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  • Vitamin C Levels in Critically Ill COVID-19 Patients

    by Michael Passwater From the COVID-19 pandemic, we continue to learn about the critical importance of maintaining adequate levels of essential nutrients. When the body is under stress from an illness such as an infection, merely eating an excellent diet may not provide sufficient nutrients to support the immune system. To stave off a fast-moving infection may require higher levels of essential vitamins and minerals. Vitamin C has an essential role in empowering the immune system. Its oxidized form can be recycled by red blood cells (erythrocytes), but a fast-moving illness can overpower this system, causing vitamin C levels to precipitously drop. A recent study in Spain measured plasma vitamin C levels in 67 critically ill hospitalized adult COVID-19 patients meeting the Berlin criteria for acute respiratory distress syndrome (ARDS).1 The results fell into three categories: undetectable (<0.1 mg/dL), low (0.1 – 0.4 mg/dL), and “normal” (0.4 – 2 mg/dL). Twelve (18%) patients had undetectable plasma vitamin C, 43 (64%) patients had low levels of plasma vitamin C (mean for this group was 0.14 mg/dL with a standard deviation of 0.05), and 12 (18%) patients had vitamin C levels within the normal range (mean for this group was 0.59 mg/dL with a standard deviation of 0.18). In summary, 82% of patients had low or undetectable plasma vitamin C levels, and 18% had values within the reference range, mostly on the low side of the reference range. (Riordon Clinic Bio-Center Laboratory has an established reference range of 0.6 – 2.0 mg/dL for plasma vitamin C). A smaller study of 18 adult COVID-19 patients with ARDS found similar results: 17 (94%) patients had undetectable plasma vitamin C, and 1 (6%) patient had a plasma vitamin C level of 0.24 mg/dL.2 The assay used in this study had a lower limit of detection of 0.15 mg/dL, above the mean of the low-level group in the first study. Finding low levels of vitamin C in critically ill patients is not new and has been reported in a variety of studies over the last several decades. In 2017, a study of 44 critical care patients receiving recommended amounts of enteral and parenteral vitamin C (125 +/- 88 mg/day, max 448 mg/day) showed 70% of patients had vitamin C deficiency.3 Among septic shock patients, 90% had vitamin C deficiency. Borrelli et al published findings in 1996 showing that the lower the plasma ascorbic acid level in septic patients the greater the risk of organ failure and death.4 Even in presumed healthy people in the USA, vitamin C deficiency is found. In 2003-2004, NHANES samples from noninstitutionalized civilians found a vitamin C deficiency prevalence of 7.1% +/- 0.9%.5 This was a 44% reduction in vitamin C deficiency from the 1988 – 1994 national study. Smoking and low income were associated with higher rates of vitamin C deficiency. People in a deficient state can avoid acute illness for a time but have impaired capacity to respond to infections and other stress challenges. Why Critically Ill People Require More Vitamin C to Maintain Adequate Levels of Plasma Vitamin C Increased consumption. White blood cells, such as neutrophils and monocytes, actively take up ascorbic acid from plasma (fluid portion of blood) to achieve intracellular levels of 1 mM, 50-100 -fold higher than the typical vitamin C level of plasma. When stimulated to produce an oxidative burst, these white blood cells will pull in more vitamin C to increase intracellular concentrations ten-fold to 10 mM. If there is not enough vitamin C available, the white blood cell’s oxidative burst intended to kill an invading pathogen may destroy the WBC itself instead. Cytokines, inflammation, fever, and other biological stresses of illness also increase the metabolic demand for vitamin C throughout the body.6 Decreased recycling of dehydroascorbic acid (DHAA) back to ascorbic acid (AA). Healthy blood plasma must contain antioxidants to counteract the effects of oxygen. Ascorbic acid (AA) is a major antioxidant which serves to maintain the reductive capacity of circulating blood.7 AA has a short half-life of minutes in human blood before being oxidized to dehydroascorbic acid (DHAA). Humans cannot make their own ascorbic acid. However, survival is possible with meager milligram amounts of AA intake due to recycling of the oxidized DHAA back to AA within red blood cells (RBCs) in the circulatory system and between astrocytes and tanycytes with GLUT1-DHAA receptors and neurons with SVCT2-AA receptors in the central nervous system. RBCs are the most numerous cell type in the body and have a large number of GLUT1 receptors that preferentially take in DHAA. With 20-30 trillion RBCs circulating in a healthy person, DHAA in the blood can be recycled to AA every three minutes in a healthy person. Vitamin C (ascorbic acid) is oxidized to dehydroascorbic acid, which can be reduced back to ascorbic acid (vitamin C). The recycling process is primarily dependent on glutathione peroxidases (GPx, a family of antioxidant selenoproteins), and to a lesser extent on NADH and NADPH oxidoreductases within the red blood cells. Damage or destruction of the RBCs, damage to or shortage of the intracellular reducing agents, or hypoxic conditions