The Gary Null Show

The Gary Null Show - 10.08.21

October 8, 2021

Raspberries, ellagic acid reveal benefits in two studies

Oregon State University, October 1, 2021. 


Articles that appeared recently in the Journal of Berry Research report that raspberries and compounds present in the fruit could help support healthy body mass and motor function, including balance, coordination and strength.


In one study, Neil Shay and colleagues at Oregon State University fed mice a high fat, high sugar diet plus one of the following: raspberry juice concentrate, raspberry puree concentrate, raspberry fruit powder, raspberry seed extract, ellagic acid (a polyphenol that occurs in a relatively high amount in raspberries), raspberry ketone, or a combination of raspberry ketone and ellagic acid. Additional groups of animals received a high fat, high sugar diet alone or a low fat diet.


While mice that received the high fat and sugar diet alone experienced a significant increase in body mass, the addition of raspberry juice concentrate, raspberry puree concentrate or ellagic acid plus raspberry ketone helped prevent this effect. Of note, mice that received raspberry juice concentrate experienced gains similar to those of animals given a low fat diet. "We hope that the findings from this study can help guide the design of future clinical trials," Dr Shay stated.


In another study, Barbara Shukitt-Hale, PhD, and her associates at Tufts University's Human Nutrition Research Center on Aging gave 19 month old rats a control diet or a diet enhanced with raspberry extract for 11 weeks. Psychomotor behavior was assessed during week 7 and cognitive testing was conducted during weeks 9-10.


Animals that received raspberry performed better on psychomotor coordination and balance, and had better muscle tone, strength and stamina than those that received a control diet. "These results may have important implications for healthy aging," stated Dr Shukitt-Hale. "While further research in humans is necessary, animal model studies are helpful in identifying deficits associated with normal aging."




Massage doesn't just make muscles feel better, it makes them heal faster and stronger

Harvard University, October 6, 2021

Massage has been used to treat sore, injured muscles for more than 3,000 years, and today many athletes swear by massage guns to rehabilitate their bodies. But other than making people feel good, do these "mechanotherapies" actually improve healing after severe injury? According to a new study from researchers at Harvard's Wyss Institute for Biologically Inspired Engineering and John A. Paulson School of Engineering and Applied Sciences (SEAS), the answer is "yes."

Using a custom-designed robotic system to deliver consistent and tunable compressive forces to mice's leg muscles, the team found that this mechanical loading (ML) rapidly clears immune cells called neutrophils out of severely injured muscle tissue. This process also removed inflammatory cytokinesreleased by neutrophils from the muscles, enhancing the process of muscle fiber regeneration. The research is published in Science Translational Medicine.

"Lots of people have been trying to study the beneficial effects of massage and other mechanotherapies on the body, but up to this point it hadn't been done in a systematic, reproducible way. Our work shows a very clear connection between mechanical stimulation and immune function. This has promise for regenerating a wide variety of tissues including bone, tendon, hair, and skin, and can also be used in patients with diseases that prevent the use of drug-based interventions," said first author Bo Ri Seo, Ph.D., who is a Postdoctoral Fellow in the lab of Core Faculty member Dave Mooney, Ph.D. at the Wyss Institute and SEAS.

Seo and her coauthors started exploring the effects of mechanotherapy on injured tissues in mice several years ago, and found that it doubled the rate of muscle regeneration and reduced tissue scarring over the course of two weeks. Excited by the idea that mechanical stimulation alone can foster regeneration and enhance muscle function, the team decided to probe more deeply into exactly how that process worked in the body, and to figure out what parameters would maximize healing.

They teamed up with soft robotics experts in the Harvard Biodesign Lab, led by Wyss Associate Faculty member Conor Walsh, Ph.D., to create a small device that used sensors and actuators to monitor and control the force applied to the limb of a mouse. " The device we created allows us to precisely control parameters like the amount and frequency of force applied, enabling a much more systematic approach to understanding tissue healing than would be possible with a manual approach," said co-second author Christopher Payne, Ph.D., a former Postdoctoral Fellow at the Wyss Institute and the Harvard Biodesign Lab who is now a Robotics Engineer at Viam, Inc. 

Once the device was ready, the team experimented with applying force to mice's leg muscles via a soft silicone tip and used ultrasound to get a look at what happened to the tissue in response. They observed that the muscles experienced a strain of between 10-40%, confirming that the tissues were experiencing mechanical force. They also used those ultrasound imaging data to develop and validate a computational model that could predict the amount of tissue strain under different loading forces.

