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3 Main Causes of Hypertension, 3 Ways to Lower Blood Pressure Without Taking Medicine

Hypertension is sometimes called a “silent killer,” and is feared by many. According to the 2017 American Heart Association guidelines, when blood pressure is measured during a tranquil, unagitated state and reads high more than three times within two consecutive weeks, one is considered to be suffering from high blood pressure (hypertension).

Once diagnosed, simply lowering the blood pressure is not the only goal. What is equally important is to find the cause of it. When the cause is resolved, the “silent killer” will instead become your “assistant” to alert you to the state of your health.

There are several causes of high blood pressure. Anger, nervousness, fear, stiff shoulders, and chilly weather are all contributing factors.

1. Ways to Resolve Hypertension Due to an Angry or Tense Environment

Some people are more easily agitated than others—even in watching TV their emotions may elevate, causing outward expressions of anger such as becoming red-faced, with a bulging neck, and having a high temper. This phenomenon arises as the sympathetic nerves become hyperactive, causing the peripheral blood vessels to contract. In this state, blood fails to send oxygen directly to all parts of the body, resulting in high blood pressure.

Once I had a patient in her 50s, who was slightly obese, and whose blood pressure readings were consistently around 200. After trying six different Western medicine types of blood pressure-lowering drugs with no effect, she came to me for treatment. After treatments, her blood pressure dropped to 140 or 150. She was so happy she told people everywhere, “Dr. Hu cured my blood pressure problem.”

I told her at the time, “Your high blood pressure was not cured by me, but by yourself.” How? “The medicine I prescribed to you is a medicine for soothing emotions. So you are also adjusting your emotions, and you become happier every day. Once you achieve the ‘don’t get angry, feel good’ state, high blood pressure will go away by itself.”

2 Teas to Soothe Emotions and Lower Blood Pressure

The following two teas can help soothe your emotions, achieving a calm and happy mood.

Chrysanthemum tea

Put 10 pieces of chrysanthemum into a mug and brew with hot water. Whether it is the yellow, white, or wild chrysanthemums, they are all fine. Drink the tea once the chrysanthemums are fully soaked, expanded, and exude a fragrance. To make the drink more appealing and elevate the desire to drink more, add a little licorice or wolfberry.

Licorice jujube decoction

This was one of the remedies for the patient mentioned above.

In a pot of1500cc (about 3.2 pints) of water, boil four maces (about 0.52 oz) of licorice, 1 tael (about 1.33 oz) of wheat, and 12 red dates and reduce until 1000cc (about 2.1 pints) remains. Drink daily as a tea.

Note: It is best to choose “floating wheat,” that is, wheat that has been stored for a longer time.

Chrysanthemum tea with goji berries. (Hu Naiwen/The Epoch Times)

Exercise Daily to Raise the Happiness Index

Exercise will soften the blood vessels, and once the peripheral blood vessels expand, blood can efficiently pass through, flushing the cholesterol in the blood vessels at the same time. Once blood flow in the large blood vessels becomes normal, blood pressure will drop. Moreover, during exercise, the brain produces hormones called endorphins—so-called “happy hormones,” which make people feel happier and naturally lowers blood pressure.

How do people fully occupied at home and work find time to exercise? The benefits of exercising every day can be accumulated. For example, while riding the bus on the way to work, get off one stop early and walk the rest of the distance. Or when going to lunch, spend five or six minutes walking up and down some stairs. When the workday is over and after dinner, take a walk. In this way, at the end of the day, you’ve accumulated about 30 minutes of exercise—and the more ways you can find the better.

You can also “ground” negative energy in the body by wearing soft, cloth shoes, just socks, or going barefoot and walking on grass or soil. In this way, in addition to getting some exercise, the blood supply in the brain is also increased. With sufficient oxygen, blood pressure will naturally drop.

2. Tap 3 Acupoints to Ease Hypertension With Stiff Neck

Having a stiff neck and shoulders is another condition that can add to hypertension.

