All About Nutrition, essential Vitamins, essential Minerals and essential Amino-acids for a Maximum Health.
I love to discuss Nutrition Deficiencies and Benefits.
Frank clinical selenium deficiency has been described in cystic fibrosis (CF), and a relative deficiency has been proposed as contributing to the pathogenesis of the disease. Because of these possibilities, we investigated the relationship between overall nutritional status in CF with measures of selenium nutriture. Fifteen stable outpatients with CF (group I) were compared to 13 age-matched controls (group II) and 27 healthy adults (group III).
Whole blood, plasma, and red blood cell selenium levels were reduced by 31%, 29%, and 33%, respectively, in CF patients vs controls (all p less than 0.001). In addition, both groups I and II showed significantly lower blood selenium levels than healthy adults (p less than 0.005).
Nutritional assessment revealed CF patients to be undernourished, with significant decreases in serum albumin (p less than 0.025), weight-for-height deficit (p less than 0.01), and weight-for-age (p less than 0.025) vs controls. However, only the triceps skinfold (TSF) measurement correlated significantly with selenium status (r = 0.56: p less than 0.05 for whole blood selenium vs TSF).
We conclude, based on the magnitude of decrement in blood selenium, that it is unlikely that selenium plays a significant primary pathogenic role in cystic fibrosis. However, these patients are at high risk for developing clinical selenium deficiencies. The measurement of blood selenium levels using appropriate age-matched normal standards should be mandatory in all CF patients with malnutrition, or in those requiring parenteral nutritional support.
Deficiency of Fat-Soluble Vitamins in Treated Patients With Pancreatic Insufficiency
S K Dutta et al. Ann Intern Med..
Abstract
Deficiency of fat-soluble vitamins (A,D,E, and K) was evaluated in 15 patients with exocrine pancreatic insufficiency secondary to chronic alcoholic pancreatitis. Mild to moderate steatorrhea was present in all patients despite oral pancreatic enzyme therapy for 27 +/- 4 months (mean +/- SE). Deficiency of a single fat-soluble vitamin was seen in six patients and deficiency of two fat-soluble vitamins was seen in two patients. One patient was deficient in three fat-soluble vitamins. Deficiency of vitamins A and E was most frequent. Treatment with specific vitamin supplements resulted in correction of these vitamin deficiencies. These data suggest that deficiency of a single or multiple fat-soluble vitamins is frequent even in treated patients with pancreatic insufficiency.
Fat-soluble vitamin status was assessed in 36 infants diagnosed with cystic fibrosis by newborn screening in the Colorado Program. At the time of diagnosis of cystic fibrosis, 36% of infants were hypoalbuminemic, 21% had vitamin A deficiency, 35% had vitamin D deficiency, and 38% had vitamin E deficiency. None had vitamin K deficiency. Supplementation with pancreatic enzymes, a multiple vitamin preparation, and additional vitamin E was associated with normalization of serum albumin, retinol, and 25-hydroxyvitamin D and negative PIVKA testing at age 6 and 12 months. Several patients remained vitamin E deficient, but this was felt to be due to poor compliance. Biochemical evidence of fat-soluble vitamin deficiency is common before age 3 months in infants with CF and responds to supplementation in the first year of life.
[Wallach goes on to cite additional evidence that cystic fibrosis is caused by a selenium deficiency and throughout his books reveals methods for treating CF patients.] - Joel Wallach, DVM, ND, and Ma Lan, MD, MS, Let's Play Doctor!, p. 77. Date: 10/30/2006 10:28:42 PM ( 14 y ) ... viewed 6051 times Today's medical fad: The Genetic Myth [Posted 26 October 2003, Last updated 16 November 2003] I have to admit... This article is inspired by TELEVISION, of all things. Either Thursday or Wednesday, I was at a Mexican restaurant having lunch when CNN Headline News ran two "medical" stories in the half-hour, blaming genetics for breast cancer and OCD (Obsessive-Compulsive Disorder). Now I know, as do most well-educated people, that TV news stories are often bogus, and I don't have time to respond to them. Big advertisers (think drug commercials) heavily influence news content, making independent radio stations and certain internet news services (see the news links on my main page) the last bastions of "honest" news, with their news largely uncontrolled by corporate advertising dollars. In this case, knowing that neither cancer nor OCD is caused by genetics, and that effective cancer cures have been available yet deliberately suppressed since the early 1900s, today I'll write a short article about the Genetic Fad.
