No Smell, No Taste—Dealing With a “Senseless” Phase of the Pandemic

Abstract

The SARS-CoV-2 infection alters smell and taste sensations in many patients. These 2 neurosensory impairments, namely, (1) the loss of smell, an olfactory dysfunction (OD) or anosmia, and (2) the loss of taste, a gustatory dysfunction (GD) or ageusia, are often the earliest and, sometimes, the only signs in otherwise asymptomatic individuals. Both OD and GD are recognized by the international scientific community as one of the critical symptoms of COVID-19. The prevalence of COVID-19–related OD is higher among women (although less likely to experience severe forms of SARS-CoV-2 infection) than men. The total loss of taste sense or GD is more common among the elderly COVID-19 patients than in the younger population. In “long” COVID or postacute sequelae of COVID-19 (PASC) patients, OD/GD could persist for months to years, depending on the extent of damage caused by the SARS-CoV-2 infection to the olfactory and gustatory systems. Olfactory dysfunction and GD manifestations may severely disrupt quality of life, which includes altered eating habits, loss of appetite, weight change, and loss of pleasure in food consumption, and may further affect psychological well-being, social bonding, altered intimacy, and relationship to self and others. The hedonic value of diet relies exclusively on its flavor; however, the onset of OD/GD during SARS-CoV-2 infection deprives such organoleptic experiences of nutrition. To compensate for these OD/GD issues, the chemosensory focus of COVID-19/PASC patients during dietary consumption may shift toward food texture (to stimulate trigeminal nerves) and food colors (to stimulate brain activity), to sustain appetite as well as enhance the pleasure of eating. Olfactory training with repeated exposure to 4 intense odors twice daily has been a traditional rehabilitation practice to alleviate olfactory impairments in COVID-19. The neurosensory impairments in COVID-19 pathobiology culminate from iron-redox dysregulation, viral-induced host metabolic reprogramming, and host mitochondrial dysfunction. Therefore, nutritional restoration of host metabolic reprogramming and mitochondrial function could provide an effective strategy to reverse iron-redox dysregulation syndrome and combat OD/GD in COVID-19 and PASC patients. Innate regulators of iron-redox homeostasis, such as lactoferrin, heme oxygenase-1, erythropoietin, and hepcidin modulators, could serve as potential interventions for OD/GD recovery.

Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID

“…During host cell entry, the viral S-protein disrupts BBB function, damages neurons, and activates brain mast cells 196 . Neuro-invasion of SARS-CoV-2 occurs via transcribrial (nose) route with damage to olfactory mucosa, and olfactory nerves, ultimately manifesting into anosmia (loss of smell) 197 , 198 . COVID-19 patients also display diffused white matter damage, microglial activation, and neuroinflammation at different CNS regions with olfactory neuritis (25%), nodular brainstem encephalitis (31%), and cranial nerve neuritis (6%) 199 .…”

“…Viral infection of astrocytes resembles reactive astrogliosis with elevated type-I IFN production, increased inflammation, and down-regulation of transporters for water, ions, choline, and neurotransmitters 312 . These events lead to dysfunction and death of uninfected bystander neurons that could inflict severe symptoms of neuro-COVID including anosmia, ageusia, headache, delirium, acute psychosis, seizures, and stroke 171 , 197 .…”

“…Ferroptosis, the programmed cell death due to iron and lipid dependent peroxidation, is associated with ageusia and anosmia, the early clinical manifestations of COVID-19 197 , 599 , 600 . Ferroptosis is regulated by lipid repair enzymes, which also include GSH and GPx4 reducing lipid hydroperoxides (L-OOH) to lipid alcohols (L-OH) 601 .…”