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Optimizing Vitamin D Status Improves Outcomes in
Critical Ill and Injured Patients
Omar K Danner1*, Erin Danielle Danner2 and Leslie Ray Matthews1
1
Department of Surgery, Morehouse School of Medicine, USA
2
College of Arts and Sciences, University of Georgia, USA
*Corresponding author: Omar K Danner, Department of Surgery, Morehouse School of Medicine, USA.
To Cite This Article: Omar K Danner, Optimizing Vitamin D Status Improves Outcomes in Critical Ill and Injured Patients. 2020 - 8(2). AJBSR.
MS.ID.001250. DOI: 10.34297/AJBSR.2020.08.001250.
Received: March 03, 2020; Published: March 16, 2020
Copy Right@ Omar K Danner
This work is licensed under Creative Commons Attribution 4.0 License AJBSR.MS.ID.001250.
American Journal of
Biomedical Science & Research
www.biomedgrid.com
---------------------------------------------------------------------------------------------------------------------------------
ISSN: 2642-1747
Review Article
Abbreviations: ICU: Intensive Care Unit; BMD: Maximal Bone Density; VDR: Vitamin D Receptors; ARDS: Acute Respiratory Distress Syndrome
114
Introduction
In 2008, Giovanucci et al. [1] showed that men with low vitamin
D levels suffered 2.42 times more myocardial infarctions than
those with normal vitamin D status [1]. Alternatively, a sufficient
amount of serum 25-hydroxyvitamin D3, [25(OH)D], appears to
improve the risk of almost every disease of aging. Dobnig et al.
[2] similarly demonstrated people with an inadequate vitamin D
status have twice the likelihood of death over seven years [2,3].
Vitamin D sufficiency, define as serum 25(OH)D levels of 30ng/
mL (75nmol/L) and above, improves various health outcomes,
including bone mineral density, fractures, and colorectal cancer,
based on analysis of observational studies [4]. Vitamin D levels of
21-29ng/mL delineates insufficiency and a concentration of 20ng/
mL or less defines vitamin D deficiency [4]. When vitamin D levels
are inadequate, and particularly fall below17.8ng/mL, mortality risk
increases by as much as 26% from all-cause mortality in the general
population [3,5]. Current data suggests hypovitaminosis D plays a
significant role in the development of numerous common chronic
diseases and inflammatory conditions, including coronary artery
disease, cerebrovascular disease, diabetes mellitus, autoimmune
disorders, such as systemic lupus erythematosus, scleroderma and
multiple sclerosis and 17 different forms of cancer [6-12]. Vitamin
D deficiency is arguably one of the most prevalent but underrated
nutritional deficiency worldwide [6,7]. It continues to be associated
with increased overall mortality risk in several studies [8-12].
Several observational studies on hypovitaminosis D over the past
decade support the persistent existence of a high prevalence of
vitamin D insufficiency and deficiency in as many as 50 to 90%
of hospitalized patients, with a particular predilection in the setting
of critical illness [6-9, 12-14]. Although full elucidation of the role
vitamin D status plays in patients requiring admission to the
intensive care unit (ICU) is an area undergoing active investigation,
epidemiological data supports the findings that vitamin D
sufficiency may decrease the risk of systemic inflammatory from
all causes as well as sepsis in general [12,15]. Investigations by
our group examining the prevalence and effects of insufficient or
deficient serum vitamin D levels on our critically-ill and/or severelyinjured trauma patients revealed increased risk of unfavorable
outcomes when serum vitamin D levels fell below a level of 30ng/
mL (75nmol/mL] in SICU trauma patients who survived their initial
injury and resuscitative efforts [6,16]. According to some of the
world’s leading vitamin D experts, optimal serum levels of 25[OH]D
range between 30 and 50ng/mL. Those individuals with 25 (OH) D3
(calcidiol) levels below 30 ng/mL are considered to have vitamin D
insufficiency as noted above [5,6, 8,15,16] looked at the risk of 30-
day and in-hospital mortality after initiation of critical care services
in patients with severe vitamin D deficiency. There was a 1.9-fold
higher risk of death than in those patients with vitamin D levels
of ≤30ng/mL [7]. Inadequate levels of 25[OH]D in the insufficient
cohort remained a significant predictor of increased likelihood of
mortality, even after multivariate adjustment [7].
Under normal circumstances, vitamin D is a hormone produced
principally by the skin in response to natural sunlight. However,
American Journal of Biomedical Science & Research
Am J Biomed Sci & Res Copy@ Omar K Danner
115
when the sun hits the northern hemisphere below 45 degrees
in the spring and summer, it cannot produce UVB rays of the
proper wavelengths from 290 to 315 nm, which is required for
the production of vitamin D in the skin between 10:00 a.m. and
approximately 3:00 p.m. [6,17]. At latitudes of 32 degrees or above,
vitamin D levels are the lowest, particularly during the winter
months and early spring, due to the lack of sunlight at the suitable
wavelength [6,17]. During the fall and winter months, vitamin
D stores decrease by approximately 20 to 30%. Furthermore,
vitamin D deficiency is very common in Western society as it is
nearly impossible to get adequate amounts of vitamin D from diet
alone without purposeful exogenous supplementation [6,7,17].