I'm not the first to notice that blaming everything on genetics has become a fad in the medical field. About ten years ago in his Rare Earths, Forbidden Cures book, Dr. Joel Wallach made the assertion that genetic explanations of numerous diseases were just another fad. Genetic models of disease are encouraged by research grant funding sources, often companies that stand to profit from experimental "gene therapy" treatments.
Wallach is a colourful character. If you search the internet for him, you'll find two photos of the man used over and over, one in a cowboy hat and American flag shirt, the other in combat fatigues driving a Humvee. Well, my favourite photo of Wallach isn't a flaky guy on an internet site -- it's found in his Rare Earths, Forbidden Cures book: Wallach in his younger days, wearing a white lab coat, holding an infant monkey with cystic fibrosis. Wallach was the first research scientist to discover cystic fibrosis (CF) in monkeys. He also discovered what caused cystic fibrosis shortly thereafter -- a prenatal selenium deficiency in the mother. Until then (and even now, among traditional doctors), cystic fibrosis was promoted as a "genetic" disease. So Wallach reported these landmark findings to his bosses at the National Institutes of Health, and was promptly fired the next day. Why? Well, isn't it obvious? There goes their cystic fibrosis research money! Who's going to give all those high-priced scientists cushy jobs for their entire lives if the problem has been SOLVED?? And solved with inexpensive vitamins and minerals for a woman during pregnancy, no less!
In 1978, I (Wallach) discovered the first agreed upon CF [cystic fibrosis] in nonhumans; the test animals were NASA monkeys; the diagnosis was agreed to by experts from Johns Hopkins Medical School, Emory University and the CF Foundation!!!! Once they realized that this wasn't a genetic accident but CF was a recreatable selenium deficiency, they fired me within 24 hours' notice, 10 days after my wife had died. Dr. Paul de St. Agnese stated that "if anything important was to be discovered on CF, it would be in his NIH laboratory." Since 1978, we have treated 450 CF patients with excellent results; we have essentially cured infants three months old who started on the program (they are 12 years old today) and have helped CF women have healthy pregnancies and normal babies! [Wallach goes on to cite additional evidence that cystic fibrosis is caused by a selenium deficiency and throughout his books reveals methods for treating CF patients.] - Joel Wallach, DVM, ND, and Ma Lan, MD, MS, Let's Play Doctor!, p. 77.
Wallach was a hard-working Veterinarian and research scientist, his first major project a cause-of-death study for thousands of zoo animals. His research then expanded to cause-of-death in humans, and he eventually became an ND (Naturopathic Doctor) in order to treat humans with nutrient-based therapies used by Vets and farmers for their animals. His patients "were treated like dogs, but they got better." He particularly wanted to treat cystic fibrosis cases, as no one else in the field was willing to accept a new paradigm for the disease. As he explains in his books, there are no health insurance policies for farm animals -- Vets and farmers are very familiar with the common deficiency causes of most disease, and blend supplements into farm feed to prevent such disorders from occurring in the fist place. Wallach is very aware of simple deficiency diseases being passed off as genetics or other complicated theories. He wrote several books covering the vitamin and mineral deficiencies that cause these "genetic" diseases in humans.
