The relationship between peripheral blood mononuclear cells telomere length and diet – unexpected effect of red meat – PMC

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4944490/

 

Conclusions

Unexpected correlation of telomere length with the frequency of consumption of red meat indicates the need for further in-depth research and may undermine some accepted concepts of adverse effects of this diet on the health status and life longevity.

 

Kasielski M, Eusebio MO, Pietruczuk M, Nowak D. The relationship between peripheral blood mononuclear cells telomere length and diet – unexpected effect of red meat. Nutr J. 2016;15(1):68. Published 2016 Jul 14. doi:10.1186/s12937-016-0189-2

Pre-infection 25-hydroxyvitamin D3 levels and association with severity of COVID-19 illness

https://pubmed.ncbi.nlm.nih.gov/35113901/

Conclusions: Among hospitalized COVID-19 patients, pre-infection deficiency of vitamin D was associated with increased disease severity and mortality.”

Dror AA, Morozov N, Daoud A, Namir Y, Yakir O, Shachar Y, Lifshitz M, Segal E, Fisher L, Mizrachi M, Eisenbach N, Rayan D, Gruber M, Bashkin A, Kaykov E, Barhoum M, Edelstein M, Sela E. Pre-infection 25-hydroxyvitamin D3 levels and association with severity of COVID-19 illness. PLoS One. 2022 Feb 3;17(2):e0263069. doi: 10.1371/journal.pone.0263069. PMID: 35113901; PMCID: PMC8812897.

Association between vitamin D status and risk of covid-19 in-hospital mortality: A systematic review and meta-analysis of observational studies

https://pubmed.ncbi.nlm.nih.gov/34882024/

”We found a significant direct association between vitamin D deficiency and elevated risk of COVID-19 in-hospital mortality. Moreover, each unit increment in serum vitamin D levels was associated to significant reduction in risk of COVID-19 mortality.”

Ebrahimzadeh A, Mohseni S, Narimani B, Ebrahimzadeh A, Kazemi S, Keshavarz F, Yaghoubi MJ, Milajerdi A. Association between vitamin D status and risk of covid-19 in-hospital mortality: A systematic review and meta-analysis of observational studies. Crit Rev Food Sci Nutr. 2021 Dec 9:1-11. doi: 10.1080/10408398.2021.2012419. Epub ahead of print. PMID: 34882024.

Riboflavin (vitamin B-2) and health

https://pubmed.ncbi.nlm.nih.gov/12791609/

”Riboflavin is unique among the water-soluble vitamins in that milk and dairy products make the greatest contribution to its intake in Western diets. Meat and fish are also good sources of riboflavin”

”Biochemical signs of depletion arise within only a few days of dietary deprivation.”

”There is reasonably good evidence that poor riboflavin status interferes with iron handling and contributes to the etiology of anemia when iron intakes are low. Various mechanisms for this have been proposed, including effects on the gastrointestinal tract that might compromise the handling of other nutrients.”

Powers HJ. Riboflavin (vitamin B-2) and health. Am J Clin Nutr. 2003 Jun;77(6):1352-60. doi: 10.1093/ajcn/77.6.1352. PMID: 12791609.

Role of Vitamins in Neurodegenerative Diseases: A Review

https://pubmed.ncbi.nlm.nih.gov/34802410/

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity.”

Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington’s disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington’s disease disrupts the synthesis of acetylcholine and hormones in the brain.”

Kumar RR, Singh L, Thakur A, Singh S, Kumar B. Role of Vitamins in Neurodegenerative Diseases: A Review. CNS Neurol Disord Drug Targets. 2021 Nov 19. doi: 10.2174/1871527320666211119122150. Epub ahead of print. PMID: 34802410.

Vitamin A supplementation and serum Th1- and Th2-associated cytokine response in women

https://pubmed.ncbi.nlm.nih.gov/24024773/

Conclusions: Decline in serum concentrations of IL-1β and IL-1β/IL-4 ratio in obese women suggests that vitamin A is capable of regulating the immune system and possibly reducing the risk of autoimmune disease in this group.”

Farhangi MA, Keshavarz SA, Eshraghian M, Ostadrahimi A, Saboor-Yaraghi AA. Vitamin A supplementation and serum Th1- and Th2-associated cytokine response in women. J Am Coll Nutr. 2013;32(4):280-5. doi: 10.1080/07315724.2013.816616. PMID: 24024773.