Therefore, reversal of hypovitaminosis D may not be quick or easy
without supplementation.
There is a suggestion by researchers that vitamin D deficiency
is present in at least 50% to 80% of critically ill patients admitted
to surgical and medical ICUs. Nevertheless, based on the definition
of normal and subtherapeutic vitamin D status, vitamin D
insufficiency in western society may be grossly underestimated
[6-14,16]. The true prevalence and extent of vitamin D deficiency
might be much worse. This understanding is particularly pertinent
considering we have entered the season of increased risk for acute
respiratory illness, where a robust immune system is of paramount
importance for fighting off upper respiratory tract infections. This
underappreciation of vitamin D deficiency may be associated with
increased relative risk of adverse outcomes in fragile and critically
ill patient populations [6-14,16]. In our prior investigations, we
evaluated a cutoff ≥40 ng/mL as a surrogate marker to define
a normal vitamin D level, and levels of <40 ng/mL to represent
a relative insufficiency in our ICU patients [6]. We found higher
25[OH]D levels improved outcomes in surgical ICU patients
[6,8,16]. There is other evidence that supports the body functions
better at this higher vitamin D level. Other authors have suggested
that maximal bone density (BMD) can only be achieved when the
25-hydroxyvitamin D level reaches 40ng/mL or greater [17]. As
fractures are very common in critically injured elderly trauma
patients, achieving adequate vitamin D levels becomes increasingly
important in this fragile, at-risk patient population. Based on prior
observations demonstrating the need for calcidiol levels ≥ 40ng/
mL to adequately suppress serum parathyroid hormone levels
and achieve maximal bone density in the hips and lumbar spine
patients, it is plausible to suggest that higher vitamin D levels may
portend a protective effect in the other severely injured and/or
critically ill individuals [5,6,15,18-20].
To achieve a vitamin D of 30 to 50ng/mL and maintain it long
term, investigators have found that it takes over 4,000 to 5,000
units of 25-(0H) vitamin D supplementation per day [18,20]. This
amounts to over 5 to 10 times the current recommended daily
intake [20]. The importance of this recommendation is that optimal
local concentrations of serum 25-(OH) D ≥30 ng/mL [6,24,25] are
required for optimal paracrine conversion to 1,25-(OH)2-vitamin
D (calcitriol) by macrophages and other immune cells. The serum
concentration needs to be ≥ 30 (>75 nmol/L) [6,7,21-24] to activate
the vitamin D receptors (VDR) that regulates the immune response.
Activation of the VDR by bioactive vitamin D up-regulates the
anti-inflammatory cytokines IL-8 and IL-10, which promotes the
expression of a T-suppressor cell lineage and helps to turn off the
adaptive immune response once the job is complete [23-25]. Thus,
it is understandable that patients with moderate to severe vitamin
D deficiency syndromes are less capable of mounting a successful
immune response to severe insults, injury, and acute viral and
bacterial infections. Furthermore, they have higher risk of ICUrelated septic complications, acute respiratory distress syndrome
(ARDS) and death.
Conclusion
Published data suggests critically-ill patients with inadequate
serum vitamin D stores may enter into a vicious inflammatory cycle
due to low levels of the bioactive form of vitamin D, calcitriol, which
leads to increased production of pro-inflammatory cytokines,
which may not be easily reversed with vitamin D supplementation
[6,8,24]. This review may provide a plausible link between the
excess mortality observed in people during an acute outbreak
of novel acute respiratory syndromes in the general population
and especially patients in the ICU setting who are at a higher risk
of frankly deficient vitamin D levels. Therefore, we recommend
checking serum 25-OH vitamin D levels on all hospitalized
ICU patients, and particularly those with acute respiratory or
unexplained infectious/inflammatory illness. Although it is difficult
to prove clinical effectiveness in the setting of acute infectious
illness, supplementation of vitamin D stores to augment the
immune system using cholecalciferol (Vitamin D3) at doses of 4,000
to 5,000 units daily may not be unreasonable, especially during this
uncharacteristically aggressive flu season, and more so in light of
the worldwide coronavirus [COVID-19] epidemic.
References
1. Giovannucci E, Liu Y, Hollis BW, Rimm EB (2008) 25-hydroxyvitamin
D and risk of myocardial infarction in men: a prospective study. Arch
Intern Med 168(11): 1174-1180.
2. Dobnig H, Pilz S, Scharnagi H, Renner W, Seelhorst U, et al. (2008)
Independent association of low serum 25-hydroxyvitamin d and
1,25-dihydroxyvitamin D levels with all-cause and cardiovascular
mortality, Arch Intern Med 168(12): 1340-1349.
3. Melamed ML, Michos ED, Post W, Astor B (2008) 25-hydroxyl vitamin
D levels and the risk of mortality in the general population, Arch Intern
Med 168(15): 1629-1637.
4. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, DawsonHughes B, et al. (2006) Estimation of optimal serum concentrations
of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr
84(1): 18-28.