impair or halt the recycling process.8,9 Additionally, as the reductive capacity of plasma decreases, the amount of DHAA lost to irreversible oxidation to 2,3-diketo-L-gulonic acid further depletes the body’s pool of AA. To maintain AA levels in the body as intracellular recycling decreases, intake of AA must increase. In addition to maintaining antioxidant capacity, RBCs are responsible for the management of the three gases of life, O2, CO2, and NO, throughout the body.10 RBCs (erythrocytes) are produced from erythroid precursor cells in the bone marrow and circulate for approximately four months. They are biconcave discs, with very flexible membranes to allow them to flow smoothly throughout the body’s 60,000 miles of blood vessels. Capillaries in the body’s extremities become so narrow that the RBCs flow single file, underscoring the necessity of cell membrane flexibility. RBC Membrane Components, Interferon, and Selenoproteins New research reveals that RBC membrane components, interferon, and selenoproteins are targets of the SARS-CoV-2 virus, and along with NAD are all depleted by the virus.11-15 In addition to GLUT1 receptors, RBC membranes also can express ACE2 receptors, which are well established as a cellular entry point for the SARS-CoV-2 virus. CD147 and the RBC structural protein Band3 have also been shown to serve as attachment points for the virus. Mature RBCs do not have a nucleus and cannot support viral replication. However viral attachment and entry can disrupt the RBC’s ability to transport and transfer oxygen to tissues, as well as destroy selenoproteins which in turn disrupts DHAA – AA recycling. RBC membrane disturbances and loss of antioxidant capacity results in a more spherical and less flexible RBC, and oxidation causes phosphatidyl serine and other lipids to flip from the inner side of the membrane to the outer side of the membrane. These changes inhibit the RBC from bending and twisting to travel through the small capillaries of the circulatory system, and accelerate the RBC’s clearance from circulation by the reticuloendothelial system monocytes in the spleen and liver. Immature RBC precursor cells have a nucleus, numerous ACE2 receptors, and can support viral replication. Invasion of these cells by the SARS-CoV-2 virus is even more damaging. Release of RBC precursor cells into the blood stream in response to hypoxia, can intensify the disease by causing immunosuppression and serving as a rich source of selenocysteine and other nutrients for the rapidly replicating virus. The virally induced structural, functional, and metabolic damage to RBCs helps explain cases of COVID-19 presenting with hypoxia disproportional to the degree of pneumonia present. In addition to elucidating the interactions of SARS-CoV-2 with the RBCs and RBC precursor cells, recent genetics, proteomics, metabolomics, and lipidomics research has identified specific interactions leading to interferon and selenoprotein destruction and suppression. These studies have also identified nicotinamide phosphoribosyltransferase, nicotinamide, and nicotinamide riboside as therapeutic options to boost innate immunity and counteract NAD depletion by the virus. Importance of Adequate Niacin, Glutathione/Cysteine (NAC and alpha lipoic acid), and Selenium The findings of recent studies on the effect of nutrient deficiencies in COVID-19 add empirical evidence in support of hypotheses published early in the pandemic. In March of 2020, Yufang Shi and team in China recommended the use of niacin (vitamin B3) whenever lung damage was detected by CT scan.16 Miller, Wentzel, and Richards in South Africa pointed to the importance of NAD+ deficiency.17 Over a decade ago, Ethan Will Taylor proposed the oxidative stress-induced niacin sink (OSINS) model for HIV, another RNA virus.18 Taylor, along with Hiffler, Vavougios, Polonikov and others also suggested glutathione and selenium as central in the etiology of SARS-CoV-2 disease.19-21 Additionally, a German study showed an inverse association between COVID-19 mortality or severe illness and selenium and selenoprotein P levels.22 And in the USA, two cases of severe COVID-19 were successfully treated with oral and intravenous glutathione, N-acetyl-cysteine (NAC), and lipoic acid have been published.23

  • Zero Deaths From Vitamins, Zero Deaths From Minerals

    Written by Andrew W. Saul The 39th annual report from the American Association of Poison Control Centers shows zero deaths from vitamins Confirming data is in Table 22B, p 1613-1615, at the very end of the lengthy report published in Clinical Toxicology. [1] It is interesting that it is placed way back there where nary a news reporter is likely to see it. But there it is: no deaths, none whatsoever, from vitamin A, niacin, pyridoxine (B-6) or from any other B-vitamin. There were no deaths from vitamin C, vitamin D, or vitamin E. There were no deaths from multiple vitamins. There were no deaths from any vitamin at all. Furthermore, there were no fatalities from mineral supplements. Two fatalities from “Iron and Iron Salts” were clearly stated as not being due to supplemental iron (p 1607). No deaths from vitamins. No deaths from minerals. Want to bet this will never be on the evening news? Well, have you seen it there? And why not? This is of real importance to