The symptoms associated with virus infections vary; some patients report physical pain, others have gastrointestinal issues, others say their mucous production is elevated, and others may complain about fatigue. However, these symptoms are likely reported at the same time by the same patient. Imagine a patient who suffers from irritable bowel syndrome (IBS), is overweight and gets a virus infection? Chronic conditions add an extra layer of inflammation to the acute infection, promoting a more severe reaction. Our role is to create awareness about the link between gut health, vitamin deficiency, and their effect on mitochondrial dysfunction and pain. Prevention is key.
Gut health and mitochondrial dysfunction:
There is a clear association between dietary ingestion and wellbeing. Indeed, the nutritional status assessment depends on a multi-focal approach, evaluating body composition, laboratory findings, clinical and dietetic analysis. Furthermore, in the clinical evaluation, it is crucial to determine the presence of gut health issues due to their link with micronutrient absorption.
The literature supports the association between malnutrition and an increase in mitochondrial dysfunction. In addition, malnutrition coincides with the ingestion of inadequate diet. This means that the diet can be energetically sufficient or insufficient and deficient in nutrients to support mitochondrial function.
Furthermore, gut issues coincide with detrimental gastrointestinal symptoms such as bloating, pain, constipation, and diarrhea. Consequently, these symptoms may keep the patient from ingesting a specific group of foods, leading to micronutrient deficiencies. Preventing and correcting micronutrient depletion promotes the maintenance of optimal immune status. Also, this can mitigate exaggerated immune responses, decrease the infection impact and create an anti-inflammatory and antioxidant milieu, thus improving mitochondrial function.
Micronutrient supplementation and the improvement of dietary intake are safe ways to improve immune reactions. Also, current literature reports a decrease in inflammatory diseases and pro-oxidant with the use of therapies based on micronutrient intake. Furthermore, vitamins like folic acid, vitamin C, tocopherols, and minerals like selenium and zinc promote cellular mechanisms that promote mitochondrial function and reduce inflammatory mechanisms.
Vitamin B9 (folic acid)
Vitamin B9 depletion alters mtDNA stability, affecting the function and structure of this organelle. Studies performed in mice with cardiac hypertrophy significantly improved fatty acid oxidation and mitochondrial biogenesis after vitamin B9 supplementation.
Furthermore, vitamin B9 is a critical factor in synthesizing methionine, generating the intracellular antioxidant glutathione.
Vitamin C (ascorbic acid)
Vitamin C plays the role of a free radical scavenger, preventing lipid peroxidative damage and reestablishing vascular endothelial function.
Maintaining proper vitamin C levels may help prevent vascular dysfunction and the progression of pro-oxidative and pro-inflammatory disorders that contribute to neurological and cardiometabolic diseases.
Septic shock studies propose using combined selenium, vitamin C, zinc, and melatonin as “metabolic resuscitators” in mitochondrial dysfunction.
The functional structure of vitamin E, tocotrienols, and tocopherols have therapeutic potential to improve epileptic seizures associated with neuroinflammation and mitochondrial dysfunction. Indeed, vitamin E is a cofactor to multiple enzymes found in the polyunsaturated lipid metabolism and inflammatory signaling pathways.
The role of vitamin D in mitochondrial function and its effects on health and disease is linked with its receptors. Indeed, optimal vitamin D plasma levels improve mitochondrial function by the modulation of the renin-angiotensin system. Consequently, this mechanism positively affects conditions like hypertension, cardiometabolic, neurodegenerative, bone and kidney diseases.
Vitamin D also has antioxidant properties, as it is a promoter of antioxidant enzymes at neuronal levels, thus reducing free radical generation and inflammatory/oxidative injuries.
This mineral is crucial for the action of over 25 cellular enzymes called selenoproteins. Within these selenoproteins, glutathione peroxidase, thioredoxin reductase, and methionine sulfoxide reductase are vital modulators of oxidation and inflammation.
Indeed, selenium deficiency is associated with a detrimental immune response leading to cytokine storm and chronic inflammation. In addition, proper selenium status has a neuroprotective effect against glutamate-induced cell damage. Furthermore, selenium supplementation suppressed the NLRP3 inflammatory cascade, thus reducing exaggerated inflammatory and immune responses.
Our body’s systems are interconnected; they all form a part of a whole. Indeed, this makes it clear that we have to treat chronic and acute diseases with a multiple focus approach. How to start? Let’s start with the gut! Focusing on improving our gastrointestinal symptoms might lead to better micronutrient absorption, resulting in better mitochondrial function. Consequently, this will lead to better anti-inflammatory and antioxidant mechanisms, clearing the path to better health and fast recovery.- Ana Paola RodrÃguez Arciniega, MS
MartÃn GimÃ©nez, Virna Margarita et al. “Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases.” Diseases (Basel, Switzerland) vol. 9,2 30. 14 Apr. 2021, doi:10.3390/diseases9020030
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