21 research outputs found

    The Experience of Meditation and Healing in Practitioners of the Wim Hof Method

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    The practice of meditation for the purpose of increasing mental clarity, health, and healing has grown steadily over the past 50 years or more. While meta-analyses and literature reviews of hundreds of studies have shown that individuals who meditate improve neuro-biopsychosocial functions and recover from illness, few studies have examined these benefits within specific systems of practice. This qualitative study explored the experience of meditation and healing in adults who have trained in the Wim Hof Method (WHM). Transpersonal psychology and placebo theory served as the conceptual framework of this research. Narrative analysis was used to guide data collection and analysis. The narrative interviews of 10 participants who experienced the WHM were transcribed and analyzed using both structural and thematic strategies. The results indicated that WHM practitioners experienced neuro-biopsychosocial and emotional well-being through the use of breath, cold-immersion, and/or meditation. All participants reported profound experiences involving symptomatic reduction and/or the healing of maladies, as well as transpersonal/transcendental experiences that transformed their lives. Future research is encouraged to study the experience in more diverse populations (gender, nationality and age), and to explore participants’ worldviews prior to, during, and following the practice of the Wim Hof Method. Quantitative research assessing effectiveness and the influence of individual difference factors is recommended. Given the benefits associated with engaging in the WHM, as well as its low cost, ease of access and simplicity, this method could be deployed across a variety of venues to inspire social change

    L-type Voltage-Gated Calcium Channels in Fear Conditioning, Fear Extinction, and Amygdala Neurophysiology.

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    Fear conditioning is a form of learning in which an initially neutral stimulus (e.g., tone or context) comes to be feared after being paired with an aversive stimulus (e.g., shock). After pairing, the neutral stimulus alone can elicit fear responses (e.g., freezing behavior, autonomic arousal, stress hormone release). The initially neutral stimulus is referred to as the "conditioned stimulus" (CS) once it is able to bring about fear responses on its own, the aversive stimulus is the "unconditioned stimulus" (US), and the fear responses elicited by the CS are the "conditioned responses" (CRs). Fear extinction is a process by which the previously conditioned fear responses can be reduced by repeated presentation of the CS alone, in the absence of the aversive US. Fear conditioning and fear extinction are both critically dependent on the amygdala, a medial temporal lobe brain structure. Interestingly, it has been previously demonstrated that L-type voltage-gated calcium channels (L-VGCCs) have a role in fear conditioning, fear extinction, and amygdala neurophysiology. All of the studies implicating L-VGCCs in these phenomena used L-VGCC antagonists to demonstrate the role for L-VGCCs. There are two brain-expressed L-VGCCs, Cav1.2 and Cav1.3, both of which are the targets of currently-available L-VGCC antagonists. In this dissertation, I address the contribution of each of these L-VGCCs to fear conditioning, fear extinction, and amygdala neurophysiology using mouse models in which the genes for either Cav1.2 or Cav1.3 deleted. First, I demonstrate that Cav1.3, but not Cav1.2, mediates consolidation of fear conditioning. Next, I show that neither Cav1.2 nor Cav1.3 alone is necessary for fear extinction. Instead, I find that the L-VGCC antagonist nifedipine used in the previous experiments implicating L-VGCCs in fear extinction impairs locomotion and induces an aversive state. Further, I demonstrate that this aversive state can enter into associations with stimuli present at the time that it is experienced, suggesting that previous studies using nifedipine were likely confounded by drug toxicity. Finally, I show that Cav1.3 mediates long-term potentiation of afferents to the basolateral amygdala (BLA) as well as the afterhyperpolarization in principal neurons of the BLA.Ph.D.NeuroscienceUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/75966/1/bcmckinn_1.pd

    The Age-by-Disease Interaction Hypothesis of Late-Life Depression

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