doi:10.1037/11859-000
Field, T., Diego, M., Pelaez ,M., Deeds, O., & Delgado, J. (2009).
Breakup distress in university students. Adolescence, 44, 705-727.
Fisher, H. E. (2004). Why we love: The nature and chemistry of roman-
tic love. New York: Holt Paperbacks.
Fisher, H. E., Aron, A., & Brown, L. L. (2006). Romantic love: A
mammalian brain system for mate choice. Philosophical Transac-
tions of the Royal Society, 361, 2173-2186.
doi:10.1098/rstb.2006.1938
Frazier, T. W., Strauss, M. E., & Steinhauer, S. R. (2004). Respiratory
sinus arrhythmia as an index of emotional response in young adults.
Psychophysiology, 41, 75-83.
doi:10.1046/j.1469-8986.2003.00131.x
Freyd, J. J., Klest, B., & Allard, C. B. (2005). Betrayal trauma: Rela-
tionship to physical health, psychological distress, and a written dis-
closure intervention. Journal of Trauma Dissociation, 6, 83-104.
doi:10.1300/J229v06n03_04
Gerra, G., Monti, D., Panerai, A. E., Sacerdote, P., Anderlini, R.,
Avanzini, P. et al. (2003). Long-term immune-endocrine effects of
bereavement: Relationships with anxiety levels and mood, Psychia-
try Research, 121, 145-158. doi:10.1016/S0165-1781(03)00255-5
T. FIELD
387
Griffin M. G., & Taylor, G. T. (1995). Norephinephrine modulation of
social memory: Evidence for a time-dependent functional recovery
of behavior. Behavioral Neuroscience, 109, 466-538.
doi:10.1037/0735-7044.109.3.466
Gündel, H., O’Connor, M. F., Littrell, L., Fort, C., & Lane, R. (2003).
Functional neuroanatomy of grief: An fMRI study. American Journal
of Psychiatry, 160, 1946-1953.
doi:10.1176/appi.ajp.160.11.1946
Hardison, H. G., Neimeyer, R. A., & Lichstein, K. L. (2005). Insomnia
and complicated grief symptoms in bereaved college students. Be-
havioral Sleep Medicine, 3, 99-111.
doi:10.1207/s15402010bsm0302_4
Hofer, M. A. (1984). Relationships as regulators: A psychobiologic
perspective on bereavement. Psychosomatic Medicine, 46, 183-197.
Hofer, M. A. (1996). On the nature and consequences of early loss.
Review. Psychosomatic Medicine, 58, 570-581.
Johnson, A. K., & Grippo, A. J. (2006). Sadness and broken hearts:
Neurohumoral mechanisms and co-morbidity of ischemic heart dis-
ease and psychological depression. Journal of Physiology and
Pharmacology, 57, 529-534.
Kawai, S., Suzuki, H., Yamaguchi, H., Tanaka, K., Sawada, H., Aizawa,
T
. et al. (2000). Ampulla cardiomyopathy (Takotsubo’ cardio-
myopathy)—reversible left ventricular dysfunction: With ST seg-
ment elevation. Japan Circulation Journal, 64, 156-159.
doi:10.1253/jcj.64.156
Kiecolt-Glaser, J. K., McGuire, L., Robles, T. F., & Glaser, R. (2002).
Emotions, morbidity, and mortality: New perspectives from psycho-
neuroimmunology. Annual Review of Psychology, 53, 83-107.
doi:10.1146/annurev.psych.53.100901.135217
Kleinman, A., & Good, B. (1985). Introduction: Culture and depression.
In A. Kleinman and B. Good (Eds.), Culture and depression: Studies
in the anthropology and cross-cultural psychiatry of affect and dis-
order. Berkeley and Los Angeles: University of California Press.
Kurisu, S., Sato, H., Kawagoe, T., Masaharu, I., Yuji, S., Kenji, N. et al.
(2002). Tako-Tsubo-like left ventricular dysfunction with ST-seg-
ment elevation: A novel cardiac syndrome mimicking acute myocar-
dial infarction. American Heart Journal, 143, 448-455.
doi:10.1067/mhj.2002.120403
Leonard, B. (2006). HPA and immune axes in stress: involvement of
the serotonergic system. Neuroimmunomodulation, 13, 268-276.
doi:10.1159/000104854
Luciana, M., Collins, P. F., & Depue, R. A. (1998). Opposing roles for
dopamine and serotonin in the modulation of human spatial working
memory functions. Cerebral Cortex, 8, 218-244.
d
oi:10.1093/cercor/8.3.218
McDermott, O. D., Prigerson, H. G., Reynolds, C. F. III, Houck, P. R.,
Dew, M. A., Hall, M. et al. (1997). Sleep in the wake of complicated
grief symptoms: An exploratory study. Biological Psychiatry, 41,
710-716.
doi:10.1016/S0006-3223(96)00118-7
Monk, T. H., Houck, P. R., & Shear, M. K. (2006). The daily life of
complicated grief patients-what gets missed, what gets added? Death
Studies, 30, 77-85.
doi:10.1080/07481180500348860
Najib, A., Lorberbaum, J. P., Kose, S., Bohning, D. E., & George, M. S.