5. Amer M, Qayyam R (2013) Relationship between 25-Hydroxyvitamin D
and All-Cause and Cardiovascular Disease Mortality. Am J Med 126(6):
509-514.
Am J Biomed Sci & Res C
Critical Ill and Injured Patients
Omar K Danner1*, Erin Danielle Danner2 and Leslie Ray Matthews1
1
Department of Surgery, Morehouse School of Medicine, USA
2
College of Arts and Sciences, University of Georgia, USA
*Corresponding author: Omar K Danner, Department of Surgery, Morehouse School of Medicine, USA.
To Cite This Article: Omar K Danner, Optimizing Vitamin D Status Improves Outcomes in Critical Ill and Injured Patients. 2020 - 8(2). AJBSR.
MS.ID.001250. DOI: 10.34297/AJBSR.2020.08.001250.
Received: March 03, 2020; Published: March 16, 2020
Copy Right@ Omar K Danner
This work is licensed under Creative Commons Attribution 4.0 License AJBSR.MS.ID.001250.
American Journal of
Biomedical Science & Research
www.biomedgrid.com
---------------------------------------------------------------------------------------------------------------------------------
ISSN: 2642-1747
Review Article
Abbreviations: ICU: Intensive Care Unit; BMD: Maximal Bone Density; VDR: Vitamin D Receptors; ARDS: Acute Respiratory Distress Syndrome
114
Introduction
In 2008, Giovanucci et al. [1] showed that men with low vitamin
D levels suffered 2.42 times more myocardial infarctions than
those with normal vitamin D status [1]. Alternatively, a sufficient
amount of serum 25-hydroxyvitamin D3, [25(OH)D], appears to
improve the risk of almost every disease of aging. Dobnig et al.
[2] similarly demonstrated people with an inadequate vitamin D
status have twice the likelihood of death over seven years [2,3].
Vitamin D sufficiency, define as serum 25(OH)D levels of 30ng/
mL (75nmol/L) and above, improves various health outcomes,
including bone mineral density, fractures, and colorectal cancer,
based on analysis of observational studies [4]. Vitamin D levels of
21-29ng/mL delineates insufficiency and a concentration of 20ng/
mL or less defines vitamin D deficiency [4]. When vitamin D levels
are inadequate, and particularly fall below17.8ng/mL, mortality risk
increases by as much as 26% from all-cause mortality in the general
population [3,5]. Current data suggests hypovitaminosis D plays a
significant role in the development of numerous common chronic
diseases and inflammatory conditions, including coronary artery
disease, cerebrovascular disease, diabetes mellitus, autoimmune
disorders, such as systemic lupus erythematosus, scleroderma and
multiple sclerosis and 17 different forms of cancer [6-12]. Vitamin
D deficiency is arguably one of the most prevalent but underrated
nutritional deficiency worldwide [6,7]. It continues to be associated
with increased overall mortality risk in several studies [8-12].
Several observational studies on hypovitaminosis D over the past
decade support the persistent existence of a high prevalence of
vitamin D insufficiency and deficiency in as many as 50 to 90%
of hospitalized patients, with a particular predilection in the setting
of critical illness [6-9, 12-14]. Although full elucidation of the role
vitamin D status plays in patients requiring admission to the
intensive care unit (ICU) is an area undergoing active investigation,
epidemiological data supports the findings that vitamin D
sufficiency may decrease the risk of systemic inflammatory from
all causes as well as sepsis in general [12,15]. Investigations by
our group examining the prevalence and effects of insufficient or
deficient serum vitamin D levels on our critically-ill and/or severelyinjured trauma patients revealed increased risk of unfavorable
outcomes when serum vitamin D levels fell below a level of 30ng/
mL (75nmol/mL] in SICU trauma patients who survived their initial
injury and resuscitative efforts [6,16]. According to some of the
world’s leading vitamin D experts, optimal serum levels of 25[OH]D
range between 30 and 50ng/mL. Those individuals with 25 (OH) D3
(calcidiol) levels below 30 ng/mL are considered to have vitamin D
insufficiency as noted above [5,6, 8,15,16] looked at the risk of 30-
day and in-hospital mortality after initiation of critical care services
in patients with severe vitamin D deficiency. There was a 1.9-fold
higher risk of death than in those patients with vitamin D levels
of ≤30ng/mL [7]. Inadequate levels of 25[OH]D in the insufficient
cohort remained a significant predictor of increased likelihood of
mortality, even after multivariate adjustment [7].
Under normal circumstances, vitamin D is a hormone produced
principally by the skin in response to natural sunlight. However,
American Journal of Biomedical Science & Research
Am J Biomed Sci & Res Copy@ Omar K Danner
115
when the sun hits the northern hemisphere below 45 degrees
in the spring and summer, it cannot produce UVB rays of the
proper wavelengths from 290 to 315 nm, which is required for
the production of vitamin D in the skin between 10:00 a.m. and
approximately 3:00 p.m. [6,17]. At latitudes of 32 degrees or above,
vitamin D levels are the lowest, particularly during the winter
months and early spring, due to the lack of sunlight at the suitable
wavelength [6,17]. During the fall and winter months, vitamin
D stores decrease by approximately 20 to 30%. Furthermore,
vitamin D deficiency is very common in Western society as it is
nearly impossible to get adequate amounts of vitamin D from diet
alone without purposeful exogenous supplementation [6,7,17].