For example, many office workers spend their days in front of a computer screen in a “turtle-neck” posture and have to sit still for many hours on end. When they get home, they lie again on the sofa—not moving—or bend their heads to their phones, contributing even more to their stiff necks and shoulders, which in turn can lead to high blood pressure.

I have another patient who would go to a hospital for examinations, and each time his blood pressure was measured at nearly 200. He always felt uncomfortable after taking all the blood pressure-lowering drugs prescribed by the doctor, whether they were cholesterol-lowering or blood vessel dilating. Later, I helped him stretch his carotid artery, and his high blood pressure problem disappeared.

There is an acupoint for neck and shoulder stiffness, the Chize (LU 5) acupoint. Gently press the Chize point on the left and right hands every day for 3 to 5 minutes, and shake and move the neck while pressing. In this way, the blood circulation in the neck will improve, and the blood in the carotid artery will flow to the brain. When the blood supply is sufficient, the blood pressure will naturally drop.

In addition to Chize, two other points can enhance blood circulation. One is Zusanli (ST 36)and the other is Sanyinjiao (SP 6).

In addition, people who cannot accurately press the acupuncture points can also use the method of tapping. By hitting the upper part of the acupoint, and tapping the lower part too, they can sometimes hit the exact acupoint location, and the effect is also very good.

Note: Pregnant women should avoid massaging or tapping the Sanyinjiao point.

Chize point location. ( The Epoch Times)
Zusanli (L) and Sanyinjiao(R) acupoints location. (The Epoch Times)

3. Cold Type Hypertension–Keep the Body Warm

Chilly weather can also cause blood pressure to rise.

During cold seasons, to preserve the heat in the body, the blood vessels around the body will shrink, that is, they become thinner, and shrink in size. This reduces the blood flow around the body, and much of the blood stays inside the large blood vessels, causing the blood pressure to remain high.

What to do? Wear warm layers of clothing and drink warm beverages. This will aid the narrowed blood vessels in return to their normal width, blood will then be evenly sent to all other blood vessels, and blood pressure will drop without the use of antihypertensive drugs.

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Scientists Create Semi-Living ‘Cyborg’ Cells That Could Transform Medicine : ScienceAlert

Through a complex chemical process, scientists have been able to develop versatile, synthetic ‘cyborg’ cells in the lab. They share many characteristics of living cells while lacking the ability to divide and grow.

That non-replication part is important. For artificial cells to be useful, they need to be carefully controlled, and that can’t happen as easily if they’re propagating in the same way that actual cells do.

The researchers behind the new development think these cyborgs could have a huge variety of applications, from improving treatments for diseases like cancer to cleaning up pollution through targeted chemical processes.

“The cyborg cells are programmable, do not divide, preserve essential cellular activities, and gain nonnative abilities,” says biomedical engineer Cheemeng Tan from the University of California, Davis.

Cell engineering is currently based on two key approaches: genetically remodeling existing cells to give them new functions (more flexible but also able to reproduce) and building synthetic cells from scratch (which can’t replicate but have limited biological functions).

These cyborg cells are the result of a new, third strategy. The researchers took bacterial cells as their foundation and added elements from an artificial polymer. Once inside the cell, the polymer was exposed to ultraviolet light to build it into a hydrogel matrix by cross-linking, mimicking a natural extracellular matrix.

While able to maintain much of their normal biological functions, these cyborg cells proved to be more resistant to stressors like high pH and antibiotic exposure – stressors that would kill off normal cells. Much like actual cyborgs, they’re tough.

“Cyborg cells preserve essential functions, including cellular metabolism, motility, protein synthesis, and compatibility with genetic circuits,” write the researchers in their published paper.

Lab tests on tissue samples showed that the newly developed cells were able to invade cancer cells, highlighting the potential of these modified biological building blocks for health treatments further down the line – they could one day be used to deliver drugs to very specific parts of the body.

That’s still a long way off, as promising as these early results are. The researchers say they now want to experiment with the use of different materials to create these cells, as well as investigate how they could be used.

It’s also not clear exactly what is stopping the cells from replicating, which needs to be determined. The authors think the hydrogel matrix may stop cell division by inhibiting cell growth or DNA replication, or both.

