The word of Freud

Last week it was published a new and exciting study about inner speech. The authors utilized virtual reality – a system that provokes the perceptual illusion of being physically present in a non-physical world (Osimo, Pizarro, Spanlang, & Slater, 2015). The study investigated whether self-counseling experiences (that is, explaining a problem and giving advices to yourself) differ depending on whether you have the perception of being talking to yourself, or whether you have the perception of being talking to an expert counselor. The authors report that, to choose an identity of the expert counselor, they did some kind of survey at the university campus, and it turned out that male students would mainly prefer to discuss personal problems with Angelina Jolie, Nelson Mandela, or Sigmund Freud. So, dr. Freud was selected as the expert counselor avatar.

Participants were told to either (a) explain their problems to themselves, or (b) explain a personal problem to Freud. When they finished, they were moved into the other person’s body (themselves or Freud), and they were asked to offer some advice to that problem. After this, participants were moved back to the original body (themselves again), and listened to the advice that they provided while being in the other body.

When participants discussed the problem with Freud, mood improvements were stronger than when participants discussed with themselves. The authors discussed this result as an effect of perspective taking – or the benefits of creating an emotional distance to our own personal problems – and self-processing. They suggest that being embodied in a body different to our own might affect environmental perception, attitudes, or self-identity. Overall, results have interesting clinical implications, since there might exist some parallels between the aforementioned body ownership illusion and psychotherapeutic approaches like the ‘empty chair technique’.

Next time something is bothering us, we can ask Freud and listen what he has to say. Picture from wikipedia:

Next time something is bothering us, we can ask Freud and listen what he has to say. Picture from wikipedia:

The only one thing that I was missing in the study is a qualitative description of the inner speech in the two situations. For instance, it could be the case that, when participants talk to themselves, they might use non-adaptive ways to face a problem –i.e., rumination, self criticism, or self-pity – more often than when they are obliged to give advice to themselves as if they were Freud. And conversely, it could be possible that the conversations with the Freud avatar are richer in problem-solving strategies and in the search for different solutions to a certain problem.

Despite not reporting a qualitative analysis of the conversations, the authors do provide some examples of the inner speeches. I was kinda hoping that they would report some Freudian-like conversation, like, “Hey, dr. Freud, I’m dating a girl who looks exactly like my mum’s clone, do you think it’s normal?”. Instead, the conversations were pretty conventional, covering, for example, discussions with a demanding boss.

Maybe next time that something is bothering you, you can try to imagine that you are talking with somebody you admire (I always wanted to meet Frida Kahlo in my imaginary world). Maybe, a similar psychological mechanism that the one described in Osimo and cols. paper, also takes place when people engage in intimate talks or perform rituals to communicate with the God they believe in. Nevertheless, I think that the important message here is that, a number of times, the solution to our problems is in our own brain. Maybe we need some cognitive strategy to facilitate the process. Sometimes it’s useful to stop thinking negative, take care of ourselves by placing emotional distance to the problem, and avoid ruminating over and over again. And, of course, if negativity has already invaded our body and looks like it is there to stay, we can also ask Freud, and listen to what he has to say.


Osimo, S. A., Pizarro, R., Spanlang, B., & Slater, M. (2015). Conversations between self and self as Sigmund Freud—A virtual body ownership paradigm for self counselling. Scientific Reports, 5(July), 13899. doi:10.1038/srep13899

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The (forgotten) social dimension of eating disorders.

We don’t eat until your father’s at the table.

We don’t drink until the devil’s turned to dust.

 James Vincent McMorrow. We don’t eat.

Social interactions often involve drinks and food. Think about Mean Girls and the cafeteria map that Janice handles to Cady displaying where the different school tribes sit. Or the episode in The House of Cards when Frank Underwood invites the Russian President, Petrov, to a dinner in the White House in order to try to influence on a peacekeeping agreement in the Jordan Valley. Eating food can be a valuable moment to interact with our family, friends, or co-workers.

Social interactions might influence our eating behavior. In German, there is the expression “alleine Essen macht dick”, which literally, means that eating alone fattens. On the other hand, at least in Spain, you might be perceived as rude if you do not finish your meal when someone else is hosting you for dinner, so in that case, you might prefer to eat beyond satiety than to offend your host. Like, when I go visit my parents in Barcelona. My mum will always complain that I look too skinny, does not matter how many times I tell her that my weight is in the normal range. In my flight back to Germany, I will always end up weighting two more kilos.

