Peters Achim, Hartwig Mattis, Spiller Tobias
Medical Clinic 1, Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany.
German Research Center for Artificial Intelligence (DFKI), Kaiserslautern, Germany.
Front Psychol. 2022 Jun 10;13:931701. doi: 10.3389/fpsyg.2022.931701. eCollection 2022.
According to the free energy principle, all sentient beings strive to minimize surprise or, in other words, an information-theoretical quantity called variational free energy. Consequently, psychosocial "stress" can be redefined as a state of "heightened expected free energy," that is, a state of "expected surprise" or "uncertainty." Individuals experiencing stress primarily attempt to reduce uncertainty, or expected free energy, with the help of what is called an uncertainty resolution program (URP). The URP consists of three subroutines: First, an arousal state is induced that increases cerebral information transmission and processing to reduce uncertainty as quickly as possible. Second, these additional computations cost the brain additional energy, which it demands from the body. Third, the program controls which stress reduction measures are learned for future use and which are not. We refer to an episode as "good" stress, when the URP has successfully reduced uncertainty. Failure of the URP to adequately reduce uncertainty results in either stress habituation or prolonged toxic stress. Stress habituation reduces uncertainty by flattening/broadening individual goal beliefs so that outcomes previously considered as untenable become acceptable. Habituated individuals experience so-called "tolerable" stress. Referring to the Selfish Brain theory and the experimental evidence supporting it, we show that habituated people, who lack stress arousals and therefore have decreased average brain energy consumption, tend to develop an obese type 2 diabetes mellitus phenotype. People, for whom habituation is not the free-energy-optimal solution, do not reduce their uncertainty by changing their goal preferences, and are left with nothing but "toxic" stress. Toxic stress leads to recurrent or persistent arousal states and thus increased average brain energy consumption, which in turn promotes the development of a lean type 2 diabetes mellitus phenotype. In conclusion, we anchor the psychosomatic concept of stress in the information-theoretical concept of uncertainty as defined by the free energy principle. In addition, we detail the neurobiological mechanisms underlying uncertainty reduction and illustrate how uncertainty can lead to psychosomatic illness.
根据自由能原理，所有有感知的生物都努力将意外最小化，或者换句话说，将一个称为变分自由能的信息理论量最小化。因此，心理社会“压力”可以重新定义为“预期自由能增加的状态”，即“预期意外”或“不确定性”的状态。经历压力的个体主要试图借助所谓的不确定性解决程序（URP）来减少不确定性或预期自由能。URP由三个子程序组成：首先，诱导一种唤醒状态，这种状态会增加大脑信息的传输和处理，以尽快减少不确定性。其次，这些额外的计算会使大脑消耗额外的能量，而大脑会从身体获取这些能量。第三，该程序控制哪些减压措施会被学习以供未来使用，哪些则不会。当URP成功减少不确定性时，我们将这样的一段经历称为“良性”压力。URP未能充分减少不确定性会导致压力习惯化或长期的毒性压力。压力习惯化通过使个体目标信念变平/变宽来减少不确定性，这样以前被认为不可行的结果就变得可以接受了。习惯化的个体经历所谓的“可容忍”压力。参照自私大脑理论及其支持的实验证据，我们表明，缺乏压力唤醒因而平均大脑能量消耗降低的习惯化人群，往往会发展出肥胖型2型糖尿病表型。对于那些习惯化不是自由能最优解决方案的人来说，他们不会通过改变目标偏好来减少不确定性，而只会承受“毒性”压力。毒性压力会导致反复或持续的唤醒状态，从而增加平均大脑能量消耗，这反过来又会促进瘦型2型糖尿病表型的发展。总之，我们将压力的心身概念锚定在自由能原理所定义的信息理论不确定性概念中。此外，我们详细阐述了减少不确定性背后的神经生物学机制，并说明了不确定性如何导致心身疾病。
