Wednesday Jun 23, 2021
The Gary Null Show - 06.23.21
Propolis for Upper Respiratory Tract Infections
Could bees provide a solution to a prevalent and costly problem?
University of Naples (Italy), June 2, 2021
Study Objective
To evaluate the effects of a standardized oral spray of poplar-type propolis extract (M.E.D. Propolis) on the symptoms of mild upper respiratory tract infections (URTIs)
Design
A monocentric, placebo-controlled, double-blind clinical trial performed in an outpatient setting
Participants
This study involved 122 subjects (58 in the propolis group and 64 in the placebo group). The age range was from 18 to 77 years; 54 subjects were male, and 68 were female. All subjects had signs and/or symptoms of a URTI. Subjects were examined by a physician and were eligible for inclusion in the study if they suffered from 1 or more of the following common URTI symptoms: sore throat, muffled dysphonia, and swelling and redness of the throat that began on the same day as the baseline visit (t=0).
Intervention
The subjects were randomly assigned to receive either a propolis oral spray or a placebo spray from t1 to t3 (5 days). Dose was 2 to 4 sprays 3 times daily. Researchers evaluated each participant at 4 time points: baseline=t0, after 3 days=t1, after 5 days=t2, and at 15 days=t3.
The propolis spray was standardized to contain 15 mg/mL of polyphenols. The spray had a reproducible composition of the 6 major flavonoids found in this type of propolis (ie, galangin, chrysin, pinocembrin, apigenin, pinobanksin, quercetin). Each participant used 2 to 4 sprays 3 times daily for 5 days. The placebo spray had an identical appearance and flavor to the propolis spray.
Study Parameters Assessed
Apart from the primary outcome measure, the researchers evaluated the persistence of positive bacterial throat cultures at t3. They performed throat swabs on all subjects at t0 and then again at t2 and t3 on those subjects who had an initially positive throat culture. At t0, 8 people in the treatment group and 7 people in the placebo group were positive for a bacterial URTI. At t3, none of the subjects in either the treatment or placebo group were found to have a positive bacterial throat culture.
Primary Outcome Measures
The primary outcome measure was the resolution of URTI symptoms. Researchers assessed these symptoms at baseline (t0), 3 days (t1), after 5 days (t2), and at the final timepoint (t3) of the study, 15 days.
At t1, 17% of the participants in the treatment group still had 1 symptom of an URTI. In contrast, about 72% of people in the placebo group still displayed 1 symptom (RR: 2.93, CI: 1.95–4.42).
The results of a univariate analysis showed that only treatment with oral propolis spray was related to the disappearance of symptoms (resolution of all symptoms in the treatment group vs the placebo group: X2=35.57, df=1, P<0.001; resolution from sore throat in the propolis vs placebo group: X2=28.38, df=1, P<0.001; resolution of muffled dysphonia in the propolis vs placebo group: X2=4.38, df=1, P=0.036; and resolution of swelling and redness of the throat in the propolis vs placebo group: X2=16.85, df=1, P<0.001).
There was no relationship noted between the resolution of symptoms after 3 days and the type of infection (bacterial or viral) or the age or gender of the subjects.
Key Findings
The disappearance of all URTI symptoms occurred 2 days earlier in the propolis group vs the placebo group. Symptoms were gone within 5 days in the placebo group and within 3 days for the treatment group. This finding held true for both viral and bacterial URTIs. Since there were so few bacterial URTIs noted in this study, the authors were not able to make any conclusions related to the effects of propolis on antibiotic-resistant bacteria.
Yoga And Meditation Could Potentially Reverse The Genetic Effects Of Stress
Coventry University (UK), Antwerp University (Belgium), Radboud University (Netherlands), June 21, 2021
Mind-body interventions (MBIs) such as meditation, yoga and Tai Chi don't simply relax us; they can 'reverse' the molecular reactions in our DNA which cause ill-health and depression, according to a study by the universities of Coventry and Radboud.
The research, published in the journal Frontiers in Immunology, reviews over a decade of studies analysing how the behaviour of our genes is affected by different MBIs including mindfulness and yoga.
Experts from the universities conclude that, when examined together, the 18 studies -- featuring 846 participants over 11 years -- reveal a pattern in the molecular changes which happen to the body as a result of MBIs, and how those changes benefit our mental and physical health.
