Trial Report The effects of chronic fatigue and chronic stress on alterations in immune cell responses to acute psychosocial stress, 2024, Nater

[Dolphin]

https://www.sciencedirect.com/science/article/pii/S0889159124006536

Brain, Behavior, and Immunity
Available online 13 October 2024
In Press, Journal Pre-proof

The effects of chronic fatigue and chronic stress on alterations in immune cell responses to acute psychosocial stress

Nida Ali, Jana Strahler, Urs M. Nater,

https://doi.org/10.1016/j.bbi.2024.10.013
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open access

Highlights

• •
  Acute stress induced changes in lymphocyte subpopulations.
• •
  Low fatigue individuals had steeper changes in cell populations following stress.
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  Both chronic fatigue and stress have blunting effects on adaptive immune functioning.

Abstract

Fatigue is a common and debilitating symptom of a broad spectrum of diseases.

Previous research has shown that individuals suffering from chronic forms of fatigue experience significantly more stress compared to healthy individuals, suggesting that stress is a potential pathophysiological factor in the onset and maintenance of chronic fatigue.

Individually, chronic experiences of fatigue and stress have been associated with disruptions in adaptive immunity.

However, how chronic fatigue and chronic stress together affect immune regulation is not fully understood.

Here, we investigated the unique and combined contribution of chronic fatigue and chronic stress on immune cell redistribution in response to, and recovery from, acute psychosocial stress.

Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor.

Blood samples were collected 10 min before and then at 10, 40, and 100 min after the end of stress.

The main lymphocyte subpopulations (CD3+, CD3 + CD4+, CD3 + CD8+, CD16 + CD56+, and CD19 + cells) were enumerated via flow cytometry.

Acute stress resulted in an increase in CD8 + and CD16+/CD56 + cells, a decline in CD4 + cells, and no effects on CD19 + B lymphocytes.

Importantly, the magnitude of immune cell redistribution during stress reactivity (CD3+, CD4+, CD16+/CD56 + ) and recovery (CD3 + ) was contingent on fatigue and chronic stress levels of individuals.

Notably, in contrast to low-fatigued individuals, who showed steeper changes in cell populations, increasing levels of chronic stress did not impact immune cell migration responses in high-fatigued individuals.

Our findings demonstrate the compounded blunting effects of fatigue and chronic stress on adaptive immune functioning, highlighting a potential pathway for vulnerability and detrimental effects on long-term health.

Keywords
Chronic fatigue
Chronic stress
Acute stress
TSST
CD3+ T cells
CD3+CD4+ T helper cells
CD3+CD8+ T-suppressor cells
CD16+CD56+ NK cells
CD19+ B cells

 

[Dolphin]

2. Methods
2.1. Participants
This study was part of a larger project investigating the psychological and biological mechanisms that underlie chronic fatigue and chronic stress. For the current study, 80 participants were recruited from the general population. Eligible participants were fluent in German, 18 years or older, self-identified as female, and had a Body Mass Index (BMI) range of 18–30 kg/m2 to exclude weight-related immune dysfunction. Individuals were deemed ineligible if they were pregnant or lactating, met the diagnostic criteria for CFS, took medication that influenced neuroendocrine, autonomic, or immune function, had major physical health conditions (e.g., cancer, hepatic, hematological, neurological, autoimmune, or endocrinological diseases), or were diagnosed with psychological disorders (i.e., substance abuse/dependence within the past 2 years, eating disorders within the past 5 years, lifetime psychotic or bipolar disorder). The study was conducted at the University of Marburg, Germany, between 2013 and 2018. Participants provided informed written consent for the study, which was approved by the ethics committee at the University of Marburg.

 

[Dolphin]

Urs Nater was lead author on a number of CDC CFS research papers around 15 years ago.

 

[rvallee]

Acute stress induced changes in lymphocyte subpopulations

Given that exercise has similar effects, and that in about 99% of cases stress can be substituted for exertion, isn't this just the normal effect of literally any exertion above base metabolism? Because it just creates completely unnecessary confusion to use the common terminology of stress in popular psychology when it mostly means cellular stress, making any type of effort. Those are just very different, and give rise to nonsense like the notion of psychosocial stress, like it's some magical thing happening in a parallel mind field, rather than simply the body doing work.

The point being mainly that there is no such thing as psychosocial stress. It's just exertion, and whether it's physical or cognitive, or even immune, doesn't change much. That's just exertion:

The TSST consists of an anticipation phase, followed by a testing phase encompassing a 5-minute speech and a 5-minute mental arithmetic task, performed in front of trained confederates

I know it's popular to have this notion of such things being stressful, but to a lot of people, myself included, this rates a 0 on the anxiety scale, which is what psychosocial stress usually means. Here it's about "performance anxiety", even though the performance is entirely inconsequential and therefore irrelevant. The anticipation phase, i.e. "take a 5 minute break", is frankly just weird to me.

I don't really know what this has to do with chronic fatigue or chronic pain either, aside from participants meeting some arbitrary definition.

 

[Sean]

Eighty women with high or low levels of chronic fatigue and varying levels of chronic stress were exposed to a psychosocial laboratory stressor.

No control for non-psychosocial stressors?

Or direction of causation?

If patients are already stressed due to persistent fatigue and/or the underlying causes of it (especially undiagnosed and untreated medical problems, and associated misattribution by clinicians), then adding any sort of stressor on top is hardly likely to be beneficial.