They then applied consistent, repeated force to injured muscles for 14 days. While both treated and untreated muscles displayed a reduction in the amount of damaged muscle fibers, the reduction was more pronounced and the cross-sectional area of the fibers was larger in the treated muscle, indicating that treatment had led to greater repair and strength recovery. The greater the force applied during treatment, the stronger the injured muscles became, confirming that mechanotherapy improves muscle recovery after injury. But how?

Evicting neutrophils to enhance regeneration

To answer that question, the scientists performed a detailed biological assessment, analyzing a wide range of inflammation-related factors called cytokines and chemokines in untreated vs. treated muscles. A subset of cytokines was dramatically lower in treated muscles after three days of mechanotherapy, and these cytokines are associated with the movement of immune cells called neutrophils, which play many roles in the inflammation process. Treated muscles also had fewer neutrophils in their tissue than untreated muscles, suggesting that the reduction in cytokines that attract them had caused the decrease in neutrophil infiltration.

The team had a hunch that the force applied to the muscle by the mechanotherapy effectively squeezed the neutrophils and cytokines out of the injured tissue. They confirmed this theory by injecting fluorescent molecules into the muscles and observing that the movement of the molecules was more significant with force application, supporting the idea that it helped to flush out the muscle tissue.

To pick apart what effect the neutrophils and their associated cytokines have on regenerating muscle fibers, the scientists performed in vitro studies in which they grew muscle progenitor cells (MPCs) in a medium in which neutrophils had previously been grown. They found that the number of MPCs increased, but the rate at which they differentiated (developed into other cell types) decreased, suggesting that neutrophil-secreted factors stimulate the growth of muscle cells, but the prolonged presence of those factors impairs the production of new muscle fibers.

"Neutrophils are known to kill and clear out pathogens and damaged tissue, but in this study we identified their direct impacts on muscle progenitor cell behaviors," said co-second author Stephanie McNamara, a former Post-Graduate Fellow at the Wyss Institute who is now an M.D.-Ph.D. student at Harvard Medical School (HMS). "While the inflammatory response is important for regeneration in the initial stages of healing, it is equally important that inflammation is quickly resolved to enable the regenerative processes to run its full course."

Seo and her colleagues then turned back to their in vivo model and analyzed the types of muscle fibers in the treated vs. untreated mice 14 days after injury. They found that type IIX fibers were prevalent in healthy muscle and treated muscle, but untreated injured muscle contained smaller numbers of type IIX fibers and increased numbers of type IIA fibers. This difference explained the enlarged fiber size and greater force production of treated muscles, as IIX fibers produce more force than IIA fibers.

Finally, the team homed in on the optimal amount of time for neutrophil presence in injured muscle by depleting neutrophils in the mice on the third day after injury. The treated mice's muscles showed larger fiber size and greater strength recovery than those in untreated mice, confirming that while neutrophils are necessary in the earliest stages of injury recovery, getting them out of the injury site early leads to improved muscle regeneration.

"These findings are remarkable because they indicate that we can influence the function of the body's immune system in a drug-free, non-invasive way," said Walsh, who is also the Paul A. Maeder Professor of Engineering and Applied Science at SEAS and whose group is experienced in developing wearable technology for diagnosing and treating disease. "This provides great motivation for the development of external, mechanical interventions to help accelerate and improve muscle and tissue healing that have the potential to be rapidly translated to the clinic."

The team is continuing to investigate this line of research with multiple projects in the lab. They plan to validate this mechanotherpeutic approach in larger animals, with the goal of being able to test its efficacy on humans. They also hope to test it on different types of injuries, age-related muscle loss, and muscle performance enhancement.

"The fields of mechanotherapy and immunotherapy rarely interact with each other, but this work is a testament to how crucial it is to consider both physical and biological elements when studying and working to improve human health," said Mooney, who is the corresponding author of the paper and the Robert P. Pinkas Family Professor of Bioengineering at SEAS.

"The idea that mechanics influence cell and tissue function was ridiculed until the last few decades, and while scientists have made great strides in establishing acceptance of this fact, we still know very little about how that process actually works at the organ level. This research has revealed a previously unknown type of interplay between mechanobiology and immunology that is critical for muscle tissue healing, in addition to describing a new form of mechanotherapy that potentially could be as potent as chemical or gene therapies, but much simpler and less invasive," said Wyss Founding Director Don Ingber, M.D., Ph.D., who is also the Judah Folkman Professor of Vascular Biology at (HMS) and the Vascular Biology Program at Boston Children's Hospital, as well as Professor of Bioengineering at SEAS.