The researchers focus on how gene expression is affected; in other words the way that genes activate to produce proteins which influence the biological make-up of the body, the brain and the immune system.
When a person is exposed to a stressful event, their sympathetic nervous system (SNS) -- the system responsible for the 'fight-or-flight' response -- is triggered, in turn increasing production of a molecule called nuclear factor kappa B (NF-kB) which regulates how our genes are expressed.
NF-kB translates stress by activating genes to produce proteins called cytokines that cause inflammation at cellular level -- a reaction that is useful as a short-lived fight-or-flight reaction, but if persistent leads to a higher risk of cancer, accelerated aging and psychiatric disorders like depression.
According to the study, however, people who practise MBIs exhibit the opposite effect -- namely a decrease in production of NF-kB and cytokines, leading to a reversal of the pro-inflammatory gene expression pattern and a reduction in the risk of inflammation-related diseases and conditions.
The study's authors say the inflammatory effect of the fight-or-flight response -- which also serves to temporarily bolster the immune system -- would have played an important role in humankind's hunter-gatherer prehistory, when there was a higher risk of infection from wounds.
In today's society, however, where stress is increasingly psychological and often longer-term, pro-inflammatory gene expression can be persistent and therefore more likely to cause psychiatric and medical problems.
Lead investigator Ivana Buric from the Brain, Belief and Behaviour Lab in Coventry University's Centre for Psychology, Behaviour and Achievement said:
"Millions of people around the world already enjoy the health benefits of mind-body interventions like yoga or meditation, but what they perhaps don't realise is that these benefits begin at a molecular level and can change the way our genetic code goes about its business.
"These activities are leaving what we call a molecular signature in our cells, which reverses the effect that stress or anxiety would have on the body by changing how our genes are expressed. Put simply, MBIs cause the brain to steer our DNA processes along a path which improves our wellbeing.
"More needs to be done to understand these effects in greater depth, for example how they compare with other healthy interventions like exercise or nutrition. But this is an important foundation to build on to help future researchers explore the benefits of increasingly popular mind-body activities."
The Role of Plant-Based Protein Functional Food in Preventing Acute Respiratory Disease: A Case Study
Abstract
Exposure to pollutants, increased free-radical damage speeds up aging
West Virginia University, June 22, 2021
Every day, our bodies face a bombardment of UV rays, ozone, cigarette smoke, industrial chemicals and other hazards.
This exposure can lead to free-radical production in our bodies, which damages our DNA and tissues. A new study from West Virginia University researcher Eric E. Kelley--in collaboration with the University of Minnesota--suggests that unrepaired DNA damage can increase the speed of aging.
The study appears in the journal Nature.
Kelley and his team created genetically-modified mice with a crucial DNA-repair protein missing from their hematopoietic stem cells, immature immune cells that develop into white blood cells. Without this repair protein, the mice were unable to fix damaged DNA accrued in their immune cells.
"By the time the genetically-modified mouse is 5 months old, it's like a 2-year-old mouse," said Kelley, associate professor and associate chair of research in the School of Medicine's Department of Physiology and Pharmacology. "It has all the symptoms and physical characteristics. It has hearing loss, osteoporosis, renal dysfunction, visual impairment, hypertension, as well as other age-related issues. It's prematurely aged just because it has lost its ability to repair its DNA."
According to Kelley, a normal 2-year-old mouse is about equivalent in age to a human in their late 70s to early 80s.
Kelley and his colleagues found that markers for cell aging, or senescence, as well as for cell damage and oxidation were significantly greater in the immune cells of genetically-modified mice compared to normal, wild-type mice. But the damage was not limited to the immune system; the modified mice also demonstrated aged, damaged cells in organs such as the liver and kidney.
These results suggest that unrepaired DNA damage may cause the entire body to age prematurely.
When we are exposed to a pollutant, such as radiation for cancer treatment, energy is transferred to the water in our body, breaking the water apart. This creates highly reactive molecules--free radicals--that will quickly interact with another molecule in order to gain electrons. When these free radicals interact with important biomolecules, such as a protein or DNA, it causes damage that can keep that biomolecule from working properly.