(2004). Regional brain activity in women grieving a romantic rela-
tionship breakup. American Journal of Psychiatry, 161, 2245-2256.
doi:10.1176/appi.ajp.161.12.2245
Nelson, J., & Harvey, A. G. (2002). The differential functions of im-
agery and verbal thought in insomnia. Journal of Abnormal Psy-
chology, 111, 665-673. doi:10.1037/0021-843X.111.4.665
Nelson, J., & Harvey, A. G. (2003). Pre-sleep imagery under the mi-
croscope: A comparison of patients with insomnia and good sleepers.
Behaviour Research and Therapy, 41, 273-356.
doi:10.1016/S0005-7967(02)00010-4
Nyui, N., Yamanaka, O., Nakayama, R., Sawano, M., & Kawai, S.
(2000). Takotsubo’ transient ventricular dysfunction: A case report.
Japanese Circulation Journal, 64, 715-723.
doi:10.1253/jcj.64.715
O’Connor, M. F., Wellisch, D. K., Stanton, A. L., Eisenberger, N. I.,
I
rwin, M. R., & Lieberman, M. D. (2008). Craving love? Enduring
grief activates brain reward center. Neuroimage, 42, 969-972.
doi:10.1016/j.neuroimage.2008.04.256
Powell, L. H., Lovallo, W. R., Matthews, K. A., Meyer, P., Midgley, A.
R., Baum, A., et al. (2002). Physiologic markers of chronic stress in
premenopausal, middle-aged women. Psychosomatic Medicine, 64,
502-509.
Prigerson, H., & Jacobs, S. (2001). Traumatic grief as a distinct disor-
der: A rationale, consensus criteria, and a preliminary empirical test.
In M. S. Stroebe, R. O. Hansson, W. Stroebe and H. Schut, (Eds.),
Handbook of bereavement research: consequences, coping, and care.
Washington, DC: American Psychological Association, 613-645.
doi:10.1037/10436-026
Raphael, B., Minkov, C., & Dobson, M. (2001). Psychotherapeutic and
pharmacological intervention for bereaved persons. In M. S. Stroebe,
R. O. Hansson, W. Stroebe and H. Schut, (Eds.), Handbook of be-
reavement research: Consequences, coping, and care. Washington,
DC: American Psychological Association, 587-612.
doi:10.1037/10436-025
Reynolds, C. F., Hoch, C. C., Buysse, D. J., Houck, P. R., Schlernit-
zauer, M., Frank, E. et al. (1992). Electroencephalographic sleep in
spousal bereavement and bereavement-related depression of late life.
Biological Psychiatry, 31, 69-82.
doi:10.1016/0006-3223(92)90007-M
Sbarra, D. A., & Hazan, C. (2008). Coregulation, dysregulation, self
regulation: An integrative analysis and empirical agenda for under-
standing adult attachment, separation, loss, and recovery. Personality
and Social Psychology Review, 12, 141-167.
doi:10.1177/1088868308315702
Simon, G., VonKorff, M., Piccinelli M., Fullerton, C., & Ormei J.
(1999). An international study of the relation between somatic
symptoms and depression. The New England Journal of Medicine,
341, 1329-1334.
doi:10.1056/NEJM199910283411801
Taylor, F., & Bryant, R. A. (2007). The tendency to suppress inhibiting
thoughts, and dream rebound. Behavior Research and Therapy, 45,
163-168. doi:10.1016/j.brat.2006.01.005
Uchino, B. N., Kiecolt-Glaser, J. K., & Glaser, R. (2000). Psychologi-
cal modulation of cellular immunity. In J. T. Cacioppo, L. G. Tassi-
nary and G. G. Berntson (Eds.), Handbook of psychophysiology (2nd
ed., pp. 397-424). New York: Cambridge University Press.
Uvnäs-Moberg, K. (1998). Oxytocin may mediate the benefits of posi-
tive social interaction and emotions. Psychoneuroendocrinology, 23,
819-835. doi:10.1016/S0306-4530(98)00056-0
Villareal, R. P., Achari, A., Wilansky, S., & Wilson, J. M. (2001).
Anteroapical stunning and left ventricular outflow tract obstruction.
Mayo Clinic Proceedings, 76, 79-83.
doi:10.4065/76.1.79
Vrana, S. R., Cuthbert, B. N., & Lang, P. J. (1986). Fear imagery and
text processing. Psychophysiology, 23, 247-253.
doi:10.1111/j.1469-8986.1986.tb00626.x
Wegner, D. M., Wenzlaff, R. M., & Kozak, M. (2004). Dream rebound:
The retuned of suppressed/thoughts in dreams. Psychological Sci-
ence, 15, 232-236.
doi:10.1111/j.0963-7214.2004.00657.x
Wikan, U. (1988). Bereavement and loss in two Muslin communities:
Egypt and Bali. Social Science and Medicine, 27, 451-460.
doi:10.1016/0277-9536(88)90368-1
Wittstein, L. S., Thiemann, D. R., Lima, J. A. C., Baughman, K. T.,
Schulman, S. P., Gerstenblith, G. et al. (2005). Neurohumoral fea-
tures of myocardial stunning due to sudden emotional stress. The
New England Journal of Medicine, 352, 539-548.
doi:10.1056/NEJMoa043046