Therefore, reversal of hypovitaminosis D may not be quick or easy
without supplementation.
There is a suggestion by researchers that vitamin D deficiency
is present in at least 50% to 80% of critically ill patients admitted
to surgical and medical ICUs. Nevertheless, based on the definition
of normal and subtherapeutic vitamin D status, vitamin D
insufficiency in western society may be grossly underestimated
[6-14,16]. The true prevalence and extent of vitamin D deficiency
might be much worse. This understanding is particularly pertinent
considering we have entered the season of increased risk for acute
respiratory illness, where a robust immune system is of paramount
importance for fighting off upper respiratory tract infections. This
underappreciation of vitamin D deficiency may be associated with
increased relative risk of adverse outcomes in fragile and critically
ill patient populations [6-14,16]. In our prior investigations, we
evaluated a cutoff ≥40 ng/mL as a surrogate marker to define
a normal vitamin D level, and levels of <40 ng/mL to represent
a relative insufficiency in our ICU patients [6]. We found higher
25[OH]D levels improved outcomes in surgical ICU patients
[6,8,16]. There is other evidence that supports the body functions
better at this higher vitamin D level. Other authors have suggested
that maximal bone density (BMD) can only be achieved when the
25-hydroxyvitamin D level reaches 40ng/mL or greater [17]. As
fractures are very common in critically injured elderly trauma
patients, achieving adequate vitamin D levels becomes increasingly
important in this fragile, at-risk patient population. Based on prior
observations demonstrating the need for calcidiol levels ≥ 40ng/
mL to adequately suppress serum parathyroid hormone levels
and achieve maximal bone density in the hips and lumbar spine
patients, it is plausible to suggest that higher vitamin D levels may
portend a protective effect in the other severely injured and/or
critically ill individuals [5,6,15,18-20].
To achieve a vitamin D of 30 to 50ng/mL and maintain it long
term, investigators have found that it takes over 4,000 to 5,000
units of 25-(0H) vitamin D supplementation per day [18,20]. This
amounts to over 5 to 10 times the current recommended daily
intake [20]. The importance of this recommendation is that optimal
local concentrations of serum 25-(OH) D ≥30 ng/mL [6,24,25] are
required for optimal paracrine conversion to 1,25-(OH)2-vitamin
D (calcitriol) by macrophages and other immune cells. The serum
concentration needs to be ≥ 30 (>75 nmol/L) [6,7,21-24] to activate
the vitamin D receptors (VDR) that regulates the immune response.
Activation of the VDR by bioactive vitamin D up-regulates the
anti-inflammatory cytokines IL-8 and IL-10, which promotes the
expression of a T-suppressor cell lineage and helps to turn off the
adaptive immune response once the job is complete [23-25]. Thus,
it is understandable that patients with moderate to severe vitamin
D deficiency syndromes are less capable of mounting a successful
immune response to severe insults, injury, and acute viral and
bacterial infections. Furthermore, they have higher risk of ICUrelated septic complications, acute respiratory distress syndrome
(ARDS) and death.
Conclusion
Published data suggests critically-ill patients with inadequate
serum vitamin D stores may enter into a vicious inflammatory cycle
due to low levels of the bioactive form of vitamin D, calcitriol, which
leads to increased production of pro-inflammatory cytokines,
which may not be easily reversed with vitamin D supplementation
[6,8,24]. This review may provide a plausible link between the
excess mortality observed in people during an acute outbreak
of novel acute respiratory syndromes in the general population
and especially patients in the ICU setting who are at a higher risk
of frankly deficient vitamin D levels. Therefore, we recommend
checking serum 25-OH vitamin D levels on all hospitalized
ICU patients, and particularly those with acute respiratory or
unexplained infectious/inflammatory illness. Although it is difficult
to prove clinical effectiveness in the setting of acute infectious
illness, supplementation of vitamin D stores to augment the
immune system using cholecalciferol (Vitamin D3) at doses of 4,000
to 5,000 units daily may not be unreasonable, especially during this
uncharacteristically aggressive flu season, and more so in light of
the worldwide coronavirus [COVID-19] epidemic.
References
1. Giovannucci E, Liu Y, Hollis BW, Rimm EB (2008) 25-hydroxyvitamin
D and risk of myocardial infarction in men: a prospective study. Arch
Intern Med 168(11): 1174-1180.
2. Dobnig H, Pilz S, Scharnagi H, Renner W, Seelhorst U, et al. (2008)
Independent association of low serum 25-hydroxyvitamin d and
1,25-dihydroxyvitamin D levels with all-cause and cardiovascular
mortality, Arch Intern Med 168(12): 1340-1349.
