A recently published study in The New England Journal of Medicine found that among 1,497 fully vaccinated healthcare workers in Israel, 39 SARS-CoV-2 breakthrough infections were documented.2 19% of patients with breakthrough infections still had symptoms six weeks later.2 Patients with long COVID report prolonged, multisystem involvement and significant disability.3 By seven months, many patients have not yet recovered (mainly from systemic and neurological/cognitive symptoms), have not returned to previous levels of work, and continue to experience significant symptom burden.3
GUT FUNCTION BREAKTHROUGH – RESTORE
Increasing evidence suggests that the gastrointestinal (GI) tract may influence the severity and outcome of COVID-19, particularly the gut microbiome.5-8 An online survey of 3,762 patients published on July 15, 2021, in the Lancet found that 84% to 86.6% of patients with long COVID experience gastrointestinal distress, including diarrhea, loss of appetite, vomiting, abdominal pain, nausea, constipation, and gastroesophageal reflux.3 Studies like these are ongoing and provide insight into the prevalence, etiology, and potential mechanisms of COVID-19 in the GI tract crucial for defining prevention measures, clinical care, and treatment strategies.9 Scientists are hopeful that therapeutic interventions to restore the gut microbiome may mitigate systemic inflammation and intestinal damage and even limit the effects on the central nervous system through the brain-gut axis10 in patients with acute and long COVID.
A more recent study suggests that gut dysbiosis may also be associated with the recovery process following SARS-CoV-2 infection, perhaps linking it to long COVID risks.19 Chen et al conducted this prospective study to longitudinally monitor alterations of gut microbiota in patients with COVID-19 using 16S rDNA sequencing. Fecal microbiota was monitored at three timepoints: acute phase (from illness onset to viral clearance), convalescence (from viral clearance to two weeks after hospital discharge), and postconvalescence (six months after hospital discharge). The small study found that microbiota diversity was not restored to normal levels after six-month recovery. Patients with lower postconvalescence diversity showed higher levels of C-reactive protein and illness severity during the acute phase, suggesting close correlations between the inflammatory response and gut dysbiosis in COVID-19.19 Patients with lower postconvalescence diversity showed higher levels of hs-CRP and illness severity during the acute phase, suggesting close correlations between inflammatory response and gut dysbiosis in COVID-19, as illustrated in previous studies. The authors hypothesize that the persistent reduction of gut microbiota diversity may have long-term biological influence.19
With respect to interventions, the practice of functional medicine emphasizes the primacy of safety, validity, and effectiveness. Functional medicine practitioners are trained in providing personalized guidance to patients in the use of nutrition, nutraceuticals, and lifestyle to prevent, reverse, and decrease the burden of complex, chronic diseases like long COVID. IFM has assembled a wealth of resources for functional medicine clinicians, including clinical recommendations and mechanisms of action; virus-specific nutraceuticals and botanical agents, nutrition, and lifestyle practices for strengthening host defense; practice considerations; testing; and COVID-19 vaccines.
The National Institutes of Health estimates that nearly 1/4 of us (about 70 million people) suffer from digestive issues: gas, bloating, heartburn, diarrhea, constipation, and nausea. In functional medicine, we believe that these symptoms are often a result of a leaky gut.
Amy Myers, MD is a two-time New York Times bestselling author and an internationally acclaimed functional medicine physician. Dr. Myers specializes in empowering those with autoimmune, thyroid, and digestive issues to reverse their conditions and take back their health. In addition, she is a wife, mother, and the successful founder and CEO of Amy Myers MD.
Having been failed by conventional medicine myself, I understand the hesitancy to trust someone new with your health. However, as a functional medicine physician and two-time New York Times bestselling author on the topics of autoimmunity and thyroid health, I have spent the better part of my professional life dedicated to empowering people just like you to take back their health.
Finally, supplements from a source you can actually trust. After receiving my medical degree (M.D.) at Louisiana State University, I completed my residency in Emergency Medicine at the University of Maryland Medical Center. In 2012, I became a certified functional medicine physician, so I could help my patients get to the root cause of their health problems.