Some exposure to pollutants is unavoidable, but there are several lifestyle choices that increase exposure to pollution and thus increase free radicals in the body. Smoking, drinking and exposure to pesticides and other chemicals through occupational hazards all significantly increase free radicals.
"A cigarette has over 10 to the 16th free radicals per puff, just from combusted carbon materials," Kelley said.
In addition to free radicals produced by pollutant exposure, the human body is constantly producing free radicals during a process used to turn food into energy, called oxidative phosphorylation.
"We have mechanisms in the mitochondria that mop free radicals up for us, but if they become overwhelmed--if we have over-nutrition, if we eat too much junk, if we smoke--the defense mechanism absolutely cannot keep up," Kelley said.
As bodies age, the amount of damage caused by free-radical formation becomes greater than the antioxidant defenses. Eventually, the balance between the two tips over to the oxidant side, and damage starts to win out over repair. If we are exposed to a greater amount of pollutants and accumulate more free radicals, this balance will be disrupted even sooner, causing premature aging.
The issue of premature aging due to free-radical damage is especially important in West Virginia. The state has the greatest percentage of obese citizens in the nation and a high rate of smokers and workers in high-pollution-exposure occupations.
"I come from an Appalachian background," Kelley said. "And, you know, I'd go to funerals that were in some old house--an in-the-living-room-with-a-casket kind of deal--and I'd look at people in there, and they'd be 39 or 42 and look like they were 80 because of their occupation and their nutrition."
Many West Virginians also have comorbidities, such as diabetes, enhanced cardiovascular disease, stroke and renal issues, that complicate the situation further.
Although there are drugs, called senolytics, that help to slow the aging process, Kelley believes it is best to prevent premature aging through lifestyle change. He says that focusing on slowing the aging process through preventive measures can improve the outcome for each comorbidity and add more healthy years to people's lives.
"The impact is less on lifespan and more on healthspan," he said. "If you could get people better access to healthcare, better education, easier ways for them to participate in healthier eating and a healthier lifestyle, then you could improve the overall economic burden on the population of West Virginia and have a much better outcome all the way around."
Vitamin B6 status among vegetarians: findings from a population-based survey
University of Heidelberg (Germany), June 21, 2021
According to news reporting out of Heidelberg, Germany, by NewsRx editors, research stated, “Vitamin B6 from plant foods may have lower bioavailability than vitamin B6 from animal foods, but studies on objectively measured vitamin B6 status among vegetarians compared to non-vegetarians are lacking.”
The news reporters obtained a quote from the research from University of Heidelberg: “Thus, the vitamin B6 status among vegetarians, but also pescatarians, and flexitarians, compared to meat-eaters was assessed in the population-based NHANES study (cycles 2007-2008 and 2009-2010). Data on serum pyridoxal-5’-phosphate (PLP) and 4-pyridoxic acid (4-PA) measured by high-performance liquid chromatography (HPLC) as well as dietary intakes from 24-h recalls were available for 8968 adults aged 20-80 years. Geometric mean (±standard error) PLP concentrations were 58.2 ± 6.0, 52.1 ± 3.7, 49.2 ± 4.6 and 51.0 ± 1.1 nmol/L among vegetarians, pescatarians, flexitarians, and meat-eaters. The 4-PA concentrations were 32.7 ± 4.0, 29.0 ± 2.5, 34.8 ± 5.6 and 33.0 ± 0.7, respectively. There were no statistically significant differences in PLP, 4-PA, and their ratio across the groups in multivariable linear regression models. Overall, the use of vitamin B6 supplements was the strongest predictor of the vitamin B6 status, followed by the dietary vitamin B6 intake.”
According to the news editors, the research concluded: “Interestingly, several other covariates were significantly associated with vitamin B6 biomarker levels, particularly serum albumin, creatinine and alkaline phosphatase, and should be considered when assessing the vitamin B6 status. In summary, our findings suggest that a vegetarian diet does not pose a risk for vitamin B6 deficiency.”
Compound made inside human body stops viruses from replicating
Penn State University & Albert Einstein College of Medicine, June 20, 2021The newest antiviral drugs could take advantage of a compound made not by humans, but inside them. A team of researchers has identified the mode of action of viperin, a naturally occurring enzyme in humans and other mammals that is known to have antiviral effects on a wide variety of viruses, including West Nile, hepatitis C, rabies, and HIV.