Vitamin E could help protect older men from pneumonia

University of Helsinki (Finland), October 7 2021. 


An article that appeared in Clinical Interventions in Aging reported a protective role for vitamin E against pneumonia in older men.


For the current investigation, Dr Harri Hemilä of the University of Helsinki, Finland analyzed data from the Alpha-Tocopherol Beta-Carotene (ATBC) Cancer Prevention Study conducted in Finland. The trial included 29,133 men between the ages of 50 to 69 years who smoked at least five cigarettes daily upon enrollment. Participants received alpha tocopherol (vitamin E), beta carotene, both supplements, or a placebo for five to eight years.


The current study was limited to 7,469 ATBC participants who started smoking at age 21 or older. Among this group, supplementation with vitamin E was associated with a 35% lower risk of developing pneumonia in comparison with those who did not receive the vitamin.  Light smokers who engaged in leisure time exercise had a 69% lower risk compared with unsupplemented members of this subgroup. The risk in this subgroup of developing pneumonia by age 74 was 12.9%.


Among the one-third of the current study's population who quit smoking for a median period of two years, there was a 72% lower risk of pneumonia in association with vitamin E supplementation. In this group, exercisers who received vitamin E experienced an 81% lower pneumonia risk.


Dr Hemilä observed that the benefit for vitamin E in this study was strongest for older subjects—a group at higher risk of pneumonia.


"The current analysis of individual-level data suggests that trials on vitamin E and pneumonia on nonsmoking elderly males are warranted," he concluded.




Toxic fatty acids to blame for brain cell death after injury

New York University, October 7, 2021

Cells that normally nourish healthy brain cells called neurons release toxic fatty acids after neurons are damaged, a new study in rodents shows. This phenomenon is likely the driving factor behind most, if not all, diseases that affect brain function, as well as the natural breakdown of brain cells seen in aging, researchers say.

Previous research has pointed to astrocytes—a star-shaped glial cell of the central nervous system—as the culprits behind cell death seen in Parkinson's disease and dementia, among other neurodegenerative diseases. While many experts believed that these cells released a neuron-killing molecule to "clear away" damaged brain cells, the identity of this toxin has until now remained a mystery.

Led by researchers at NYU Grossman School of Medicine, the new investigation provides what they say is the first evidence that tissue damage prompts astrocytes to produce two kinds of fats, long-chain saturated free fatty acids and phosphatidylcholines. These fats then trigger cell death in damaged neurons, the electrically active cells that send messages throughout nerve tissue.

Publishing Oct. 6 in the journal Nature, the study also showed that when researchers blocked fatty acid formation in mice, 75 percent of neurons survived compared with 10 percent when the fatty acids were allowed to form. The researchers' earlier work showed that brain cells continued to function when shielded from astrocyte attacks. 

"Our findings show that the toxic fatty acids produced by astrocytes play a critical role in brain cell death and provide a promising new target for treating, and perhaps even preventing, many neurodegenerative diseases," says study co-senior author Shane Liddelow, Ph.D.

Liddelow, an assistant professor in the Department of Neuroscience and Physiology at NYU Langone Health, adds that targeting these fats instead of the cells that produce them may be a safer approach to treating neurodegenerative diseasesbecause astrocytes feed nerve cells and clear away their waste. Stopping them from working altogether could interfere with healthy brain function.

Although it remains unclear why astrocytes produce these toxins, it is possible they evolved to destroy damaged cells before they can harm their neighbors, says Liddelow. He notes that while healthy cells are not harmed by the toxins, neurons become susceptible to the damaging effects when they are injured, mutated, or infected by prions, the contagious, misfolded proteins that play a major role in mad cow disease and similar illnesses. Perhaps in chronic diseases like dementia, this otherwise helpful process goes off track and becomes a problem, the study authors say.

For the investigation, researchers analyzed the molecules released by astrocytes collected from rodents. They also genetically engineered some groups of mice to prevent the normal production of the toxic fats and looked to see whether neuron death occurred after an acute injury.

"Our results provide what is likely the most detailed molecular map to date of how tissue damage leads to brain cell death, enabling researchers to better understand why neurons die in all kinds of diseases," says Liddelow, also an assistant professor in the Department of Ophthalmology at NYU Langone.