the public. After all, at least two-thirds of the U.S. population takes daily nutritional supplements. A Harris Poll indicated that for American adults, the number is 86 percent. [2] But let’s just use the lower number. Should each of those people take only one single tablet daily, that still makes over 220,000,000 individual doses per day, for a total of well over 80 billion doses annually. Since many persons take far more than just one single vitamin tablet, actual consumption is considerably higher, and the safety of vitamin supplements is all the more remarkable. Throughout the entire year, coast to coast across the entire USA, there was not one single death from a vitamin or mineral supplement. If supplements are allegedly so “dangerous,” as the FDA, the news media, and even some physicians still claim, then where are the bodies? References: Gummin DD, Mowry JB, Beuhler MC et al. (2022) 2021 Annual Report of the National Poison Data System (NPDS) from America’s Poison Centers: 39th Annual Report, Clinical Toxicology, 60:12, 1381-1643, DOI: 10.1080/15563650.2022.2132768 2. See more here orthomolecular

  • Foggy Memory After Anesthesia? Support Brain Resiliency

    Dr. Linda J. Dobberstein, DC, Board Certified in Clinical Nutrition Have you ever had general anesthesia or know someone who has? Did you notice any subtle changes since that time to your long-term memory? Research suggests that general anesthesia use even after one exposure poses long-term challenges in susceptible individuals and age groups. Over the course of your lifetime, you encounter a vast array of challenges and stressors that affect brain health even once the event is over. Building brain resiliency and optimal nutritional reserves through good self-care habits impacts your overall tolerance to many things. Anesthesia Lingering Effects General anesthesia exposure is much more commonplace today than any other time in history. You may have had it with a tonsillectomy, appendix or gall bladder removal, joint replacement surgery, birth defect repair, or repair of broken bones and torn ligaments, heart surgery, etc. Over 300 million surgeries are performed globally each year since anesthetics were introduced in 1842. When you think about your experience with anesthetics, you might recall the nausea and upset stomach, mental fuzziness and “out-of-it behaviors” that occur immediately after the procedure. For some individuals, subtle effects may linger for weeks or longer. You may find that you lose your “train of thought”, have poorer memory recall, or experience more brain fog than usual. These lingering effects may be more noticeable in your aging parent, but they can also happen in kids too. These slight changes are often attributed to stress and/or age. Whether it is a short, single event or multiple, extended procedures, general anesthesia can create neurological effects that may last longer than you think. New evidence shows that common general anesthetics affect the brain’s memory centers in ways that were previously not understood. Memory Center Affected General anesthetics naturally shut down the memory center of your brain’s hippocampus during surgery and make you feel like you are sleeping. This is a desirable effect during the procedure. Anesthetics, however, work on various mechanisms different than sleep. They impact nerve networks in the hippocampus and interfere with natural activity and connections long after the exposure. The greatest negative risks and effects have been identified in the preborn infant to the three-year-old preschooler as well the elderly. Concerns for Children An increasing body of medical literature suggests that general anesthesia and sedation medications4 are neurotoxic and poses harmful effects to a young child’s brain and neurodevelopment. These effects have been studied primarily in animals. In a recent study, rats were exposed to a single, short-term general anesthesia in early infancy. They were raised in a controlled environment. Later in adulthood, brain samples were analyzed and compared to the norm. Adverse cellular and mitochondrial changes were identified. Their research findings suggested that limited, early life exposure resulted in “persistent neuroinflammation” and caused neurotoxicity “mimicking aspects of chronic neurodegenerative diseases”. Another rodent study demonstrated that after a single, short exposure of general anesthesia, “disturbing” mitochondrial changes were observed. These changes were like those seen in neurodevelopmental disorders. Concerns for the Elderly Elderly individuals are also at high risk. In serious cases, postoperative cognitive dysfunction complications can occur, which significantly impairs brain health and quality of life. General anesthetics and surgery are hypothesized to cause neuroinflammation and neurodegeneration likely related with build-up of amyloid beta or changes in tau protein management. Individuals who have poor blood flow to the brain from blood pressure dysregulation or blocked circulation are at greater risk. Other Risk Groups The literature focuses on young children and elderly as the most vulnerable to general anesthesia effects due to their stages in life and neurological development or burden of wear and tear. Individuals of other age groups who have had multiple or