Stress can kill you and that’s no metaphor

85heart - CopyThe term ‘heartbreak’ is used as a metaphor to describe the intense feeling of loss, sometimes also called emotional pain. But what if the metaphor has roots into something more tangible than a feeling, that of the actual muscular organ giving signs of failure?

Although there have been previous reports that found stress causes cardiovascular problems, including myocardial infarction, Graff et al. (2016) conducted the largest study to date that investigated this link: they had almost 1 million subjects. That’s right, 1 million people (well, actually 974 732). Out of these, almost 20% of them had a partner who died between 1995 and 2014. The chosen stressor was the loss of a loved one because “the loss of a partner is considered one of the most severely stressful life events and is likely to affect most people, independently of coping mechanisms” (p. 1-2). The authors looked at Danish hospital records for people who were diagnosed with atrial fibrillation (AF) for the first time and correlated that data with bereavement information. AF increases the risk of death due to stroke or heart failure.

The people who underwent loss had an increased risk to develop AF for 1 year after the loss. The risk was more pronounced in the first 8-14 days after the loss, the bereaved people having a 90% higher risk of developing AF than non-bereaved people. By the end of the first month the risk had declined, but still was a whooping 41% higher than the average. Only 1 year after the loss the risk of developing AF was similar to that of non-bereaved people.

The risk was even higher in young people or if the death of the partner was unexpected. The authors also looked to see if other variables play a role in the risk, like gender, civil status, education, diabetes, or cardiovascular medication and none influenced the results.

I suspect the number of people that have heart problems after major stress is actually a lot higher because of the under-reporting bias. In other words, not everybody who feels their heart aching would go to the hospital, particularly in the first couple of weeks after losing a loved one.

As for the mechanism, there is some data pointing to some stress hormones (like adrenaline or cortisol) which can damage the heart. Other substances released in abundance during stress and likely to act in concert with the stress hormones are proinflamatory cytokines which also can lead to arrhythmias.

Reference: Graff S, Fenger-Grøn M, Christensen B, Søndergaard Pedersen H, Christensen J, Li J, & Vestergaard M (2016). Long-term risk of atrial fibrillation after the death of a partner. Open Heart, 3: e000367. doi:10.1136/openhrt-2015-000367. Article  | FREE FULTEXT PDF

By Neuronicus, 16 April 2016

Advertisements

Intracranial recordings in human orbitofrontal cortex

81 ofc - CopyHow is reward processed in the brain has been of great interest to neuroscience because of the relevance of pleasure (or lack of it) to a plethora of disorders, from addiction to depression. Among the cortical areas (that is the surface of the brain), the most involved structure in reward processing is the orbitofrontal cortex (OFC). Most of the knowledge about the human OFC comes from patients with lesions or from imaging studies. Now, for the first time, we have insights about how and when the OFC processes reward from a group of scientists that studied it up close and personal, by recording directly from those neurons in the living, awake, behaving human.

Li et al. (2016) gained access to six patients who had implanted electrodes to monitor their brain activity before they went into surgery for epilepsy. All patients’ epilepsy foci were elsewhere in the brain, so the authors figured the overall function of OFC is relatively intact.

While recording directly form the OFC the patients performed a probabilistic monetary reward task: on a screen, 5 visually different slot machine appeared and each machine had a different probability of winning 20 Euros (0% chances, 25%, 50%, 75% and 100%), fact that has not been told to the patients. The patients were asked to press a button if a particular slot machine is more likely to give money. Then they would use the slot machine and the outcome (win 20 or 0 Euros) would appear on the screen. The patients figured out quickly which slot machine is which, meaning they ‘guessed’ correctly the probability of being rewarded or not after only 1 to 4 trails (generally, learning is defined in behavioral studies as > 80% correct responses). The researchers also timed the patients during every part of the task.

Not surprisingly, the subjects spent more time deciding whether or not the 50% chance of winning slot machine was a winner or not than in all other 4 possibilities. In other words, the more riskier the choice, the slower the time reaction to make that choice.