Liddelow cautions that while the findings are promising, the genetic techniques used to block the enzyme that produces toxic fatty acids in mice are not ready for use in humans. As a result, the researchers next plan is to explore safe and effective ways to interfere with the release of the toxins in human patients. Liddelow and his colleagues had previously shown these neurotoxic astrocytes in the brains of patients with Parkinson's, Huntington's disease, and multiple sclerosis, among other diseases.


Clinical trial for nicotinamide riboside: Vitamin safely boosts levels of important cell metabolite linked to multiple health benefits

University of Iowa Health Care, October 3, 2021


In the first controlled clinical trial of nicotinamide riboside (NR), a newly discovered form of Vitamin B3, researchers have shown that the compound is safe for humans and increases levels of a cell metabolite that is critical for cellular energy production and protection against stress and DNA damage.


Studies in mice have shown that boosting the levels of this cell metabolite -- known as NAD+ -- can produce multiple health benefits, including resistance to weight gain, improved control of blood sugar and cholesterol, reduced nerve damage, and longer lifespan. Levels of NAD+ diminish with age, and it has been suggested that loss of this metabolite may play a role in age-related health decline.


These findings in animal studies have spurred people to take commercially available NR supplements designed to boost NAD+. However, these over-the-counter supplements have not undergone clinical trials to see if they work in people.


The new research, reported in the journal Nature Communications, was led by Charles Brenner, PhD, professor and Roy J. Carver Chair of Biochemistry at the University of Iowa Carver College of Medicine in collaboration with colleagues at Queens University Belfast and ChromaDex Corp. (NASDAQ: CDXC), which supplied the NR used in the trial. Brenner is a consultant for ChromaDex. He also is co-founder and Chief Scientific Adviser of ProHealthspan, which sells NR supplements under the trade name Tru NIAGEN®.


The human trial involved six men and six women, all healthy. Each participant received single oral doses of 100 mg, 300 mg, or 1,000 mg of NR in a different sequence with a seven-day gap between doses. After each dose, blood and urine samples were collected and analyzed by Brenner's lab to measure various NAD+ metabolites in a process called metabolomics. The trial showed that the NR vitamin increased NAD+ metabolism by amounts directly related to the dose, and there were no serious side effects with any of the doses.


"This trial shows that oral NR safely boosts human NAD+ metabolism," Brenner says. "We are excited because everything we are learning from animal systems indicates that the effectiveness of NR depends on preserving and/or boosting NAD+ and related compounds in the face of metabolic stresses. Because the levels of supplementation in mice that produce beneficial effects are achievable in people, it appears than health benefits of NR will be translatable to humans safely."


The next step will be to study the effect of longer duration NR supplementation on NAD+ metabolism in healthy adults, but Brenner also has plans to test the effects of NR in people with diseases and health conditions, including elevated cholesterol, obesity and diabetes, and people at risk for chemotherapeutic peripheral neuropathy.


Prior to the formal clinical trial, Brenner conducted a pilot human study -- on himself. In 2004, he had discovered that NR is a natural product found in milk and that there is pathway to convert NR to NAD+ in people. More than a decade of research on NR metabolic pathways and health effects in mice and rats had convinced him that NR supplementation had real promise to improve human health and wellness. After consulting with UI's institutional review board, he conducted an experiment in which he took 1 gram of NR once a day for seven days, and his team analyzed blood and urine samples using mass spectrometry. The experiment showed that Brenner's blood NAD+ increased by about 2.7 times. In addition, though he reported immediate sensitivity to flushing with the related compound niacin, he did not experience any side effects taking NR.


The biggest surprise from his metabolomic analysis was an increase in a metabolite called NAAD, which was multiplied by 45 times, from trace levels to amounts in the micromolar range that were easily detectable.


"While this was unexpected, I thought it might be useful," Brenner says. "NAD+ is an abundant metabolite and it is sometimes hard to see the needle move on levels of abundant metabolites. But when you can look at a low-abundance metabolite that goes from undetectable to easily detectable, there is a great signal to noise ratio, meaning that NAAD levels could be a useful biomarker for tracking increases in NAD+ in human trials."


Brenner notes this was a case of bidirectional translational science; having learned something from the initial human experiment, his team was able to return to laboratory mice to explore the unexpected NAAD finding in more detail.


Brenner's mouse study showed that NAAD is formed from NR and confirmed that NAAD levels are a strong biomarker for increased NAD+ metabolism. The experiments also revealed more detail about NAD+ metabolic pathways.