The blending of the natural and the artificial demonstrated here in some ways takes the best elements of both, opening up new possibilities – a state of “quasi vita” or “almost life”, as the researchers put it.

“We are interested in the bioethics of applying cyborg cells as they are cell-derived biomaterials that are neither cells nor materials,” says Tan.

The research has been published in Advanced Science.

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Newly Discovered VEXAS Syndrome May Affect Thousands More Americans Than Thought

The patient, Hector Campos, came into the emergency department with shortness of breath, erratic fever, and swollen, itchy ears. His wife explained that Campos had tested negative for COVID-19. “What do you think this might be?” Campos asked the chief of emergency medicine, Ethan Choi, who was similarly befuddled by the man’s symptoms.

Scary, right? But it’s not real—Campos and Choi are both characters on the NBC medical drama Chicago Med. Over the course of the episode, which aired in March 2021, Choi initially misdiagnoses Campos’ symptoms as pneumonia and a bacterial infection, but a test comes back for widespread inflammation. Campos’ condition rapidly deteriorates, and the team of doctors is mystified until fellow ER surgeon Dean Archer suggests it might be VEXAS, a rare autoinflammatory syndrome. Genetic sequencing ultimately finds a mutation confirming the diagnosis, and Choi begins treating the patient.

The episode is fictional, but depictions like this one are surprisingly accurate to real-life cases of VEXAS, said David Beck, a clinical genetics researcher at New York University Grossman School of Medicine. “In terms of clinical manifestations,” he told The Daily Beast, “they’ve been spot on.” Beck ought to know: He and his colleagues first named the syndrome in a study published in The New England Journal of Medicine in 2020. “I’ve been impressed, actually, with depictions in popular media, because [it shows] they’ve read the paper.”

Even so, these representations of VEXAS syndrome tend to highlight severe cases, in part because the NEJM paper did, too. Of the 25 cases the researchers studied, 10 of the patients died from VEXAS-related causes.

But more recent research has expanded the case definition of VEXAS to include a milder side. In a paper published in JAMA on Jan. 24, Beck and his colleagues scanned genetic sequencing readings from more than 160,000 people to determine how common VEXAS syndrome really is, and how its symptoms manifest in patients. The research team found that nine male patients and two female patients in their study had mutations that caused VEXAS.

And as a result, the researchers estimated that the syndrome affects about 13,200 men and 2,300 women over age 50 in the U.S. alone.

“It’s thrilling to go from trying to understand a few patients to finding that the same genetic cause and the same disease is found in tens of thousands of individuals,” Beck said. “Not just because we know that there are many patients out there who are suffering, who don’t get a diagnosis, or who don’t get the treatment that can help them and just taking a step in that direction; it’s also very surprising that you can still make these sort of discoveries despite all of the biomedical research going on.”

VEXAS is an acronym that stands for several key features of the syndrome. In every case of the syndrome, a patient has a genetic mutation coding for the enzyme E1. The mutation occurs on a gene on the X chromosome, which as you might recall from biology class, is a sex chromosome—men only have one, making them more prone to coming down with VEXAS. And the mutation is somatic, which means it is acquired during life as opposed to being inherited from a parent. That last feature, which gives VEXAS its “S,” is crucial: Because VEXAS is caused by a somatic mutation, the syndrome isn’t passed down and only occurs in older patients, typically over the age of 50, Beck said.

This type of research, Beck emphasized, has been made possible by recent advances in genetic sequencing that make it readily available and affordable to patients. The participants in the study all sought care at a Geisinger health care facility in central and northeastern Pennsylvania between 1996 and 2022. As part of a collaboration between Geisinger and the Regeneron Genetics Center to map genetic variation across the human genome, the participants’ exomes—regions of their genomes that encode proteins—were sequenced.

I’ve been impressed, actually, with depictions in popular media, because [it shows] they’ve read the paper.