ICC may be considered to be a specialized population of smooth muscle cells. Both arise from common mesenchymal cells[1-3]. However, whereas smooth muscle cells develop an extensive array of contractile elements, ICC have few contractile elements but contain large numbers of mitochondria, an abundance of endoplasmic reticulum and distinct sets of channels in their membrane. The ICC consist of a fusiform cell body with a thin cytoplasm, a large oval nucleus and dendritic-like processes[4]. Two to five primary dendritic processes divide further into secondary and tertiary processes[5]. Many ICC express Kit, a tyrosine kinase receptor (Kit-ir); this allows them to be recognized by their ability to bind antibodies to Kit[4]. Similarly ICC readily react with antibodies to vimentin whereas nearby smooth muscle cells do not[6]. The presence of ICC is not restricted to the GI tract. They can be found in the bladder[7,8], the ureteropelvic junction[9], the vas deferens[10], the prostate[11], the penis[12,13], the mammary gland, the uterus[14], the pancreas[15], blood vessels[16] such as the portal vein[17] and the vagina[18]. More recently, they have been found in the vermiform appendix in childhood[19]. Some of these cells are thought to have a pacemaker function (such as those in the portal vein, in the lymphatics or prostate) but not those in the arteries, uterus (where the influence is, if any, an inhibitory one) or bladder[20].
Achalasia: Achalasia is a disorder of esophageal motility that has been well documented for over 300 years[61]. Achalasia is characterized by relaxation failure of the LES and lack of peristaltic contraction of the esophageal body[62]. The mechanism of LES relaxation is complex, requiring the coordinated interaction of nerves, smooth muscle, ICC and hormones. The LES is a functional and anatomic barrier between the stomach and esophagus. It consists of a thickening of the circular smooth muscle layer of the esophagus at the gastroesophageal junction. It is anatomically asymmetric, and this is reflected in the physiology of the sphincter as demonstrated by ultrasound and pharmacologic manometric studies[63]. The LES is tonically contracted. Initiation of a peristaltic wave in the esophagus is accompanied by a decrease in LES pressure as a result of smooth muscle relaxation. This allows the swallowed bolus to enter the stomach[61].
Slow transit constipation: Functional constipation encompasses a group of functional disorders that exhibit persistent difficult, infrequent, or seemingly incomplete defecation and infrequent, lumpy, or hard stools[115,116]. This symptom is very common and may occur in up to 20% of populations, depending on demographic factors, sampling, and the definitions employed[115,117]. The term constipation is probably better viewed as a sort of semantic umbrella, covering pathophysiologic subtypes, among which 2 major groups may now be identified: slow transit constipation (STC) and pelvic floor dysfunction[118].
The deposition of alpha-synuclein (α-syn) in neuronal cells could contribute to the development of PD. The α-syn is the most abundant protein constituent of Lewy bodies(LBs), which are generally described as round lamellar eosinophilic cytoplasmic inclusions (Braak et al., 2003a). LBs are the hallmark pathologic features of PD. Whether LBs are cytotoxic or cytoprotective to neuronal cells remains debatable. It could potentially be toxic since the number of cortical LBs positively correlated with the severity of symptoms of dementia in PD (Hurtig et al., 2000). However, in some cases, Lewy pathology is also found but without present parkinsonism (Parkkinen et al., 2008; Adler et al., 2010; Milber et al., 2012). Some studies have also suggested that α-syn aggregates might be protective (da Costa et al., 2000; Tanaka et al., 2004), while oligomers and pre-fibrillar α-syn are the toxic species responsible for neurodegeneration (Chen et al., 2009). The excessive accumulation of a-syn can enhance its toxicity and lead to the degeneration of DA (dopamine) neurons in the substantia nigra of the midbrain in PD, and the loss of neurons is associated with motor symptoms (Dickson et al., 2009). It is also possible rather than the neuronal loss, the presynaptic terminal failure may be the more critical pathogenic factor for motor symptoms of PD (Schulz-Schaeffer, 2010). Besides motor symptoms, PD is also associated with non-motor symptoms. In the early stage of PD, non-motor symptoms such as insomnia, impairment of smell (Shah et al., 2009) as well as gastrointestinal (GI) dysfunction (nausea, abnormal salivation, constipation, prolonged intestinal transit time etc.) (Cersosimo et al., 2013; Mulak and Bonaz, 2015) can be found. The typical movement-related symptoms, such as tremor, rigidity, bradykinesia, and postural instability are reported in the second stage of PD. In the final stage, the severe psychotic symptoms such as motor disorders and neuropsychiatric disturbances which including depression (Marsh, 2013; Parashar and Udayabanu, 2017; Guo et al., 2020; Park et al., 2020), dementia (Tsuang et al., 2013) can be observed in PD patients. The interesting phenomenon is that PD patients who suffer from GI symptoms can occur several years ahead of classic motor symptoms (Chen et al., 2015). The GI dysfunction caused by gut microbiota disorder which can initiate α-syn accumulation in the enteric nerve cell, causing concurrent mucosal inflammation and oxidative stress (Chen et al., 2019). So scientists give the hypothesis that PD may begin in the gastrointestinal tract and transfer to the brain through the gut-brain axis (Hawkes et al., 2007). 2ff7e9595c
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