In particular, the researchers compared the ability of all three NAD+ precursor vitamins -- NR, niacin, and nicotinamide -- to boost NAD+ metabolism and stimulate the activity of certain enzymes, which have been linked to longevity and healthbenefits. The study showed for the first time that oral NR is superior to nicotinamide, which is better than niacin in terms of the total amount of NAD+ produced at an equivalent dose. NR was also the best of the three in stimulating the activity of sirtuin enzymes. However, in this case, NR was the best at stimulating sirtuin-like activities, followed by niacin, followed by nicotinamide.


The information from the mouse study subsequently helped Brenner's team design the formal clinical trial. In addition to showing that NR boosts NAD+ in humans without adverse effects, the trial confirmed that NAAD is a highly sensitive biomarker of NAD+ supplementation in people.


"Now that we have demonstrated safety in this small clinical trial, we are in a position to find out if the health benefits that we have seen in animals can be reproduced in people," says Brenner, who also is co-director of the Obesity Research and Education Initiative, professor of internal medicine, and a member of the Fraternal Order of Eagles Diabetes Research Center at the UI.


Protecting the ozone layer is delivering vast health benefits

Montreal Protocol will spare Americans from 443 million skin cancer cases

National Center for Atmospheric Research, October 7, 2021

An international agreement to protect the ozone layer is expected to prevent 443 million cases of skin cancer and 63 million cataract cases for people born in the United States through the end of this century, according to new research.

The research team, by scientists at the National Center for Atmospheric Research (NCAR), ICF Consulting, and U.S. Environmental Protection Agency (EPA), focused on the far-reaching impacts of a landmark 1987 treaty known as the Montreal Protocol and later amendments that substantially strengthened it. The agreement phased out the use of chemicals such as chlorofluorocarbons (CFCs) that destroy ozone in the stratosphere.

Stratospheric ozone shields the planet from harmful levels of the Sun’s ultraviolet (UV) radiation, protecting life on Earth.

To measure the long-term effects of the Montreal Protocol, the scientists developed a computer modeling approach that enabled them to look to both the past and the future by simulating the treaty’s impact on Americans born between 1890 and 2100. The modeling revealed the treaty’s effect on stratospheric ozone, the associated reductions in ultraviolet radiation, and the resulting health benefits. 

In addition to the number of skin cancer and cataract cases that were avoided, the study also showed that the treaty, as most recently amended, will prevent approximately 2.3 million skin cancer deaths in the U.S.

“It’s very encouraging,” said NCAR scientist Julia Lee-Taylor, a co-author of the study. “It shows that, given the will, the nations of the world can come together to solve global environmental problems.”

The study, funded by the EPA, was published in ACS Earth and Space Chemistry. NCAR is sponsored by the National Science Foundation.

Mounting concerns over the ozone layer

Scientists in the 1970s began highlighting the threat to the ozone layer when they found that CFCs, used as refrigerants and in other applications, release chlorine atoms in the stratosphere that set off chemical reactions that destroy ozone. Concerns mounted the following decade with the discovery of an Antarctic ozone hole.

The loss of stratospheric ozone would be catastrophic, as high levels of UV radiation have been linked to certain types of skin cancer, cataracts, and immunological disorders. The ozone layer also protects terrestrial and aquatic ecosystems, as well as agriculture.

Policy makers responded to the threat with the 1987 Montreal Protocol on Substances that Deplete the Ozone Layer, in which nations agreed to curtail the use of certain ozone-destroying substances. Subsequent amendments strengthened the treaty by expanding the list of ozone-destroying substances (such as halons and hydrochlorofluorocarbons, or HCFCs) and accelerating the timeline for phasing out their use. The amendments were based on Input from the scientific community, including a number of NCAR scientists, that were summarized in quadrennial Ozone Assessment reports.

To quantify the impacts of the treaty, the research team built a model known as the Atmospheric and Health Effects Framework. This model, which draws on various data sources about ozone, public health, and population demographics, consists of five computational steps. These simulate past and future emissions of ozone-destroying substances, the impacts of those substances on stratospheric ozone, the resulting changes in ground-level UV radiation, the U.S. population’s exposure to UV radiation, and the incidence and mortality of health effects resulting from the exposure.

The results showed UV radiation levels returning to 1980 levels by the mid-2040s under the amended treaty. In contrast, UV levels would have continued to increase throughout this century if the treaty had not been amended, and they would have soared far higher without any treaty at all. 