prolonged anesthesia exposure may also be at risk. Those who have underlying brain, gut, autoimmune, chronic inflammation, or mitochondrial challenges are also likely to be more vulnerable to neurotoxins and recovery challenges. Genetics too play a role in anesthesia tolerance and detoxification. Findings and Debates Various animal studies have shown without a doubt that anesthetics induce cell death, suppress nerve growth, disrupt synapse formation and plasticity (nerve connections), and affect learning, memory, and cognitive function. Results in animal studies, however, do not always correlate to human health. A preclinical review study suggested “a single brief exposure to general anesthesia is not associated with any long-term neurodevelopment deficits in children’s brain. They did suggest that multiple exposures may affect cognitive speed and motor skills in children. There is considerable debate and concern within medical literature. As you reflect on this information, I hope you engage in ways to protect and support your brain resiliency and overall health throughout your lifetime. Building and Protecting Brain Resiliency Building and protecting brain resiliency for you and your loved ones is an ongoing lifelong process. You have only one brain to last for a lifetime. Unexpected bumps happen. Engage in proactive brain resiliency choices with healthy lifestyle, diet and exercise and acts of prevention to reduce chances of events that need anesthesia as part of treatment. Lifestyle Choices Healthy choices include wearing a seat belt. Use a designated driver if you are under the influence or sleep deprived. Wear a helmet with various sports and recreational activities. Use proper safety equipment for dangerous work and play activities. Wear proper shoes for the environment to avoid those sudden slips and falls. Your brain needs and loves a variety of activities, playtime, and rest. Strive for consistent sleep and circadian rhythms. Participate in exercise to oxygenate your brain, keep fit and support healthy circulation and blood pressure. Do your best to keep your blood sugar levels stable and your A1C at 5.6 or lower. Engage in activities that require hand-eye coordination, handwriting, balance, and movement. Learn a new language or a musical instrument. Enjoy nature. Manage stress. Make deliberate healthy dietary choices with a whole foods diet rich in colorful fruits and vegetables, unrefined grains, beans and legumes, seeds and nuts, and organic proteins. Drink clean, filtered water and maintain adequate hydration. Reduce environmental toxins and plastics. Limit or avoid alcohol, tobacco, and/or toxic inhalants. If you use medications, replenish drug-nutrient depletions. Check with your health care professional for this information. Nutrients for Adult Brain and Mitochondrial Support Provide your brain with essential fats and oils necessary for its normal structure, repair, and cell membrane stability. Omega-3 DHA, choline, and phosphatidyl serine are required structures for neurological repair. Mitochondrial protection and function require several antioxidants and co-factors. Ensure optimal nutrient reserves to protect against mitochondrial decay. Important nutrients include: coenzyme Q10 PQQ glutathione B vitamins grape seed extract OPCs tocotrienols and tocopherols lipoic acid carnitine iron magnesium manganese zinc and copper biotin vitamin K In addition, these nutrients have also been found helpful: melatonin resveratrol curcumin/turmeric butyric acid Support Your Gut Flora Too Support your gut microbiome with beneficial flora. Animal studies demonstrated that anesthesia altered gut flora, provoked inflammatory response in the digestive tract, and altered mitochondrial function. Probiotic support helped to mitigate these stress responses and supported neurological tolerance to the anesthetic. Dietary fiber and prebiotics like arabinogalactan found in Immune Plus help make the short chain fatty acid butyric acid for your gut. Choices for Children Nutritional status during your infant and child’s formative years affects their development and health for life. Ask yourself a few questions. What is their overall picture of support like? Was it a healthy pregnancy or was it high risk, high stress or with limited prenatal nutrition? How about breast-fed versus formula? If you used baby formula, was it filled with corn syrup as the first ingredient? How about their diet? Is their diet predominantly whole foods or processed fast foods? Is your child engaged in regular physical exercise or is their lifestyle predominantly television, device and/or gaming outside of school? Ensure children are provided with essential omega-3 DHA, a multiple vitamin, minerals, antioxidants and probiotics. Choices to consider include DHA Kids, Super Mini Multi, Coral Calcium, Grape Seed Extract and probiotic rich foods (yogurt, kefir, fermented vegetables) or supplement. Children two years and older may use Super Dophilus. Optimization of your current health status plays an important role in your resiliency. Unexpected bumps happen in life which can disrupt health and require medical intervention. If you feel that you are aging faster than you should, give your brain some tender loving care to bounce back.

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