3. Melamed ML, Michos ED, Post W, Astor B (2008) 25-hydroxyl vitamin
D levels and the risk of mortality in the general population, Arch Intern
Med 168(15): 1629-1637.
4. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, DawsonHughes B, et al. (2006) Estimation of optimal serum concentrations
of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr
84(1): 18-28.
5. Amer M, Qayyam R (2013) Relationship between 25-Hydroxyvitamin D
and All-Cause and Cardiovascular Disease Mortality. Am J Med 126(6):
509-514.
Am J Biomed Sci & Res C
f a natural cure for coronavirus is ever proven, this Chinese Medicine herb is likely to be the one (and no, we don’t sell it)
Tuesday, March 17, 2020 by: Mike Adams
Tags: artemisinin, coronavirus, Cures, goodhealth, goodmedicine, Herbs, infections, natural cures, natural medicine, Naturopathy, outbreak, pandemic, prevention, remedies, sweet wormwood
3,600
VIEWS
Image: If a natural cure for coronavirus is ever proven, this Chinese Medicine herb is likely to be the one (and no, we don’t sell it)
(Natural News) News is breaking all over the world that chloroquine, a prescription medication used to treat malaria, also appears to be effective against the coronavirus. According to local news KFOR.com, the Oklahoma Medical Research Foundation is advocating testing of the drug against COVID-19, the disease caused by the Wuhan coronavirus. From the KFOR.com website:
James explained that repurposing existing medications is often the fastest path to treating those infected by the virus in a novel way.
“That would be really exciting, because it’s a drug that already has FDA approval, and it is readily available,” she said. “If it works, it might treat COVID-19 almost instantly.”
Wider studies are now underway to confirm the results.
Chloroquine is best known as a malaria treatment, and it seems very likely to be helpful in preventing coronavirus infections. But what about natural molecules from herbs that might offer the same promise against both malaria and coronavirus?
Here’s a promising candidate herb that prevents malaria and tuberculosis
In the world of natural medicine, there are already powerful, well-known treatments against malaria that also happen to prevent tuberculosis, an aggressive infection of the respiratory tract. While nothing is yet proven to treat coronavirus, our review of herbal medicine studies and medicinal phytochemicals leads us to the conclusion that this Chinese Medicine herb may one day become known as the “natural cure” for coronavirus (although clinical trials are needed, obviously, to prove this).
The chemical is called artemesinin, and the herb is known as sweet wormwood. And no, we don’t sell it. This isn’t a commercial promotion, it’s an effort to help save millions of lives using medicine that’s available right now, all around the world.
Artemesinin is known for its ability to block the bacterial strain that causes tuberculosis, known as Mycobacterium tuberculosis. That doesn’t mean it prevents coronavirus, which is a viral infection, but it’s a strong candidate for a number of logical reasons.
According to research published in the journal Phytomedicine, artemisinin / sweet wormwood has a “100% cure rate” for treating drug-resistant malaria, at least in a small trial involving 18 patients (all of whom were cured). As Herbs.news writes in this important story:
A study led by Pamela Weathers, a professor of biology and biotechnology at the Worcester Polytechnic Institute (WPI), published in the journal Phytomedicine, describes how the Artemisia annua plant, commonly known as sweet wormwood or sweet annie, saved 18 patients with drug-resistant malaria from the brink of death.
The Congolese patients, who ranged in age from 14 months to 60 years, had all developed severe, untreatable malaria, with symptoms ranging from loss of consciousness, to trouble breathing and convulsions, among others. When they failed to respond to intravenous treatment with an ACT, compassionate doctors decided to try the dried leaves of the Artemisia annua plant as a last resort. After only five days of the treatment, all 18 patients were fully recovered, including one child who had been in a coma. Blood tests revealed that absolutely no parasites remained in their blood.
That study was published in Phytomedicine, and the full study is available at this link on ScienceDirect.com. The title of the study is, “Artemisia annua dried leaf tablets treated malaria resistant to ACT and i.v. artesunate: Case reports.”
There’s even more scientific evidence to back this up. Natural News covered another story about sweet wormwood herb in 2017, entitled, “Chinese medicine herb discovered to prevent tuberculosis infections.” The story cites a study published in Nature Chemical Biology in 2011.
Here’s part of that story:
Chinese medicine herb discovered to prevent tuberculosis infections
A recent study reveals that artemisinin, a compound found in sweet wormwood, shows potential in tuberculosis treatment. This Chinese herbal medicine is previously known for its efficacy in treating malaria. Researchers at the Michigan State University have discovered that the compound prevents Mycobacterium tuberculosis, a tuberculosis-causing bacteria, from becoming dormant. Dormancy was associated with antibiotic resistance in patients.
Lead researcher Dr. Robert Abramovitch explains that dormant bacteria become highly tolerant to antibiotic therapy. Inhibiting dormancy makes the tuberculosis bacteria more susceptible to drug treatments and shortens treatment duration. To test this, researchers engineered a tuberculosis strain that glows bright green upon the onset of dormancy. A vast number of compounds were then assessed to see if they could prevent the bacteria from becoming dormant.
