[7] Thomas Fuchs defines 6 different types of BM: procedural, situational, intercorporeal, incorporative, pain, and traumatic memory.
and "The belief in these pseudoscientific concepts appears to be related to scientific illiteracy, gullibility, and a lack of critical thinking skills and reasoning abilities in both the mental health community and in society at large"[2] A 2017 systematic review of cross-disciplinary research in body memory found that the available data neither largely support or refute the claim that memories are stored outside of the brain and more research is needed.
"[14] Cellular memory refers to the ability of cells to retain information about past states, exposures, or events and adapt their responses accordingly.
[15] This dual effect is supported by research showing that glucocorticoids improve consolidation of long-term memory, particularly for emotionally valenced information, while impairing retrieval processes.
Prolonged exposure to high cortisol levels can reduce hippocampal volume and inhibit neurogenesis, weakening the brain's capacity to form new memories while reinforcing maladaptive ones.
[17] Those same studies have shown that chronic exposure to elevated cortisol levels, whether through stress or medical conditions, can lead to morphological changes in the hippocampus, suppress neuronal proliferation, and reduce hippocampal volume.
Prolonged hyperglycemia can induce lasting epigenetic changes in glucose-regulated pathways, contributing to long-term complications of diabetes, such as vascular damage and cognitive decline.
[23] This phenomenon, known as "metabolic memory," involves persistent alterations in gene expression and cellular function even after normalization of glucose levels.
Studies have demonstrated that exposure to elevated glucose levels leads to a positive feedback loop, resulting in persistent expression of genes that promote glycolysis and inhibit alternative metabolic pathways.
[25] Similarly, during caloric deficits, the body adapts by lowering the basal metabolic rate and "remembering" prior energy-deprived states through alterations in leptin, ghrelin, and thyroid hormone signaling.
Chronic high glucose levels have been shown to alter epigenetic markers, leading to persistent vascular inflammation and oxidative stress.
Transient hyperglycemia can induce long-lasting activating epigenetic changes in the promoter of the nuclear factor κB (NF-κB) subunit p65 in aortic endothelial cells.
[27] These changes persist for at least 6 days of subsequent normal glycemia, resulting in increased expression of pro-inflammatory genes such as monocyte chemoattractant protein 1 (MCP-1) and vascular cell adhesion molecule 1 (VCAM-1).
[32] Hormonal fluctuations during critical developmental periods, such as puberty or pregnancy, create lasting imprints on cellular and systemic physiology.
Early-life estrogen exposure has been associated with long-term changes in brain plasticity and memory capacity, contributing to gender differences in neuropsychiatric conditions.
[36] Emerging studies indeed reveal that testosterone levels during puberty influence neural development, affecting synaptic pruning and myelination in the prefrontal cortex.
[40] A worm reduced to 1/279th of the original can be regrown within a few weeks and be trained much quicker to head towards light and open space for food, an unnatural behavior for a flatworm.