Given the close interrelation that exists between the presence of other people and eating behavior, it is not surprising the fact that social interactions may impact in the acquisition and maintenance of pathological eating behavior. For instance, social pressures seem to have an important role in body dissatisfaction, a well-known risk factor for the development of disordered eating behavior (1).

Amongst disordered eating behavior, two patterns seem to be quite prevalent in Western populations: (a) uncontrolled eating behavior, or loss of control over food intake; as well as (b) restrained eating behavior, or continuous conscious attempts to restrict food intake in order to lose weight.

Both problematic eating patterns are interrelated (2), however, for the sake of simplicity, I will focus here exclusively on the second one. Exaggerated restrained eating can be an indicator for the presence of restrictive types of eating disorders, such as anorexia nervosa. Anorexia nervosa is a psychiatric disease characterized by excessive concern with body weight, followed by an extreme restriction of food intake, which might lead to malnutrition and to other severe health consequences, such as endocrine dysregulations. It has been estimated that, in Western societies, 0.3% of young females suffer from this pervasive health condition.

Despite the strong interrelation between eating pathology and social pressures, cognitive neuroscience has largely omitted the inclusion of the social dimension in the study of eating disorders. Admittedly, it is certainly challenging to simulate a social interaction in a dark, tight, and extremely loud 20 to 60 minutes MRI scanner. However, the incorporation of social paradigms will certainly enrich our perspective of these pervasive disorders.

Precisely, a new fMRI study has tried to address this issue by comparing patients with anorexia nervosa and healthy controls on a social evaluation task (3). Basically, participants had to rate some photographs from strangers according to how much would they like to meet this person, and later on, they were supposed to receive also the same type of feedback from these people in the scanner. One of the results that they found was related to the dorsomedial prefrontal cortex. Patients with anorexia nervosa exhibited blunted activity in the dorsomedial prefrontal area while receiving positive feedback relative to healthy participants. This fact led the authors to hypothesize the existence of possible disruptions in areas traditionally assigned to self-evaluative processes and inferences of other’s mental states (3).

Not only social pressures might be associated with vulnerability to suffer eating disorders. Many other factors, such as personality characteristics, might likely play an important role in the vulnerability and resilience of individuals. Nevertheless, I think it is important to highlight the fact that negative social experiences might exert some influence in body dissatisfaction, which in turn, might impact on the incidence of eating disorders. I think we should recognize the fact that our “civilized” Western societies tolerate toxic social messages promoting misogyny, racism, and shaming. It is important, because, in part, it is in our hands to speak out and change it. Just think about the last two months. We are witnessing extreme violence against black people in America, and absolute passivity towards the terrible fate of war refugees in Europe. In another level, but more closely related to body shaming, we have also seen the appearance of the “harpoon project” –another unfortunate manifestation of thinspiration movements or pro-anorexia trends– the commercialization of female viagras as another attempt to pathologize women’s sexuality, the use of menstruation to discredit inconvenient questions in political debates, and public shame of non-cisgender people with total immunity.

Scientific literature also plays a role in the body-shaming problem. Just go to PubMed and select a random study on obesity. Warning! Spoiler alert in the next sentence!! Typically, the opening paragraph in the introduction will contain a “catastrophic” description about how terrible obesity is for society and for an individual, how much does it cost to European or American health systems, how many months of life expectancy it reduces, and how many times does obesity increase the risk for a range of terrible diseases, such as cancer, diabetes type II, depression, and sexual dysfunction.

While it is true that obesity – specially in combination with other vascular risk factors– might prove detrimental for health, the obesity literature tends to “forget” to disclose that a number of people with overweight or obesity live a perfectly happy, healthy, and meaningful life. Moreover, body mass index, the measure more vastly utilized as surrogate for obesity (defined by kg/m2), might not be adequate to describe overweight, specially, in people with large muscular volume.

And let’s not talk about how does the media represents obesity, when referring to some scientific study. Just imagine a hypothetical scenario in which some scientist have observed that obesity is associated with something random and, in appearance, catastrophic, like 0.25% more probabilities for using the grimacing face emoji while texting on WhatsApp (is it just me? I hate this emoji!!). And let’s imagine that newspapers want to report this important bad news to the general audience. Together with the text referring to the scientific article, I am sorry to tell you that it is highly unlikely that you will see a picture of beautiful and inspiring people with obesity, like say, Tess Holliday or Adele (I mean, the Adele from “Never mind, I’ll find someone like youuuuu”; not the new slim Adele). Rather, illustrating the alarming and apocalyptic study, you will likely see a photograph portraying the centric 20% of a person’s body (well, you guess it’s a person, but since you just see 20% of the body, it could perfectly be only a pillow with a human shape), displaying a corpulent belly wearing an extremely tight, ugly, four sizes smaller, and probably fuchsia T-shirt. And you might guess, wasn’t there any other more appropriate T-shirt to wear? Was it absolutely necessary to pick the T-shirt up from the Zara kids section? Sometimes it is useful to remember that, if some jeans make muffing tops on you, it is not you the one who has a problem: simply, your jeans are too tight for you to wear them.