So am I saying that breast cancer and OCD are deficiency diseases? Yes (to OCD) and no (to cancer), but they certainly aren't "genetic" in nature
Cystic fibrosis as a specific disease entity has been known to be associated with malnutrition for almost half a century. The importance of the malnutrition in the disease process remains unknown, as does much information about specific nutritional deficiencies in CF. Supplements for children with CF should include extra energy as fat or carbohydrate, a form of linoleic acid that can be absorbed, hydrolyzed protein, fat-soluble vitamins with vitamins A and E in a water emulsion, vitamin B12, probably B vitamins and vitamin C, and trace minerals. Routine measurements of nutritional status, particularly in children with growth failure, should be made at regular intervals and should include a three-day diet record and a simultaneous 72-hour stool fat determination. If fat malabsorption is not controlled by pancreatic enzymes, the use of antacids or cimetidine should be considered. The true role of nutrition in patients with CF will not be known until the appropriate studies are completed.
What is already known about this topic?
Preliminary evidence indicates the occurrence of presymptomatic transmission of SARS-CoV-2, based on reports of individual cases in China.
What is added by this report?
Investigation of all 243 cases of COVID-19 reported in Singapore during January 23–March 16 identified seven clusters of cases in which presymptomatic transmission is the most likely explanation for the occurrence of secondary cases.
What are the implications for public health practice?
The possibility of presymptomatic transmission increases the challenges of containment measures. Public health officials conducting contact tracing should strongly consider including a period before symptom onset to account for the possibility of presymptomatic transmission. The potential for presymptomatic transmission underscores the importance of social distancing, including the avoidance of congregate settings, to reduce COVID-19 spread.
Presymptomatic transmission of SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19), might pose challenges for disease control. The first case of COVID-19 in Singapore was detected on January 23, 2020, and by March 16, a total of 243 cases had been confirmed, including 157 locally acquired cases. Clinical and epidemiologic findings of all COVID-19 cases in Singapore through March 16 were reviewed to determine whether presymptomatic transmission might have occurred.
Presymptomatic transmission was defined as the transmission of SARS-CoV-2 from an infected person (source patient) to a secondary patient before the source patient developed symptoms, as ascertained by exposure and symptom onset dates, with no evidence that the secondary patient had been exposed to anyone else with COVID-19. Seven COVID-19 epidemiologic clusters in which presymptomatic transmission likely occurred were identified, and 10 such cases within these clusters accounted for 6.4% of the 157 locally acquired cases. In the four clusters for which the date of exposure could be determined, presymptomatic transmission occurred 1–3 days before symptom onset in the presymptomatic source patient. To account for the possibility of presymptomatic transmission, officials developing contact tracing protocols should strongly consider including a period before symptom onset. Evidence of presymptomatic transmission of SARS-CoV-2 underscores the critical role social distancing, including avoidance of congregate settings, plays in controlling the COVID-19 pandemic.
Early detection and isolation of symptomatic COVID-19 patients and tracing of close contacts is an important disease containment strategy; however, the existence of presymptomatic or asymptomatic transmission would present difficult challenges to contact tracing. Such transmission modes have not been definitively documented for COVID-19, although cases of presymptomatic and asymptomatic transmissions have been reported in China (1,2) and possibly occurred in a nursing facility in King County, Washington (3). Examination of serial intervals (i.e., the number of days between symptom onsets in a primary case and a secondary case) in China suggested that 12.6% of transmission was presymptomatic (2). COVID-19 cases in Singapore were reviewed to determine whether presymptomatic transmission occurred among COVID-19 clusters.
The surveillance and case detection methods employed in Singapore have been described (4). Briefly, all medical practitioners were required by law to notify Singapore’s Ministry of Health of suspected and confirmed cases of COVID-19. The definition of a suspected case was based on the presence of respiratory symptoms and an exposure history. Suspected cases were tested, and a confirmed case was defined as a positive test for SARS-CoV-2, using laboratory-based polymerase chain reaction or serologic assays (5). All cases in this report were confirmed by polymerase chain reaction only. Asymptomatic persons were not routinely tested, but such testing was performed for persons in groups considered to be at especially high risk for infection, such as evacuees on flights from Wuhan, China (6), or families that experienced high attack rates.