The design of the task allowed the researchers to observe three 3 phases which were linked with 3 different signals in the OFC:

1) the expected value phase where the subjects saw the slot machine and made their judgement. The corresponding signal showed an increase in the neurons’ firing about 400 ms after the slot machine appeared on the screen in moth medial and lateral OFC.

2) the risk or uncertainty phase, when subjects where waiting for the slot machine to stop its spinners and show whether they won or not (1000-1500 ms). They called the risk phase because both medial and lateral OFC had the higher responses when there was presented the riskiest probability, i.e. 50% chance. Unexpectedly, the OFC did not distinguish between the winning and the non-wining outcomes at this phase.

3) the experienced value or outcome phase when the subjects found out whether they won or not. Only the lateral OFC responded during this phase, that is immediately upon finding if the action was rewarded or not.

For the professional interested in precise anatomy, the article provides a nicely detailed diagram with the locations of the electrodes in Fig. 6.

The paper is also covered for the neuroscientists’ interest (that is, is full of scientific jargon) by Kringelbach in the same Journal, a prominent neuroscientist mostly known for his work in affective neuroscience and OFC. One of the reasons I also covered this paper is that both its full text and Kringelbach’s commentary are behind a paywall, so I am giving you a preview of the paper in case you don’t have access to it.

Reference: Li Y, Vanni-Mercier G, Isnard J, Mauguière F & Dreher J-C (1 Apr 2016, Epub 25 Jan 2016). The neural dynamics of reward value and risk coding in the human orbitofrontal cortex. Brain, 139(4):1295-1309. DOI: http://dx.doi.org/10.1093/brain/awv409. Article

By Neuronicus, 25 March 2016

Stress can get you fat. And then kill you.

stress meSome people lose weight under stressful conditions and some gain weight. How does that play into the risk for the cardiovascular disease and subsequent mortality? Medical doctors keep warning us that fat people are at risk for diabetes and heart disease. Turns out that being a little on the heavy side might actually not be that bad. It all depends on what kind of fat and where it is.

The paper featured today reviews a series of interesting articles with surprising results. Peters & McEwen (2015) identify three distinct phenotypes:

1) The good stress leads to well-proportionate body shape. People who live in safe environments, they do well socioeconomically, they have good self-esteem, and they have a fulfilling social and family life. They experience low levels of stress, they are well proportionate, and have a low mortality rate due to cardiovascular disease. Might as well call these ones the lucky ones.

2) The tolerable stress leads to corpulent-but-narrow-waisted body shape. People who experience stress but in order to cope with it they supply the brain with more energy by eating more. So they become more corpulent, gaining subcutaneous fat, but their cardiovascular mortality risk remains low.

3) The toxic stress leads to lean-but-wide-waisted body shape. People who experience prolonged stress exposure to uncertain socioeconomic conditions, poor work, or family life. They have low self-esteem, often associated with depressive periods. They are or become lean, but they accumulate large visceral fat deposits (as opposed to subcutaneous), and their cardiovascular mortality risk is the highest. They also are at risk for other physical and mental disorders. The phenotype 3 people have a wider waist relative to their body mass index and height.

Source: Peters & McEwen (2015, p.144)
Source: Peters & McEwen (2015, p.144)

Thus, the authors propose that instead or along with the body mass index, another metric should be used to identify the ones in dire need of help: the body shape index. Also, the review outlines the mechanisms responsible for these findings.

So next time you see a not so well-proportionate person, smile. Maybe even offer to help or chat; you don’t know what they’re going through.

Reference: Peters, A. & McEwen, B. S. (September 2015, Epub 3 July 2015). Stress habituation, body shape and cardiovascular mortality. Neuroscience Biobehavioral Reviews, 56:139-50. doi: 10.1016/j.neubiorev.2015.07.001. Article | FREE PDF

By Neuronicus, 5 October 2015