I eagerly await the day when we no longer tolerate social messages that shame people’s appearance, culture, or sexuality. Perhaps we can all try to transform our immediate environment in a peaceful and tolerant space, where we all feel secure enough to freely express our own personality and our own cultural traditions. We might not only reduce the incidence of disordered eating behaviors. We might also build open and inclusive societies that fight against prejudices and narrow-minded attitudes. As the transgender Leelah Alcorn famously wrote in her suicide note at the beginning of this year, ‘fix society. Please’.


  1. Stice E, Maxfield J, Wells T. Adverse effects of social pressure to be thin on young women: An experimental investigation of the effects of “fat talk.” Int J Eat Disord. 2003; 34(1):108–17.
  2. Polivy J, Herman CP. Dieting and binging. A causal analysis. Am Psychol. 1985, 40(2):193–201.
  3. Via E, Soriano-Mas C, Sánchez I, Forcano L, Harrison BJ, Davey CG, et al. Abnormal Social Reward Responses in Anorexia Nervosa: An fMRI Study. PLoS One 2015; e0133539.


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What we do in the lab, echoes in eternity. Well, if you’re lucky, it might echo in PubMed.

If, unlike me, half of your Facebook friends are not predominantly neuroscientist, you might have missed one of the most important events happening this month.

It is not about Sergio Ramos announcing that he is leaving the Real Madrid to start a new life in Manchester (Ramos in exchange for de Gea? What’s wrong with you, Man United?). It is not about Tim Hunt articulating the ‘mea culpa’ for his unfortunate comments about women in science. It is not about Kim Kardashian and her upcoming talk about female objectivation (can somebody explain to me why TED hasn’t invited her yet as a speaker?). It is about the 2015 conference of the Organization for the Human Brain Mapping!! (#OHBM2015) (yay!!).

I love going to conferences. This year, OHBM had the additional incentive of taking place just nearby the paradise, in Honolulu. So it was just great to sneak out of the conference center and to go to the beach or around the city every time the title of the talk contained the words ‘Bayesian’ or ‘multivariate algorithm’ or, every time the presentation included more than three equations. But please, don’t judge me for that! This blog is actually called ArousedBrain for a reason. Otherwise, it would be called VectorizedBrain, ComplexBrain, or ComputationalBrain.

Going to conferences might offer you a great opportunity for meeting inspiring people and old friends working somewhere else. Additionally, it might be useful to ckeck if other groups that are working in your field are performing the same type of studies that you are carrying out. This can be an issue sometimes.

While I was in my first year of my PhD in Barcelona, I was working hard to apply independent component analysis (ICA) to evaluate resting-state connectivity in obesity. ICA allows the evaluation of networks in the brain, which are formed by regions that tend to activate in a synchronized way. So, I had a cool result comparing participants with obesity and participants with a normal-weight, and I was getting very excited about it.

Sometimes, I feel that science is like being on a roller coaster. There are times in which you feel like being in a ‘maniac periods’, and you feel that your result will lead you to international recognition, and (using some words from ‘Gladiator’) will echo in eternity. Conversely, other times you enter ‘depressive periods’, in which you just feel like the most incompetent person in the world.

Back to the point, I was in a maniac phase with my results in resting-state and obesity. Relative to control individuals, I had discovered that participants with obesity exhibited an increased functional connectivity in the salience network. The salience network is formed by the co-activation of the anterior insula, anterior cingulate, and other limbic and striatal areas, and it has been associated with the integration of sensory and homeostatic information (1). So, I was really excited preparing my results for publication and dreaming with winning a Nobel Prize. And then, another paper on resting-state in obesity came out.

In this ‘other paper’, Kullmann et al. reported an obesity-related increased functional connectivity strength in the precuneus, inside the default mode network (2). At that time, I thought that my career as a neuroscientist was finished. I would never be the first person in the world to investigate resting state fMRI in obesity!! Such a big deal! My group in Barcelona saw me going through a depressive phase after this. I think I even told my hairdresser too much about how terrible my life was. Well… first world problems, right?