Even with the amendments, the simulations show excess cases of cataracts and various types of skin cancer beginning to occur with the onset of ozone depletion and peaking decades later as the population exposed to the highest UV levels ages. Those born between 1900 and 2040 experience heightened cases of skin cancer and cataracts, with the worst health outcomes affecting those born between about 1950 and 2000.

However, the health impacts would have been far more severe without the treaty, with cases of skin cancer and cataracts rising at an increasingly rapid rate through the century. 

“We peeled away from disaster,” Lee-Taylor said. “What is eye popping is what would have happened by the end of this century if not for the Montreal Protocol. By 2080, the amount of UV has tripled. After that, our calculations for the health impacts start to break down because we’re getting so far into conditions that have never been seen before.”

The research team also found that more than half the treaty’s health benefits could be traced to the later amendments rather than the original 1987 Montreal Protocol. Overall, the treaty prevented more than 99% of potential health impacts that would have otherwise occurred from ozone destruction. This showed the importance of the treaty’s flexibility in adjusting to evolving scientific knowledge, the authors said.

The researchers focused on the U.S. because of ready access to health data and population projections. Lee-Taylor said that the specific health outcomes in other countries may vary, but the overall trends would be similar.

“The treaty had broad global benefits,” she said.



What is Boron?

The trace mineral boron provides profound anti-cancer effects, in addition to maintaining stronger bones.

Life Extension, September 2021

Boron is a trace mineral found in the earth’s crust and in water. Its importance in human health has been underestimated.

Boron has been shown to have actions against specific types of malignancies, such as:

  • Cervical cancer: The country Turkey has an extremely low incidence of cervical cancer, and scientists partially attribute this to its boron-rich soil.1 When comparing women who live in boron-rich regions versus boron-poor regions of Turkey, not a single woman living in the boron-rich regions had any indication of cervical cancer.2(The mean dietary intake of boron for women in this group was 8.41 mg/day.) 
    Boron interferes with the life cycle of the human papillomavirus (HPV), which is a contributing factor in approximately 95% of all cervical cancers.1 
    Considering that HPV viruses are increasingly implicated in head and neck cancers,3,4 supplementation with this ultra-low-cost mineral could have significant benefits in protecting against this malignancy that is increasing in prevalence.
  • Lung cancer: A study conducted at the University of Texas MD Anderson Cancer Center between 1995 and 2005 found that increased boron intake was associated with a lower risk of lung cancer in postmenopausal women who were taking hormone replacement therapy.
  • Prostate cancer: Studies point to boron’s ability to inhibit the growth and spread of prostate cancer cells. 
    In one study, when mice were exposed to boric acid, their tumors shrank by as much as 38%.6 One analysis found that increased dietary boron intake was associated with a decreased risk of prostate cancer.7

Several human and animal studies have confirmed the important connection between boron and bone health.

Boron prevents calcium loss,8 while also alleviating the bone problems associated with magnesium and vitamin D deficiency.9 All of these nutrients help maintain bone density.

A study in female rats revealed the harmful effects a deficiency in boron has on bones, including:10

  • Decreased bone volume fraction, a measure of bone strength,
  • Decreased thickness of the bone’s spongy inner layer, and
  • Decreased maximum force needed to break the femur.

And in a study of post-menopausal women, supplementation with3 mg of boron per day prevented calcium loss and bone demineralization by reducing urinary excretion of both calcium and magnesium.8

In addition to its bone and anti-cancer benefits, there are nine additional reasons boron is an important trace mineral vital for health and longevity. It has been shown to:1

  1. Greatly improve wound healing,
  2. Beneficially impact the body’s use of estrogen, testosterone, and vitamin D,
  3. Boost magnesium absorption,
  4. Reduce levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor α (TNF-α),
  5. Raise levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase,
  6. Protect against pesticide-induced oxidative stress and heavy-metal toxicity,
  7. Improve the brain’s electrical activity, which may explain its benefits for cognitive performance, and short-term memory in the elderly,
  8. Influence the formation and activity of key biomolecules, such as S-adenosyl methionine (SAM-e) and nicotinamide adenine dinucleotide (NAD+), and
  9. Potentially help ameliorate the adverse effects of traditional chemotherapeutic agents.

Because the amount of boron varies in the soil, based on geographical location, obtaining enough boron through diet alone can be difficult.

Supplementing with low-cost boron is an effective way to maintain adequate levels of this overlooked micronutrient.

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