David Beck, New York University Grossman School of Medicine

All of the 11 participants found to have mutations in the gene for the E1 enzyme were anemic and the vast majority had abnormally large red blood cells and a low platelet count—all symptoms consistent with VEXAS syndrome. Importantly, though, some of the more severe symptoms associated with VEXAS, like inflammation in the cartilage (which caused Campos’ swollen ears), were not present in these patients. This suggests that there may be a broader spectrum of severity when it comes to cases of VEXAS syndrome.

One other puzzling aspect of the study was the fact that the two women retrospectively identified as having VEXAS syndrome only suffered from the VEXAS-related mutation on one of their X chromosomes, not both. “It’s confusing for us,” since originally the researchers thought that VEXAS only affected men, Beck said. “We’ve been slowly recognizing more females that have the disease, and we don’t understand why that is.” One phenomenon at play could be X-inactivation, a process in which one of a female’s two X chromosomes is silenced throughout their cells.

The researchers wrote in the study that future analyses will be critical to understanding the prevalence of the syndrome in diverse populations, since 94 percent of the participants in the Geisinger cohort were white.

Currently, there are no treatments for VEXAS approved by the Food and Drug Administration, but a phase II clinical trial is underway to study whether blood stem cell transplants can treat or cure the syndrome. In 2022, a team of French researchers published a study suggesting that such a transplant can lead to complete remission, but such a procedure is not without its risks.

On the research side, Beck said that scientists are still trying to figure out how a mutation in the gene that encodes E1 leads to the widespread inflammation seen in cases of VEXAS. This enzyme starts a process for a cell to eliminate proteins it no longer needs, and further research is ongoing to determine how a dysfunctional E1 enzyme impacts this process.

“If you’re an older individual with systemic inflammation, low blood counts, don’t have any clear diagnosis, and you require steroids but don’t have any clear diagnosis,” you should contact your doctor about genetic testing for VEXAS syndrome, Beck said.

“It may help lead to better treatments for you—and at least a clear diagnosis,” he said.

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Super Gonorrhea Has Reached the U.S.

An illustration of Neisseria gonorrhoeae bacteria.
Illustration: Shutterstock (Shutterstock)

Super gonorrhea has infected people in the United States for the first known time. This week, Massachusetts public health officials announced the discovery of two gonorrhea cases appearing to display increased resistance to all known antibiotic classes that can be used against it. These cases were thankfully still curable, but it’s the latest reminder that this common sexually transmitted infection is becoming a more serious threat.

Gonorrhea, caused by the namesake bacteria Neisseria gonorrhoeae, is the second most commonly reported STI in the U.S., with 677,769 cases documented in 2020. Many infected people don’t experience illness, but initial symptoms can include a discolored discharge from the genitals, painful or burning urination, and rectal bleeding if caught from anal sex. When gonorrhea is left untreated, it raises the risk of more serious complications, like damage to the reproductive tract in women and swollen testicles in men, both of which can lead to infertility. And when it’s passed down from mother to child, the infection can be fatal or cause blindness in newborns.

While gonorrhea was once easily treatable with a simple pill of penicillin or other antibiotics, the bacteria has steadily learned to resist almost every drug put in its path. These days, only one or two antibiotics taken at the same time (depending on the region) are considered reliably effective against gonorrhea and are recommended as front-line treatments. But in recent years, doctors have seen cases of gonorrhea where it’s started to evade even these drugs. These extensively hardy, or pan-resistant, infections have been documented in parts of Europe and Asia to date, but at least two similar cases have now been identified in Massachusetts.

According to the state health department, the strain of gonorrhea isolated from one case clearly showed resistance or a reduced response to five classes of antibiotics, while the strain pulled from the second case was genetically close enough that it would likely have similar resistance. A common genetic marker seen in these cases was previously identified in a case reported in Nevada, but that strain still responded normally to at least one class of antibiotics. As far as health officials know, these are the first documented gonorrhea cases to show increased resistance to all of the drug classes known to treat it ever identified in the U.S.

“The discovery of this strain of gonorrhea is a serious public health concern which DPH, the CDC, and other health departments have been vigilant about detecting in the US,” said Public Health Commissioner Margret Cooke, in a statement from the agency.

