Fitness & Nutrition News

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fitness 21 hours ago

A cross-sectional survey on depersonalization/derealization and meditation-induced alterations of the self

Depersonalization/derealization (DPDR) involves feeling detached from one’s body, thoughts, or emotions and is often triggered by trauma, stress, mental health issues, or drug use, typically causing high distress. Similar experiences are also reported in meditation contexts, where they are often described as positive, insightful, and meaningful. However, no study has systematically compared DPDR-like experiences across these contexts. This preregistered, cross-sectional study addresses this gap. Participants who had experienced DPDR-like states triggered through meditation (MEDT, n = 60) or through other triggers (NMEDT, n = 61) completed five questionnaires and provided additional information about their DPDR experience and meditation practice. The two groups significantly differed on all questionnaires except the Cambridge Depersonalisation Scale, including its subscales covering different DPDR aspects. The MEDT group rated their experiences as substantially more positive than NMEDT, though most participants in both groups described them as mixed. In MEDT, these experiences were reported across meditation types and experience levels. Overall, meditation can induce states phenomenologically similar to DPDR, but these are often experienced as more welcome, pleasant, and spiritually meaningful than those triggered by trauma, stress, or cannabis, although distress is not uncommon. These findings suggest contemplative approaches may inform clinical support for DPDR, while highlighting the need for recognition and guidance within meditation settings.

fitness 21 hours ago

Metformin inhibits mitochondrial complex I in intestinal epithelium to promote glycaemic control

Metformin is a versatile biguanide drug primarily prescribed for type II diabetes. Despite its extensive use, the mechanisms underlying its clinical effects, including attenuated postprandial glucose excursions and elevated intestinal glucose uptake, remain unclear. Here we map these and other effects of metformin to intestine-specific mitochondrial complex I inhibition. Using human metabolomic data and an orthogonal genetics approach in male mice, we demonstrate that metformin suppresses citrulline synthesis, a metabolite generated exclusively by small intestine mitochondria, and increases GDF15 by inhibiting the mitochondrial respiratory chain at complex I. This inhibition co-opts the intestines to function as a glucose sink, driving the uptake of excess glucose and its conversion to lactate and lactoyl-phenylalanine. We also find that glucose lowering by metformin is due to repeated bolus exposure rather than a cumulative chronic response. Notably, the efficacy of phenformin, another biguanide, and berberine, a structurally unrelated nutraceutical, similarly depends on intestine-specific mitochondrial complex I inhibition, underscoring a shared therapeutic mechanism. Metformin is shown to exert its glucose-lowering and additional clinical effects through inhibition of mitochondrial complex I in the intestinal epithelium in mice.

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