According to the researchers, Mycobacterium tuberculosis or Mtb requires oxygen to thrive. Artemisinin is shown to inhibit the molecule called heme found in the bacterium’s oxygen sensor, which in turn disrupts the Mtb from sensing its deteriorating oxygen levels. “When the Mtb is starved of oxygen, it goes into a dormant state, which protects it from the stress of low-oxygen environments. If Mtb can’t sense low oxygen, then it can’t become dormant and will die,” Dr. Abramovitch says. The researchers have also identified five other compounds that may potentially replicate a similar effect on the bacterium.
A 2011 study also supports artemisinin’s anti-tuberculosis potential. Researchers said using the compound as a conjugation factor induces a selective antagonistic effect against multi- and extensively drug-resistant strains of Mtb. The findings are published in the Journal of the American Chemical Society.
###
More published studies and papers discuss artemisinin as a complementary treatment against malaria or tuberculosis
The author of the paper mentioned above, Robert Abramovitch, is also a co-author of a 2016 paper, published in Nature Chemical Biology, which explores the ability of artemesinin to treat tuberculosis, a respiratory illness. This paper is entitled, “Inhibitors of Mycobacterium tuberculosis DosRST signaling and persistence.” It says: (bolding added)
The Mycobacterium tuberculosis (Mtb) DosRST two-component regulatory system promotes the survival of Mtb during non-replicating persistence (NRP)… The screen discovered novel inhibitors of the DosRST regulon, including three compounds that were subject to follow-up studies: artemisinin, HC102A and HC103A. Under hypoxia, all three compounds inhibit Mtb-persistence-associated physiological processes, including triacylglycerol synthesis, survival and antibiotic tolerance. Artemisinin functions by disabling the heme-based DosS and DosT sensor kinases by oxidizing ferrous heme and generating heme–artemisinin adducts.
In addition, the journal Nature Reviews Microbiology also discusses the use of artemisinin as a therapy against malaria. In this article by Richard. T. Eastman and David A. Fidock, it’s explained that artemisinin is now used across the world because malaria has become resistant to the prescription drugs chloroquine and sulfadoxine–pyrimethamine. From their summary:
Drug resistance, however, remains the biggest threat to current drug efficacy. The former mainstays of antimalarial chemotherapy, chloroquine and sulfadoxine–pyrimethamine, have been rendered ineffective for the treatment of Plasmodium falciparum malaria by the emergence and spread of drug-resistant parasites.
Almost all malaria-endemic regions have switched to artemisinin (ART)-based combination therapies (ACTs) for the first-line treatment of P. falciparum malaria.
The term “ACTs” means artemisinin-based combination therapies.
We caution that artemesinin is not proven to treat or cure coronavirus, but so far, nothing else is either
The upshot of all this is that artemisinin is a promising candidate that might one day be known as the “natural cure” for coronavirus. However, since nearly every government and science body in the world is run by Big Pharma and the vaccine industry, it’s almost certain that this herb will never be tested against coronavirus. The natural cures are, of course, systematically suppressed.
Fortunately, this herb is widely available right now, and it works with a very high margin of safety, efficacy and affordability. That’s precisely why the pharmaceutical industry doesn’t want you to know about it, of course: There’s not much money to be made in affordable natural cures.
Yet this is how we can best serve humanity: Find the natural cures that exist right now, test them and disseminate the information as widely as possible. But Big Tech is making sure that all voices that promote natural cures are censored, thereby protecting Big Pharma’s profit interests. The DOJ has even announced it’s going to conduct criminal investigations into “false cures” being promoted for the coronavirus, which of course means they will specifically target anyone selling herbs, colloidal silver, chlorine dioxide and so on.
It’s all a grand racket to keep the people isolated from real knowledge while protecting the profits of the corrupt pharmaceutical industry that already kills 200,000+ Americans a year. In fact, so far this year, Big Pharma has killed far more people than the coronavirus, at least for the moment.
While I can’t tell you what to do with your own personal health strategy, I encourage you to discuss artemisinin with your naturopathic physician to determine if it’s a good fit. Personally, I’m stocking up on this herb and will start taking a preventive dose immediately. Should I begin to show any symptoms of respiratory distress or fever, I’ll up my daily dose of this along with a wide assortment of other vitamins, herbs, minerals and superfoods that might also be effective.
Rest assured, the corrupt establishment will make sure that sweet wormwood never gets tested against the coronavirus. That’s how they can say, in perpetuity, there’s “no evidence” that it works. There’s no evidence because they refuse to test it, just like the CDC managed to claim coronavirus infections were “low” in America because they deliberately botched the testing kits.
It’s amazing what the corrupt establishment can achieve by avoiding testing the things they don’t want to test, isn’t it?