Patients with confirmed COVID-19 were interviewed to obtain information about their clinical symptoms and activity history during the 2 weeks preceding symptom onset to ascertain possible sources of infection. Contact tracing examined the time from symptom onset until the time the patient was successfully isolated to identify contacts who had interactions with the patient. All contacts were monitored daily for their health status, and those who developed symptoms were tested as part of active case finding.
Clinical and epidemiologic data for all 243 reported COVID-19 cases in Singapore during January 23–March 16 were reviewed. Clinical histories were examined to identify symptoms before, during, and after the first positive SARS-CoV-2 test.
Records of cases that were epidemiologically linked (clusters) were reviewed to identify instances of likely presymptomatic transmission. Such clusters had clear contact between a source patient and a patient infected by the source (a secondary patient), had no other likely explanations for infection, and had the source patient’s date of symptom onset occurring after the date of exposure to the secondary patient who was subsequently infected. Symptoms considered in the review included respiratory, gastrointestinal (e.g., diarrhea), and constitutional symptoms. In addition, the source patient’s exposure had to be strongly attributed epidemiologically to transmission from another source. This reduced the likelihood that an unknown source was involved in the cases in the cluster.
Seven Clusters of COVID-19 Cases Suggesting Presymptomatic Transmission
Investigation of COVID-19 cases in Singapore identified seven clusters (clusters A–G) in which presymptomatic transmission likely occurred. These clusters occurred during January 19–March 12, and involved from two to five patients each (Figure). Ten of the cases within these clusters were attributed to presymptomatic transmission and accounted for 6.4% of the 157 locally acquired cases reported as of March 16.
Cluster A. A woman aged 55 years (patient A1) and a man aged 56 years (patient A2) were tourists from Wuhan, China, who arrived in Singapore on January 19. They visited a local church the same day and had symptom onset on January 22 (patient A1) and January 24 (patient A2). Three other persons, a man aged 53 years (patient A3), a woman aged 39 years (patient A4), and a woman aged 52 years (patient A5) attended the same church that day and subsequently developed symptoms on January 23, January 30, and February 3, respectively. Patient A5 occupied the same seat in the church that patients A1 and A2 had occupied earlier that day (captured by closed-circuit camera) (5). Investigations of other attendees did not reveal any other symptomatic persons who attended the church that day.
Cluster B. A woman aged 54 years (patient B1) attended a dinner event on February 15 where she was exposed to a patient with confirmed COVID-19. On February 24, patient B1 and a woman aged 63 years (patient B2) attended the same singing class. Two days later (February 26), patient B1 developed symptoms; patient B2 developed symptoms on February 29.
Cluster C. A woman aged 53 years (patient C1) was exposed to a patient with confirmed COVID-19 on February 26 and likely passed the infection to her husband, aged 59 years (patient C2) during her presymptomatic period; both patients developed symptoms on March 5.
Cluster D. A man aged 37 years (patient D1) traveled to the Philippines during February 23–March 2, where he was in contact with a patient with pneumonia who later died. Patient D1 likely transmitted the infection to his wife (patient D2), aged 35 years, during his presymptomatic period. Both patients developed symptoms on March 8.
Cluster E. A man aged 32 years (patient E1) traveled to Japan during February 29–March 8, where he was likely infected, and subsequently transmitted the infection to his housemate, a woman aged 27 years (patient E2), before he developed symptoms. Both developed symptoms on March 11.
Cluster F. A woman aged 58 years (patient F1) attended a singing class on February 27, where she was exposed to a patient with confirmed COVID-19. She attended a church service on March 1, where she likely infected a woman aged 26 years (patient F2) and a man aged 29 years (patient F3), both of whom sat one row behind her. Patient F1 developed symptoms on March 3, and patients F2 and F3 developed symptoms on March 3 and March 5, respectively.
Cluster G. A man aged 63 years (patient G1) traveled to Indonesia during March 3–7. He met a woman aged 36 years (patient G2) on March 8 and likely transmitted SARS-CoV-2 to her; he developed symptoms on March 9, and patient G2 developed symptoms on March 12.