Luckily, my wise supervisors considered that our study on the salience network still provided new and relevant information to the field. So we decided to keep on working on it and we eventually submit it to a journal. After some effort, it was successfully published (3) and I sill remember being in shock when I saw our study accessible in PubMed (finally! I had published my first ‘real’ study!!!!).

After the euphoria of getting my first paper accepted, I decided to continue applying ICA-based analysis in obesity. But this time, I wanted to study differences in an fMRI task acquisition. We had an fMRI sequence available, in which the same participants from the first study were presented with a food reward paradigm. So, I wanted to analyze differences in functional networks according to the different experimental conditions (food reward, other non-food reward and neutral stimuli). I obtained a cool result, in which participants with obesity and individuals with normal-weight differed in the connectivity strength of a network containing activation in visual and lateral prefrontal areas and deactivation in the posterior part of the default mode network.

So, again, I entered a second maniac phase imagining myself being hired by a pharmaceutical company and signing multimillionaire contracts. But then, another paper was published and brought me again back to reality. Somehow similar to what I was trying to write down, the same group of Kullmann and collaborators published an elegant study in which they applied ICA-based analysis to investigate food reward processing in obesity (4). Seriously, their study is still today one of the coolest papers published in the field!! This time, my previous experience prevented me from entering in a self-pitying and depressive phase for not being the first person in the world applying ICA to study reward processing in obesity. Instead of that, I worked hard to highlight the novelty of our study, we submitted it, and after some time, we also got it accepted (5).

So, as I said before, conferences are useful because they allow you to meet inspiring people. Last year, also during the OHBM congress, I met some of the authors from the Kullmann et al. studies. In my mind, I was imagining them as scientist with dark powers and with the ability to read minds from thousands of kilometers in the distance and being able to perform better and faster studies. It turned out that they are a very friendly and nice people. It was just a pleasure to talk and exchange ideas with them.

Results in ICA-based analysis ­–like the ones in Kullmann et al. studies (2,4) or the ones in my previous studies (3,5) – could be associated with the principle of modularity or segregation in functional connectivity. This principle refers to the organization of a system (i.e., the brain) into a set of modules (i.e., networks) containing highly inter-correlated components (6). Imagine that you are in a party, and you are trying to identify sub-groups of people based on the pattern of social inter-relations that they present. You look around and you see a group of cool people happily drunk talking with each other and dancing, romantic couples on the corners kissing like there’s no tomorrow, and a group of women wearing pink ballet skirts and diadems with bunny ears that just came from a bachelorette party. If you think about the people in the party in this manner, you are segregating the different components of the system into subgroups or modules.

Another perspective would be to assess how the system as a whole becomes interconnected and how the information can be distributed through the different components. This has been referred to as the principle of integration (6). Again, taking the example of the party, you could be interested in investigating the way in which relevant information (e.g., the club is running out of gin tonic) is transmitted to the rest of the members in the party. Here, you will be especially interested in identifying those members with the highest accessibility to the other members. It is likely that waiters and some of the most popular guests in the party will be the ones spreading information to the other members.

In our most recent study in obesity, we aimed to examine functional brain differences between participants with obesity and normal-weight individuals by examining functional brain integration. We found that participants with obesity exhibited a diminished functional integration (that is, less information exchange) of the middle prefrontal gyrus and the lateral occipital cortex with the entire brain network (7). Since the middle prefrontal gyrus is a structure associated with inhibitory control processes (8) we speculated that the obesity-related differences observed could be associated with difficulties in impulse-control processes. However, this needs to be further investigated with proper fMRI tasks.

So, enough writing for today, it is time for me to procrastinate and to look at my pictures from Hawaii. Mahalo for your time reading my blog!!


  1. Seeley W, Menon V. Dissociable intrinsic connectivity networks for salience processing and executive control. J Neurosci, 2007, 27: 2349–56.
  2. Kullmann S, Heni M, Veit R, Ketterer C, Schick F, Häring H-U, et al. The obese brain: Association of body mass index and insulin sensitivity with resting state network functional connectivity. Hum Brain Mapp, 2011, 33: 11052–61.
  3. García-García I, Jurado MÁ, Garolera M, Segura B, Sala-Llonch R, Marqués-Iturria I, et al. Alterations of the salience network in obesity: a resting-state fMRI study. Hum Brain Mapp, 2013, 34: 2786–97.
  4. Kullmann S, Pape A-AA, Heni M, Ketterer C, Schick F, Häring H-U, et al. Functional Network Connectivity Underlying Food Processing: Disturbed Salience and Visual Processing in Overweight and Obese Adults. Cereb Cortex, 2013, 23:1247–56.
  5. García-García I, Jurado MA, Garolera M, Segura B, Marqués-Iturria I, Pueyo R, et al. Functional connectivity in obesity during reward processing. Neuroimage, 2013, 66C: 232–9.
  6. Sporns O. Network attributes for segregation and integration in the human brain. Curr Opin Neurobiol, 2013,
  7. García-García I, Jurado MÁ, Garolera M, Marqués-Iturria I, Horstmann A, Segura B, et al. Functional network centrality in obesity: A resting-state and task fMRI study. Psychiatry Res Neuroimaging, 2015, (in press).
  8. Hare TA, Camerer CF, Rangel A. Self-control in decision-making involves modulation of the vmPFC valuation system. Science. 2009, 324: 646–8.
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The stick, the carrot, and the brain