The Role of Vitamin A in Wound Healing

https://pubmed.ncbi.nlm.nih.gov/31389093/

Abstract

Vitamin A is an essential micronutrient that comes in multiple forms, including retinols, retinals, and retinoic acids. Dietary vitamin A is absorbed as retinol from preformed retinoids or as pro-vitamin A carotenoids that are converted into retinol in the enterocyte. These are then delivered to the liver for storage via chylomicrons and later released into the circulation and to its biologically active tissues bound to retinol-binding protein. Vitamin A is a crucial component of many important and diverse biological functions, including reproduction, embryological development, cellular differentiation, growth, immunity, and vision. Vitamin A functions mostly through nuclear retinoic acid receptors, retinoid X receptors, and peroxisome proliferator-activated receptors. Retinoids regulate the growth and differentiation of many cell types within skin, and its deficiency leads to abnormal epithelial keratinization. In wounded tissue, vitamin A stimulates epidermal turnover, increases the rate of re-epithelialization, and restores epithelial structure. Retinoids have the unique ability to reverse the inhibitory effects of anti-inflammatory steroids on wound healing. In addition to its role in the inflammatory phase of wound healing, retinoic acid has been demonstrated to enhance production of extracellular matrix components such as collagen type I and fibronectin, increase proliferation of keratinocytes and fibroblasts, and decrease levels of degrading matrix metalloproteinases.

Polcz ME, Barbul A. The Role of Vitamin A in Wound Healing. Nutr Clin Pract. 2019 Oct;34(5):695-700. doi: 10.1002/ncp.10376. Epub 2019 Aug 7. PMID: 31389093.

Obesogenic and Ketogenic Diets Distinctly Regulate the SARS-CoV-2 Entry Proteins ACE2 and TMPRSS2 and the Renin-Angiotensin System in Rat Lung and Heart Tissues

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8541329/

 

Conclusion:

Diet-induced obesity increased the levels of viral entry proteins in the lungs, providing a mechanism whereby SARS-CoV-2 infectivity can be enhanced in obese individuals. Conversely, by maintaining low levels of ACE2 and TMPRSS2 and by exerting an anti-inflammatory effect, the KD can potentially attenuate the severity of infection and migration of SARS-CoV-2 to other ACE2-expressing tissues.

 

Da Eira D, Jani S, Ceddia RB. Obesogenic and Ketogenic Diets Distinctly Regulate the SARS-CoV-2 Entry Proteins ACE2 and TMPRSS2 and the Renin-Angiotensin System in Rat Lung and Heart Tissues. Nutrients. 2021;13(10):3357. Published 2021 Sep 25. doi:10.3390/nu13103357

A Machine-Generated View of the Role of Blood Glucose Levels in the Severity of COVID-19 – PubMed

Källa: A Machine-Generated View of the Role of Blood Glucose Levels in the Severity of COVID-19 – PubMed

 

”The machine-driven framework we developed repeatedly pointed to elevated blood glucose as a key facilitator in the progression of COVID-19. Indeed, when we systematically retraced the steps of the SARS-CoV-2 infection, we found evidence linking elevated glucose to each major step of the life-cycle of the virus, progression of the disease, and presentation of symptoms. Specifically, elevations of glucose provide ideal conditions for the virus to evade and weaken the first level of the immune defense system in the lungs, gain access to deep alveolar cells, bind to the ACE2 receptor and enter the pulmonary cells, accelerate replication of the virus within cells increasing cell death and inducing an pulmonary inflammatory response, which overwhelms an already weakened innate immune system to trigger an avalanche of systemic infections, inflammation and cell damage, a cytokine storm and thrombotic events. We tested the feasibility of the hypothesis by manually reviewing the literature referenced by the machine-generated synthesis, reconstructing atomistically the virus at the surface of the pulmonary airways, and performing quantitative computational modeling of the effects of glucose levels on the infection process. We conclude that elevation in glucose levels can facilitate the progression of the disease through multiple mechanisms and can explain much of the differences in disease severity seen across the population.”

 

Logette E, Lorin C, Favreau C, Oshurko E, Coggan JS, Casalegno F, Sy MF, Monney C, Bertschy M, Delattre E, Fonta PA, Krepl J, Schmidt S, Keller D, Kerrien S, Scantamburlo E, Kaufmann AK, Markram H. A Machine-Generated View of the Role of Blood Glucose Levels in the Severity of COVID-19. Front Public Health. 2021 Jul 28;9:695139. doi: 10.3389/fpubh.2021.695139. PMID: 34395368; PMCID: PMC8356061.