The enzyme facilitates a reaction that produces the molecule ddhCTP, which prevents viruses from copying their genetic material and thus from multiplying. This discovery could allow researchers to develop a drug that induces the human body to produce this molecule and could act as a broad-spectrum therapy for a range of viruses. A paper describing the study appears online in the journal Nature.
"We knew viperin had broad antiviral effects through some sort of enzymatic activity, but other antivirals use a different method to stop viruses," said Craig Cameron, professor and holder of the Eberly Chair in Biochemistry and Molecular Biology at Penn State and an author of the study. "Our collaborators at the Albert Einstein College of Medicine, led by senior authors Tyler Grove and Steven Almo, revealed that viperin catalyzes an important reaction that results in the creation of a molecule called ddhCTP. Our team at Penn State then showed the effects of ddhCTP on a virus's ability to replicate its genetic material. Surprisingly, the molecule acts in a similar manner to drugs that were developed to treat viruses like HIV and hepatitis C. With a better understanding of how viperin prevents viruses from replicating, we hope to be able to design better antivirals."
A virus typically co-opts the host's genetic building blocks to copy its own genetic material, incorporating molecules called nucleotides into new strands of RNA. The molecule ddhCTP mimics these nucleotide building blocks and becomes incorporated into the virus's genome. Once incorporated into a new strand of the virus's RNA, these "nucleotide analogs" prevent an enzyme called RNA polymerase from adding more nucleotides to the strand, thus preventing the virus from making new copies of its genetic material.
"Long ago, the paradigm was that in order to kill a virus, you had to kill the infected cell," said Cameron. "Such a paradigm is of no use when the virus infects an essential cell type with limited capacity for replenishment. The development of nucleotide analogs that function without actually killing the infected cell changed everything."
Most nucleotide analogs on the market are manmade, but there are often complications with using these synthetic drugs. Because nucleotides are used by many proteins and enzymes of the cell, numerous opportunities exist for analogs to interfere with normal cellular function.
"The major obstacle to developing therapeutically useful antiviral nucleotides is unintended targets," said Jamie Arnold, associate research professor of biochemistry and molecular biology at Penn State and an author of the paper. "For example, a few years ago we discovered that a nucleotide analog under development for treatment of hepatitis C could interfere with the production of RNA in mitochondria, subcellular organelles important for energy production in the patient's own cells. That meant people with mitochondrial dysfunction are predisposed to any negative effects of this unintended interference."
The molecule ddhCTP, however, does not appear to have any unintended targets. The research team suspects that the natural origin of the compound within the human body necessitates that it be nontoxic.
"Unlike many of our current drugs, ddhCTP is encoded by the cells of humans and other mammals," said Cameron. "We have been synthesizing nucleotide analogs for years, but here we see that nature beat us to the punch and created a nucleotide analog that can deal with a virus in living cells and does not exhibit any toxicity to date. If there's something out there that's going to work, nature has probably thought of it first. We just have to find it."
To verify the effectiveness of ddhCTP, the research team showed that the molecule inhibited the RNA polymerases of dengue virus, West Nile virus and Zika virus, which are all in a group of viruses called flaviviruses. Then they investigated whether the molecule halted replication of Zika virus in living cells.
"The molecule directly inhibited replication of three different strains of Zika virus," said Joyce Jose, assistant professor of biochemistry and molecular biology at Penn State and an author of the paper. "It was equally effective against the original strain from 1947 as it was against two strains from the recent 2016 outbreak. This is particularly exciting because there are no known treatments for Zika. This study highlights a new avenue of research into natural compounds like ddhCTP that could be used in future treatments."
Together, these results demonstrate promising antiviral effects of ddhCTP on a variety of flaviviruses. However, the RNA polymerases of human rhinovirus and poliovirus, which are in a group called picornaviruses, were not sensitive to the molecule. The researchers plan to investigate the polymerase structures of these viruses to better understand why flaviviruses are sensitive to ddhCTP while the picornaviruses tested in this study are not. This investigation may also offer insights into how flaviviruses might develop resistance to the molecule.
"Development of resistance to an antiviral agent is always an issue," said Cameron, "Having some idea of how resistance happens, or being able to prevent it from happening, will be critical if this is to be used as a broad-spectrum therapy."