Sometimes it seems easy to discern good from bad. Surviving in complex environments requires the ability to repel stimuli that might lead us to harmful consequences. Likewise, we might spend time and energy pursuing goals that maximize our benefit and pleasure. As such, we tend to choose Gondor over Mordor. Gryffindor over Slytherin. Or being a marine biologist and tracking gray whales on their migratory routes across the Pacific Ocean over becoming a neuroscientist and working the whole day sitting in front of a computer and reading about affective stuff.

Complex organisms are fully adapted for detecting and responding to positive and negative stimuli or situations. For years, researchers have addressed the neurobehavioral mechanisms that allow us to discern between good and bad, or –put in motivation-related terms– reward and punishment.

Behaviorally, reward and punishment are not processed in equivalent ways. There is a well-documented asymmetry between them: the processing of negative stimuli is prioritized over positive stimuli, a phenomenon known as the negativity bias (1,2). This means, when facing good stimuli and bad stimuli with equal intensities, bad stimuli tend to yield greater attentional and affective processing relative to good stimuli. As such, compared with positive events, negative events elicit stronger and more rapid responses, have more powerful effects on human relationships, and are recalled more accurately (1,2).

As an example of this, this Saturday I was in the city center with my BF just looking around and buying some stuff. At some point, he suggested we could sit and drink a coffee somewhere. My BF’s favorite café in Leipzig is a small cafeteria full of tourists and with a small outdoors terrace. I don’t really like it because it is always crowded, and it is more expensive that some other nice places that are not far away. Anyways, we ended there. We just sat on a table, when all the sudden, in the next table –placed less than half a meter from ours– a group of 10 Dutch girls in their eighteens sat there to have ice-cream. They spoke so loud (OMG!). We could not even have a conversation! Then, the waiter came, so I told him in my perfect German accent ‘Hallo, ich möchte ein Espresso, bitte’. The waiter just looked at me, raised his eyebrows and asked me again what I would like to have, this time in English (!!?!) I hate when this happens. Seriously. What is the German word for being grumpy because I am sitting in a place that I have not chosen by myself, surrounded by loud tourists and because, according to the waiter, my German is not good enough? Anyways, I was being totally unfair. I did not have any valid reason to be grumpy. That morning, Leipzig looked lovely, I did not have to worry about work and I was just having a great time with my awesome-and-patient BF, who just wanted to sit down and have a nice coffee with me somewhere. So, I tried to calm down and start looking at the world in a positive manner. Well, actually it also helped that another table far from the ten eighteen years old tourists got free, so we moved there, and it was sunny and lovely. Sometimes you face good things and bad things at the same time, but you can always choose where to pay attention.

So, enough anecdotes about positive and negative stimuli, an exciting paper that revolves around the asymmetry “bad > good stimuli” has been published recently. In line with previous studies, the authors found that monetary losses had 2-3 times a stronger effect on behavior than monetary gains (3). Interestingly, the authors provided further evidence that reward and punishment might guide behavior in a differential way. That is, on one hand, monetary reward was able to influence choice according to the magnitude of the event. As such, gaining 25 cents produced comparatively higher probabilities of repeating a given behavior relative to gaining 5 cents. Conversely, the effect of monetary losses on choice behavior followed a constant function. Thereby, losing money was associated with lower probabilities for repeating a certain behavior, no matter if the monetary loss was 5 cents or 25 cents (3).

This last finding is kind of cool and also kind of unexpected. Basically, it describes the fact that punishment might affect behavior, independent on the magnitude of the punishment. It is tempting to extract conclusions out of this and, for example, to recommend tram inspectors in Leipzig not to charge with 40 € bills when someone does not have a valid ticket, but rather deliver 5 € fines because the effect will be the same. Well, actually, public transport should be free for everybody! Nevertheless, it is better to be cautions by now and to see if this same effect can be detectable by using different range of monetary penalties (e.g., from 1$ to 100 $ instead of from 5 cents to 25 cents) as well as other negative stimuli that might be more biologically relevant (e.g., pain stimuli or negative social feedback).