Tuesday, March 17, 2020 by: Mike Adams
Tags: artemisinin, coronavirus, Cures, goodhealth, goodmedicine, Herbs, infections, natural cures, natural medicine, Naturopathy, outbreak, pandemic, prevention, remedies, sweet wormwood
3,600
VIEWS
Image: If a natural cure for coronavirus is ever proven, this Chinese Medicine herb is likely to be the one (and no, we don’t sell it)
(Natural News) News is breaking all over the world that chloroquine, a prescription medication used to treat malaria, also appears to be effective against the coronavirus. According to local news KFOR.com, the Oklahoma Medical Research Foundation is advocating testing of the drug against COVID-19, the disease caused by the Wuhan coronavirus. From the KFOR.com website:
James explained that repurposing existing medications is often the fastest path to treating those infected by the virus in a novel way.
“That would be really exciting, because it’s a drug that already has FDA approval, and it is readily available,” she said. “If it works, it might treat COVID-19 almost instantly.”
Wider studies are now underway to confirm the results.
Chloroquine is best known as a malaria treatment, and it seems very likely to be helpful in preventing coronavirus infections. But what about natural molecules from herbs that might offer the same promise against both malaria and coronavirus?
Here’s a promising candidate herb that prevents malaria and tuberculosis
In the world of natural medicine, there are already powerful, well-known treatments against malaria that also happen to prevent tuberculosis, an aggressive infection of the respiratory tract. While nothing is yet proven to treat coronavirus, our review of herbal medicine studies and medicinal phytochemicals leads us to the conclusion that this Chinese Medicine herb may one day become known as the “natural cure” for coronavirus (although clinical trials are needed, obviously, to prove this).
The chemical is called artemesinin, and the herb is known as sweet wormwood. And no, we don’t sell it. This isn’t a commercial promotion, it’s an effort to help save millions of lives using medicine that’s available right now, all around the world.
Artemesinin is known for its ability to block the bacterial strain that causes tuberculosis, known as Mycobacterium tuberculosis. That doesn’t mean it prevents coronavirus, which is a viral infection, but it’s a strong candidate for a number of logical reasons.
According to research published in the journal Phytomedicine, artemisinin / sweet wormwood has a “100% cure rate” for treating drug-resistant malaria, at least in a small trial involving 18 patients (all of whom were cured). As Herbs.news writes in this important story:
A study led by Pamela Weathers, a professor of biology and biotechnology at the Worcester Polytechnic Institute (WPI), published in the journal Phytomedicine, describes how the Artemisia annua plant, commonly known as sweet wormwood or sweet annie, saved 18 patients with drug-resistant malaria from the brink of death.
The Congolese patients, who ranged in age from 14 months to 60 years, had all developed severe, untreatable malaria, with symptoms ranging from loss of consciousness, to trouble breathing and convulsions, among others. When they failed to respond to intravenous treatment with an ACT, compassionate doctors decided to try the dried leaves of the Artemisia annua plant as a last resort. After only five days of the treatment, all 18 patients were fully recovered, including one child who had been in a coma. Blood tests revealed that absolutely no parasites remained in their blood.
That study was published in Phytomedicine, and the full study is available at this link on ScienceDirect.com. The title of the study is, “Artemisia annua dried leaf tablets treated malaria resistant to ACT and i.v. artesunate: Case reports.”
There’s even more scientific evidence to back this up. Natural News covered another story about sweet wormwood herb in 2017, entitled, “Chinese medicine herb discovered to prevent tuberculosis infections.” The story cites a study published in Nature Chemical Biology in 2011.
Here’s part of that story:
Chinese medicine herb discovered to prevent tuberculosis infections
A recent study reveals that artemisinin, a compound found in sweet wormwood, shows potential in tuberculosis treatment. This Chinese herbal medicine is previously known for its efficacy in treating malaria. Researchers at the Michigan State University have discovered that the compound prevents Mycobacterium tuberculosis, a tuberculosis-causing bacteria, from becoming dormant. Dormancy was associated with antibiotic resistance in patients.
Lead researcher Dr. Robert Abramovitch explains that dormant bacteria become highly tolerant to antibiotic therapy. Inhibiting dormancy makes the tuberculosis bacteria more susceptible to drug treatments and shortens treatment duration. To test this, researchers engineered a tuberculosis strain that glows bright green upon the onset of dormancy. A vast number of compounds were then assessed to see if they could prevent the bacteria from becoming dormant.
According to the researchers, Mycobacterium tuberculosis or Mtb requires oxygen to thrive. Artemisinin is shown to inhibit the molecule called heme found in the bacterium’s oxygen sensor, which in turn disrupts the Mtb from sensing its deteriorating oxygen levels. “When the Mtb is starved of oxygen, it goes into a dormant state, which protects it from the stress of low-oxygen environments. If Mtb can’t sense low oxygen, then it can’t become dormant and will die,” Dr. Abramovitch says. The researchers have also identified five other compounds that may potentially replicate a similar effect on the bacterium.
A 2011 study also supports artemisinin’s anti-tuberculosis potential. Researchers said using the compound as a conjugation factor induces a selective antagonistic effect against multi- and extensively drug-resistant strains of Mtb. The findings are published in the Journal of the American Chemical Society.