Investigation of these clusters did not identify other patients who could have transmitted COVID-19 to the persons infected. In four clusters (A, B, F, and G), presymptomatic transmission exposure occurred 1–3 days before the source patient developed symptoms. For the remaining three clusters (C, D, and E), the exact timing of transmission exposure could not be ascertained because the persons lived together, and exposure was continual.
This investigation identified seven clusters of COVID-19 in Singapore in which presymptomatic transmission likely occurred. Among the 243 cases of COVID-19 reported in Singapore as of March 16, 157 were locally acquired; 10 of the 157 (6.4%) locally acquired cases are included in these clusters and were attributed to presymptomatic transmission. These findings are supported by other studies that suggest that presymptomatic transmission of COVID-19 can occur (1–3). An examination of transmission events among cases in Chinese patients outside of Hubei province, China, suggested that 12.6% of transmissions could have occurred before symptom onset in the source patient (3).
Presymptomatic transmission might occur through generation of respiratory droplets or possibly through indirect transmission. Speech and other vocal activities such as singing have been shown to generate air particles, with the rate of emission corresponding to voice loudness (7). News outlets have reported that during a choir practice in Washington on March 10, presymptomatic transmission likely played a role in SARS-CoV-2 transmission to approximately 40 of 60 choir members.*
Environmental contamination with SARS-CoV-2 has been documented (8), and the possibility of indirect transmission through fomites by presymptomatic persons is also a concern. Objects might be contaminated directly by droplets or through contact with an infected person’s contaminated hands and transmitted through nonrigorous hygiene practices.
The possibility of presymptomatic transmission of SARS-CoV-2 increases the challenges of COVID-19 containment measures, which are predicated on early detection and isolation of symptomatic persons. The magnitude of this impact is dependent upon the extent and duration of transmissibility while a patient is presymptomatic, which, to date, have not been clearly established. In four clusters (A, B, F, and G), it was possible to determine that presymptomatic transmission exposure occurred 1–3 days before the source patient developed symptoms. Such transmission has also been observed in other respiratory viruses such as influenza. However, transmissibility by presymptomatic persons requires further study.
The findings in this report are subject to at least three limitations. First, although these cases were carefully investigated, the possibility exists that an unknown source might have initiated the clusters described. Given that there was not widespread community transmission of COVID-19 in Singapore during the period of evaluation and while strong surveillance systems were in place to detect cases, presymptomatic transmission was estimated to be more likely than the occurrence of unidentified sources. Further, contact tracing undertaken during this period was extensive and would likely have detected other symptomatic cases. Second, recall bias could affect the accuracy of symptom onset dates reported by cases, especially if symptoms were mild, resulting in uncertainty about the duration of the presymptomatic period. Finally, because of the nature of detection and surveillance activities that focus on testing symptomatic persons, underdetection of asymptomatic illness is expected. Recall bias and interviewer bias (i.e., the expectation that some symptoms were present, no matter how mild), could have contributed to this.
The evidence of presymptomatic transmission in Singapore, in combination with evidence from other studies (9,10) supports the likelihood that viral shedding can occur in the absence of symptoms and before symptom onset. This study identified seven clusters of cases in which presymptomatic transmission of COVID-19 likely occurred; 10 (6.4%) of such cases included in these clusters were among the 157 locally acquired cases reported in Singapore as of March 16. Containment measures should account for the possibility of presymptomatic transmission by including the period before symptom onset when conducting contact tracing.
These findings also suggest that to control the pandemic it might not be enough for only persons with symptoms to limit their contact with others because persons without symptoms might transmit infection. Finally, these findings underscore the importance of social distancing in the public health response to the COVID-19 pandemic, including the avoidance of congregate settings.
In the United States, by some estimates, the coronavirus has already claimed 28,998 lives. But for some, the virus lingers in stealth mode. For many asymptomatic people, it doesn't even cause a tickle in their throat.