At the neural level, and as I already mentioned in a previous post, it is known that positive/appetitive stimuli and negative aversive stimuli present huge overlapping patterns of brain activity, including the amygdala, anterior insula, and ventral striatum (4,5). However, it is plausible that, at the cellular level, these structures undergo microscopic modifications that depend on the valence of the stimuli (positive versus negative). Due to technical limitations, these changes would not be detectable with current MRI resolutions.

According to this possibility, a recent study in rodents from Namburi et al. suggests that brain circuits linking the amygdaloid complex with the nucleus accumbens might encode the valence of the stimuli (6). The authors reported that the nucleus accumbens and the centromedial amygdala contain populations of basolateral neurons that suffer opposing synaptic modifications following fear conditioning or reward learning. As such, in the centromedial amygdala projectors, fear conditioning causes increases in synaptic strengths, while reward learning is linked with decreases in synaptic strengths. Conversely, synaptic strengths onto nucleus accumbens projectors were observed to decrease following fear conditioning and to increase following reward learning (6).

There is still lot of work to be done in order to translate Namburi’s exciting findings to humans. And at a behavioral level, using Baumeister et al.’s own words, bad seems to be stronger than good “in a disappointingly relentless pattern” (1). But, nevertheless, it is also useful to remember that the asymmetry “bad > good” might provide us with the motivation we need in order to keep on searching for happiness and creating a better world.



  1. Baumeister RF, Bratslavsky E, Finkenauer C, Vohs KD. Bad is stronger than good. Rev Gen Psychol. 2001; 5(4):323–70.
  2. Ito TA, Larsen JT, Smith NK, Cacioppo JT. Negative Information Weighs More Heavily on the Brain : The Negativity Bias in Evaluative Categorizations has noted a tendency for negative events to result in a greater. J Pers Soc Psychol. 1998; 75(4):887–900.
  3. Kubanek J, Snyder LH, Abrams RA. Reward and punishment act as distinct factors in guiding behavior. Cognition. 2015; 139:154–67.
  4. Lindquist KA, Satpute AB, Wager TD, Weber J, Barrett LF. The Brain Basis of Positive and Negative Affect: Evidence from a Meta-Analysis of the Human Neuroimaging Literature. Cereb Cortex. 2015; 1–13.
  5. Hayes DJ, Duncan NW, Xu J, Northoff G. A comparison of neural responses to appetitive and aversive stimuli in humans and other mammals. Neurosci Biobehav Rev. 2014; 45C:350–68.
  6. Namburi P, Beyeler A, Yorozu S, Calhoon GG, Halbert SA., Wichmann R, et al. A circuit mechanism for differentiating positive and negative associations. Nature. 2015; 520(7549):675–8.
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The bright side and the dark side of aging

It is well known that aging causes a decline in several domains of cognitive function. Memory tasks, speed processing and the ability to switch from one task to another are examples of cognitive skills with a tendency to diminish, as we grow older. But nevertheless, it is also known that, in the absence of neuropsychiatric pathologies, several other every-day functions tend to remain stable over time (1).

In fact, in modern societies, an increasing number of older adults maintain high levels of satisfaction, personal independence, and a relatively stable health status. Paul B Baltes, who is like a rock star in psychology of aging, described this process as ‘successful aging’ (2,3). I still want to add something more about Paul B Baltes: he was one of the great persons that made it possible the incredibly awesome idea of creating a fellowship funding program in aging research. I still don’t know why, but I was admitted as a postdoc student in that program. I still feel extremely grateful for not having to worry about money at the end of the month.

So, after having stated my deep and selfless admiration for Paul B Baltes and his work, let’s go back to aging. One of the functions that seems to be stable across life span is emotional management. In this field, it has been formulated an influential theory called the “emotional paradox”. This paradox refers to the fact that, despite being proportionally more exposed to emotional adversities (e.g. the loss of significant others, declines in physical strength, increments in the vulnerability to disability), the subjective well-being of healthy older adults is maintained or even increased with age (4,5).

Nevertheless, aging is a highly heterogeneous process, influenced by multiple genetic and environmental factors. As such, it is not surprising that emotional processes present strong differences, even across healthy older individuals.