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More published studies and papers discuss artemisinin as a complementary treatment against malaria or tuberculosis
The author of the paper mentioned above, Robert Abramovitch, is also a co-author of a 2016 paper, published in Nature Chemical Biology, which explores the ability of artemesinin to treat tuberculosis, a respiratory illness. This paper is entitled, “Inhibitors of Mycobacterium tuberculosis DosRST signaling and persistence.” It says: (bolding added)
The Mycobacterium tuberculosis (Mtb) DosRST two-component regulatory system promotes the survival of Mtb during non-replicating persistence (NRP)… The screen discovered novel inhibitors of the DosRST regulon, including three compounds that were subject to follow-up studies: artemisinin, HC102A and HC103A. Under hypoxia, all three compounds inhibit Mtb-persistence-associated physiological processes, including triacylglycerol synthesis, survival and antibiotic tolerance. Artemisinin functions by disabling the heme-based DosS and DosT sensor kinases by oxidizing ferrous heme and generating heme–artemisinin adducts.
In addition, the journal Nature Reviews Microbiology also discusses the use of artemisinin as a therapy against malaria. In this article by Richard. T. Eastman and David A. Fidock, it’s explained that artemisinin is now used across the world because malaria has become resistant to the prescription drugs chloroquine and sulfadoxine–pyrimethamine. From their summary:
Drug resistance, however, remains the biggest threat to current drug efficacy. The former mainstays of antimalarial chemotherapy, chloroquine and sulfadoxine–pyrimethamine, have been rendered ineffective for the treatment of Plasmodium falciparum malaria by the emergence and spread of drug-resistant parasites.
Almost all malaria-endemic regions have switched to artemisinin (ART)-based combination therapies (ACTs) for the first-line treatment of P. falciparum malaria.
The term “ACTs” means artemisinin-based combination therapies.
We caution that artemesinin is not proven to treat or cure coronavirus, but so far, nothing else is either
The upshot of all this is that artemisinin is a promising candidate that might one day be known as the “natural cure” for coronavirus. However, since nearly every government and science body in the world is run by Big Pharma and the vaccine industry, it’s almost certain that this herb will never be tested against coronavirus. The natural cures are, of course, systematically suppressed.
Fortunately, this herb is widely available right now, and it works with a very high margin of safety, efficacy and affordability. That’s precisely why the pharmaceutical industry doesn’t want you to know about it, of course: There’s not much money to be made in affordable natural cures.
Yet this is how we can best serve humanity: Find the natural cures that exist right now, test them and disseminate the information as widely as possible. But Big Tech is making sure that all voices that promote natural cures are censored, thereby protecting Big Pharma’s profit interests. The DOJ has even announced it’s going to conduct criminal investigations into “false cures” being promoted for the coronavirus, which of course means they will specifically target anyone selling herbs, colloidal silver, chlorine dioxide and so on.
It’s all a grand racket to keep the people isolated from real knowledge while protecting the profits of the corrupt pharmaceutical industry that already kills 200,000+ Americans a year. In fact, so far this year, Big Pharma has killed far more people than the coronavirus, at least for the moment.
While I can’t tell you what to do with your own personal health strategy, I encourage you to discuss artemisinin with your naturopathic physician to determine if it’s a good fit. Personally, I’m stocking up on this herb and will start taking a preventive dose immediately. Should I begin to show any symptoms of respiratory distress or fever, I’ll up my daily dose of this along with a wide assortment of other vitamins, herbs, minerals and superfoods that might also be effective.
Rest assured, the corrupt establishment will make sure that sweet wormwood never gets tested against the coronavirus. That’s how they can say, in perpetuity, there’s “no evidence” that it works. There’s no evidence because they refuse to test it, just like the CDC managed to claim coronavirus infections were “low” in America because they deliberately botched the testing kits.
It’s amazing what the corrupt establishment can achieve by avoiding testing the things they don’t want to test, isn’t it?
Thanks for this info. This was an interesting read. I was wondering if the idea that Blacks may be resistant to this is because we're more resistant to malaria but even some needed the artemisinin to get over the hump.
I remember (reluctantly) having to take Anti-Malaria pills while in Afghanistan but I don't remember what they were now.
With all of the shit that I've been inoculated against over the years, hopefully I have SOME type of antibodies built in to challenge a potential infection.
I noticed that in my area too. Most of the popular mixes were sold out unless you wanted certain blends, like Cajun cornbread or something.
There was little to no fresh chicken, no ground beef, no eggs, yellow rice, or many of the things that I usually shop for.
There were no paper products and I barely found any cleansers with bleach except for the shower. I was surprised that there was still water left.
Dr Berg suggested Vitamin D3. I already had that. I had to pick up the omega 3 and ordered when amazon had BOGO last week.
Was extended 60 or 90 days. I forgot which one exactly.
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Textbooks | Publications | Cambridge Core
Cambridge University Press publishes research monographs, academic reference, textbooks, books for professionals, and books for graduate students.www.cambridge.org
Cambridge University Press is making higher education textbooks in HTML format free to access online during the coronavirus outbreak.
Over 700 textbooks, published and currently available, on Cambridge Core are available regardless of whether textbooks were previously purchased.
Free access is available until the end of May 2020.
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Ohh come on.. Stop it 