Without wide-scale testing we simply don't know how many asymptomatic cases there are, nor will we know exactly whysome people don't develop symptoms.
But we know those people are out there. Speaking to NPRRobert Redfield, the director of the CDC, estimated that as many as 25 percent of people may be asymptomatic. Other estimates range from 18 to 30 percent.
While there's no clear answer yet why some people show Covid-19 symptoms and others do not, there are theories. Two of these theories are:
Some people have a stronger innate immune response to the virus.
Some people encounter a smaller viral load.
Warner Greene, is an immunologist and microbiologist at the University of California San Francisco, and the Director of the Gladstone Center for HIV Cure Research. He tells Inverse that the most compelling explanation is the idea that some people's innate immune systems respond incredibly well to the virus.
Scientists believe that there are many undetected Covid-19 cases, perhaps amongst people who show no symptoms.
The innate immune system is a generalized fighting force. It's comprised of very basic tools on the outside of the body, like our mucus membranes or our skin. It's also equipped with generalist tools inside of the body like natural killer cells —a type of a white blood cell that's trained to recognize viral invaders and destroy them. (And yes, they are actually called that.)
That makes it different from the adaptive immune systemwhich is comprised of targeted antibodies that have learned to recognize SARS-CoV-2 and kill it (now we're using those antibodies as treatment).
"I think that it’s the first line of defense in the body — innate immunity," Greene says. "It’s not antibodies, it’s not T-cells. Some people have a stronger innate immune response to this virus and are able to bring it under control."
The idea is that this first line of defense might be able to detect SARS-CoV-2 right away, launch a "vigorous" response, and perhaps even kill the cell that was first infected to limit the spread, Greene says.
For now, this is a working theory.
"It’s not highly specific, but it’s an absolutely pivotal part of our defense against viruses like this," he adds. Other theories suggest factors outside the body influence why some people don't get as sick: Like how much virus you're exposed to. Studies conducted in China suggest that people with higher "viral load" (higher amounts of virus circulating in their bodies) tend to have worse symptoms.
However, Greene doesn't favor this idea. More likely, there's some combination of factors happening inside the body that determines who gets very sick and who doesn't, he says.
We already know that underlying conditions like diabetes, obesity, asthma or other illnesses that hamper the immune system place people at higher risk. The elderly are also at-risk (and as we age, says Greene, our immune systems do tend to decline). But scientists are eagerly looking for other biomarkers that might be able to tell us more.
Greene is currently developing a study intended to search for biomarkers that might be able to predict how well someone fares against the coronavirus. Those biomarkers he says will be "very instructive." Hidden Covid-19 cases, and a second chance at a normal life
As of writing, there are over 662,000 confirmed cases of coronavirus. But Greene explains that there's a "huge amount" of cases out there that we're not counting, partially because people either show mild symptoms or none at all.
One paper, published in Science estimates that about 86 percent of cases in Wuhan, China were not counted as the virus spread, likely facilitating the early stages of the pandemic. Many of those uncounted cases were likely asymptomatic, though, not all, the authors note.
Another pre-print paper (not peer-reviewed) based on drive-through testing in Santa Clara, California, estimates that there are actually between 50 and 85 times more cases in that region than health officials originally thought.
The only thing that can truly end our fight with coronavirus is a vaccine (on that front he is assured that "science will deliver"). However, knowing who has been exposed to this virus gives us our best shot at regaining some kind of normalcy.
If we know who is infected we may be able to put them, and their direct contacts, into quarantine right away, says Greene. That means they can't stealthily, and accidentally, spread the virus. They would stay home, just like a person who exhibits clear symptoms would stay home.
"Then society can continue to work, and the economy restarts," he says.
The more scientists learn about contact tracing, the closer we become to that potential future. But we also must scale-up testing: For life to get back to normal, everyone needs to be tested — even people who don't feel sick.
"As we come out of this shelter-in-place and everyone is separated, we have another chance to do what we should have done at the very beginning of this pandemic," Greene says.