For example, subjective rates of happiness might be influenced by political and economical population characteristics. Last year, a very cool study observed marked variations across different countries in subjective rates of well-being, with relatively high rates of happiness in high-income English speaking countries, in Latin America and in Caribbean countries, and high rates of unhappiness in several transition countries, such as in Eastern Europe and in countries of the former Soviet Union (6).

Health status is obviously another factor to take into account when studying subjective well-being in aging. Here, I’m going to focus on the role of vascular burden. It seems clear now that vascular factors are associated with lower cognitive outcomes, especially in the domain of mental speed (7). In addition to this, late-life affective symptomatology seems to be closely related to vascular pathology. This phenomenon is also referred to as “vascular depression”. Essentially, the vascular depression hypothesis proposes that vascular risk factors may be associated with the beginning or with the chronicity of depressive symptoms (8). Vascular depression has been associated with several neurological, immunological and cognitive changes (8). Amongst them, the best established is the presence of ischemic lesion burden, observable via white matter hyperintensities. A meta-analysis on 30 studies reported that relative to controls, patients with late-life depression exhibited a more frequent and severe white matter hyperintensities. Interestingly, the same study reported that white matter hyperintensities were more severe in individuals with late-life depression relative to individuals with early-life depression (9). This last finding rises the interesting possibility that late-life depression might constitute a different entity of depressive disorders (9). Complementing this finding, a very recent study in community dwelling older adults has found that severity of white matter hyperintensities seems to predict the development of depressive symptoms (10).

So, to sum up, one should not neglect the deleterious effects of vascular burden in aging. Several studies seem to indicate that vascular factors might compromise subjective well-being in aging. However, there are good news too! Vascular risk factors can be highly influenced by lifestyles. I really want to avoid ending this paragraph writing a list of healthy things to do and unhealthy things to avoid. So, yah know, if you don’t really want to change your unhealthy habits at all, not even for the sake of your future health in 50 years, maybe you should consider moving to a Caribbean or Latin American country. I’m not sure if this last point makes any sense, but it won’t hurt after all!


  1. Park DC, Reuter-Lorenz P. The adaptive brain: aging and neurocognitive scaffolding. Annu Rev Psychol. 2009; 60:173–96.
  2. Baltes PB. Theoretical propositions of life-span developmental psychology: On the dynamics between growth and decline. Dev Psychol. 1987; 23(5):611–26.
  3. Baltes PB, Baltes PB. On the Incomplete Architecture of Human Ontogeny. Am Psychol. 1997; 52(4):366–80.
  4. Carstensen L. Taking time seriously: A theory of socioemotional selectivity. Am Psychol. 1999; 54:165–81.
  5. Mather M. The emotion paradox in the aging brain. Ann N Y Acad Sci. 2012; 1251: 33–49.
  6. Steptoe A, Deaton A, Stone A a. Subjective wellbeing, health, and ageing. Lancet. 2014; 6736(13):1–9.
  7. López-Olóriz J, López-Cancio E, Arenillas JF, Hernández M, Jiménez M, Dorado L, et al. Asymptomatic cervicocerebral atherosclerosis, intracranial vascular resistance and cognition: The AsIA-Neuropsychology Study. Atherosclerosis. 2013;230(2):330–5.
  8. Taylor WD, Aizenstein HJ, Alexopoulos GS. The vascular depression hypothesis: mechanisms linking vascular disease with depression. Mol Psychiatry. 2013;18(9):963–74.
  9. Herrmann LL, Le Masurier M, Ebmeier KP. White matter hyperintensities in late life depression: a systematic review. J Neurol Neurosurg Psychiatry. 2008;79:619–24.
  10. Park JH, Lee SB, Lee JJ, Yoon JC, Han JW, Kim TH, et al. Epidemiology of MRI-defined vascular depression: A longitudinal, community-based study in Korean elders. J Affect Disord. 2015; 180:200–6.
  11. Vu NQ, Aizenstein HJ. Depression in the elderly: brain correlates, neuropsychological findings, and role of vascular lesion load. Curr Opin Neurol. 2013; 6:656–61.
  12. Byrne GJ, Pachana N a. Anxiety and depression in the elderly: do we know any more? Curr Opin Psychiatry. 2010; 23(6):504–9.
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Does your brain know at all what different emotions are?

In ‘How I met your mother’, Stella decides to break up with Ted and to give another opportunity to her ex-husband on the same day they (Stella and Ted) were supposed to get married. When Ted realizes that Stella has moved to her ex-husband’s apartment, he feels enraged. Therefore, he decides to confront Stella and to tell her that she made the biggest mistake in her life. But when he is about to do so, Ted sees Stella walking towards her ex-husband’s apartment; with her ex-husband and their daughter waiting for her at the door. Suddenly, he does not feel angry anymore, because he realizes that they were meant to be a family. So, he decides to let all the anger go and to move forward.