Growing rates of resistance to the antibiotic azithromycin led the U.S. to stop recommending it for gonorrhea in late 2020. Now, only the drug ceftriaxone—taken as an injection—is considered a frontline option in the country, and at a higher dose than before. Luckily, despite the reduced response to ceftriaxone, both cases were successfully cleared after patients took these higher doses.

These cases are likely only a warning of what’s to come. Some of the important genetic markers seen in this novel strain have been spotted in pan-resistant cases from Europe and Asia, which shows that these mutations are continuing to spread around the world. Gonorrhea rates in general have increased year after year in the U.S. And perhaps most worryingly, no clear connection between the two Massachusetts cases has been found, indicating that these strains may already be circulating past the point where they could be easily contained.

There are ongoing efforts to develop vaccines and novel antibiotics against gonorrhea, but it may take years before any of these come to fruition, if any do. So it’s only become more important to take precautions against contracting and spreading these STIs in the first place. Health officials are now alerting doctors and testing labs in Massachusetts to look out for and report any similar cases.

“We urge all sexually active people to be regularly tested for sexually transmitted infections and to consider reducing the number of their sexual partners and increasing their use of condoms when having sex. Clinicians are advised to review the clinical alert and assist with our expanded surveillance efforts,” said Cooke.

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Cough Medicine Could Be Used in New Treatment for Parkinson’s Disease

Summary: Ambroxol, a common medicine used to treat respiratory illnesses shows promise as a treatment to slow the progression of Parkinson’s disease. Researchers report ambroxol increases the level of GCase, a protein that allows cells to remove waste proteins including alpha-synuclein.

Source: UCL

Ambroxol is a drug which is currently used to treat respiratory conditions. It promotes the clearance of mucus, eases coughing and has anti-inflammatory properties.

Pre-clinical studies, led By Professor Schapira at the UCL Queen Square Institute of Neurology identified ambroxol as a candidate drug to slow the progression of Parkinson’s.

Results of the Phase 2 clinical trial by Professor Schapira and performed at UCL was published in January 2020 and tested ambroxol in people with Parkinson’s. It found that ambroxol was able effectively reach the brain and increase levels of a protein known as GCase (glucocerebrosidase). GCase allows cells to remove waste proteins, including alpha-synuclein (a protein that builds up in Parkinson’s and is thought to be important in its cause), more effectively.

Additionally, the Phase 2 trial showed that ambroxol was safe for people with Parkinson’s and was well tolerated.

The world-first Phase 3 trial, named ASPro-PD, is led by Professor Anthony Schapira and is in partnership with U.K. charity Cure Parkinson’s and Van Andel Institute—following eight years of work with the Parkinson’s community.

The trial will involve 330 people with Parkinson’s across 10–12 clinical centers in the U.K. It will be placebo controlled and participants will take ambroxol for two years.

The effectiveness of ambroxol will be measured by its ability to slow the progression of Parkinson’s using a scale including quality of life and movement. Preparations for recruitment of trial participants have already started.

Professor Schapira, said, “I am delighted to be leading this exciting project. This will be the first time a drug specifically applied to a genetic cause of Parkinson’s disease has reached this level of trial and represents ten years of extensive and detailed work in the laboratory and in a proof of principle clinical trial.

“The study design is the result of valuable input from people with Parkinson’s, leaders in the field of Parkinson’s, trial design and statistics from the UCL Comprehensive Clinical Trials Unit (CCTU), the MHRA and a consortium of funders led by Cure Parkinson’s, all operating as an effective team to ensure we have reached this stage.

“We look forward to working with all these groups to ensure successful completion of the study.”

See also

It found that ambroxol was able effectively reach the brain and increase levels of a protein known as GCase (glucocerebrosidase). Image is in the public domain

After the Phase 2 data from Professor Schapira’s group at UCL found that ambroxol could increase the removal of alpha-synuclein, the international Linked Clinical Trials (iLCT) program prioritized research into the drug.