Emotions are powerful components of our day-to-day experience. Emotions guide our actions and emotions change over time. But nevertheless, we are still miles away from an accurate understanding of how emotions are represented in the brain.

Emotions are not represented in single brain areas of the brain. Rather, they are signaled in widespread locations of the brain, including perceptual areas (e.g., occipital cortex), limbic regions (e.g., amygdala) and anterior parts of the brain (e.g., anterior cingulate cortex, orbitofrontal cortex or inferior frontal gyrus) (1–3). So far it seems easy, but things get complicated.

The patterns of brain activity across different emotion categories (e.g., anger, fear or happiness) present huge overlaps. That means, most of the aforementioned areas will be activated in your brain no matter if you are feeling sad, angry or happy (1). And, even more complicated, at a first sight it might even seem as if the brain does not really differentiate between common-sense categories like ‘positive versus negative stimuli’ or ‘appetitive versus aversive stimuli’. Areas like the amygdala, anterior insula or ventral striatum are activated both during positive and during negative stimuli (4,5). Here, though, there are some exceptions. Activity in few specific areas –e.g., the anterior cingulate cortex– seems to predominate in response to appetitive or positive stimuli relative to negative stimuli (4,5). But nevertheless, this seems not to be the case for the majority of brain regions that are considered to play a role in emotional processing.

So, is the brain blind to the emotional experience? How can it be the same to feel love than to feel disgust or to feel sad than to feel happy? Even more important and transcendental: should we start creating a whole new vocabulary with words like ‘lovegust’ or ‘sadppy’ in order to refer to emotionally overlapping scenarios? Well… I’m afraid it might not be necessary…

At the beginning of this month, an exciting new study was published. The authors were able to demonstrate that each emotion category was associated with separable patterns of brain activity across multiple brain systems (6). In other words, what it might differentiate between different emotions is not the single areas that activate in response to a certain stimuli, but rather, which networks co-activate together in order to represent that emotional category in the brain (6).

The profiles obtained for each emotion are insightful, and help to understand biological mechanisms behind the emotional experience. To put a few examples of this, anger and fear recruited areas ascribed to the cortical dorsal attentional network. This fact was interpreted as reflecting an engagement of neural processes supporting orientation towards external stimuli. Contrarily, disgust was characterized by coactivity in basal ganglia and somatomotor areas. The authors proposed that this pattern might support an orientation towards internal perceptions (6).

Lots of questions in emotion research remain unanswered. How does the brain ‘move’ from one emotion to the other? Which is the influence of ‘cognitive’ processes during the perception of emotional experience? Nevertheless, the study points to the direction of the importance of focusing on patterns of co-activation in the study of the neural representation of emotions.



  1. Lindquist KA, Wager TD, Kober H, Bliss-Moreau E, Barrett LF. The brain basis of emotion: a meta-analytic review. Behav Brain Sci. 2012; 35(3):121–43.
  2. Carretié L, Albert J, López-Martín S, Tapia M. Negative brain: an integrative review on the neural processes activated by unpleasant stimuli. Int J Psychophysiol. 2009; 71(1):57–63.
  3. Fusar-Poli P, Placentino A, Carletti F, Landi P, Allen P, Surguladze S, et al. Functional atlas of emotional faces processing: a voxel-based meta-analysis of 105 functional magnetic resonance imaging studies. J Psychiatry Neurosci. 2009; 34(6):418–32.
  4. Lindquist KA, Satpute AB, Wager TD, Weber J, Barrett LF. The Brain Basis of Positive and Negative Affect: Evidence from a Meta-Analysis of the Human Neuroimaging Literature. Cereb Cortex. 2015;1–13.
  5. Hayes DJ, Duncan NW, Xu J, Northoff G. A comparison of neural responses to appetitive and aversive stimuli in humans and other mammals. Neurosci Biobehav Rev. 2014;45C:350–68.
  6. Wager TD, Kang J, Johnson TD, Nichols TE, Satpute AB, Barrett LF. A Bayesian Model of Category-Specific Emotional Brain Responses. PLOS Comput Biol. 2015;11(4):e1004066.
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Arousedbrain: the starting point

Is friendship forever? Why can we remember our first kiss? Can words truly cure? What is love? Baby don’t hurt me, don’t hurt me, no more.

Hi world, this is Arousedbrain. The purpose of this blog is to comment on recent studies in affective neuropsychology and to share my adventures as a researcher.


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