Created and operated by Cure Parkinson’s and Van Andel Institute, the iLCT program’s mission is to slow, stop and reverse the progression of Parkinson’s. It aims to significantly reduce the time to bring disease-modifying treatments to clinic for the Parkinson’s community by testing promising drugs that already have extensive safety data and, in some cases, have been approved by regulators for other medical conditions.

Will Cook, CEO of Cure Parkinson’s, said, “This trial is a big step forward in the search to find new treatments for Parkinson’s. Once the ambroxol trial is underway, it will be one of only six Phase 3 trials on public record of potentially disease-modifying drugs in Parkinson’s, worldwide.

“We at Cure Parkinson’s are working hard—through our efforts within the iLCT program and in our fundraising efforts—to increase this number significantly in the next few years, to accelerate our progress towards a cure for Parkinson’s.”

About this Parkinson’s disease and neuropharmacology research news

Author: Poppy Danby 
Source: UCL
Contact: Poppy Danby  – UCL
Image: The image is in the public domain

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Experts Recommend Drugs, Surgery for Teen Obesity in New Guidelines

Image: Shutterstock (Shutterstock)

For the first time ever, experts with the American Academy of Pediatrics are recommending proactive medical intervention against childhood obesity. The organization’s new guidelines will no longer ask doctors to simply observe or delay treatment in children with obesity, defined as a body mass index over 30. They instead now emphasize a range of options, such as dietary and lifestyle counseling for younger children as well as medications and/or surgery for children 12 and over.

Past standards for treating childhood obesity have called for “watchful waiting,” the hope being that a child’s BMI (a measure of both weight and height) would naturally lower over time as they grew. In 2007, the AAP’s previous recommendations promoted a step-based approach, where doctors might slowly escalate from observation to treatment. But these new recommendations—released Monday—are the first clinical practice guidelines to put obesity treatments front and center.

“There is no evidence that ‘watchful waiting’ or delayed treatment is appropriate for children with obesity,” said Sandra Hassink, one of the authors behind the guidelines and vice chair of the AAP Clinical Practice Guideline Subcommittee on Obesity, in a statement released by the organization. “The goal is to help patients make changes in lifestyle, behaviors or environment in a way that is sustainable and involves families in decision-making at every step of the way.”

The lengthy guidelines outline a multitude of available treatments, depending on a child’s age and other circumstances (children under 2 are not considered eligible for obesity treatment).

For younger children, these options can include intensive health behavior and lifestyle treatment, which can involve regular counseling sessions with the child and family over a 3- to 12-month period. For children 12 and over, doctors are now advised to consider medications as a front-line option. And teens 13 and over can also be evaluated for bariatric surgery as a potential treatment.

In crafting its recommendations, the AAP cites many studies suggesting that the benefits of these treatments outweigh any potential risks they can carry. Patients who have undergone bariatric surgery seem to have a lower risk of developing obesity-related complications such as type 2 diabetes and have a longer life expectancy when compared to non-surgical patients matched in age and baseline BMI, for instance. Long-term health benefits have been seen in teen bariatric patients specifically, too.

A new class of medication, called incretins, has also greatly changed the landscape of obesity treatment in recent years. These drugs, combined with diet and exercise, have led to far larger weight loss on average than most other treatments and are approaching the typical results seen with bariatric surgery.

Last month, the Food and Drug Administration extended the approval of Novo Nordisk’s Wegovy, the first drug of this new generation, to children over 12, following clinical trial data showing that teens saw a similar improvement in BMI as adults. The shortages that have plagued Wegovy’s rollout since its approval in June 2021 may finally be over as well, with the company recently announcing that its supply should now be stable. Without insurance coverage, which is often limited, the drug can still cost over $1,000 a month, however.

The AAP’s guidelines arrive at a time when the rise in U.S. obesity rates, including among children, has only accelerated, likely in part due to the covid-19 pandemic. The new recommendations notably do not cover how best to prevent obesity in children, though the organization has promised to release separate recommendations for that in the near future.

“The medical costs of obesity on children, families and our society as a whole are well-documented and require urgent action,” said lead author Sarah Hampl in a statement. “This is a complex issue, but there are multiple ways we can take steps to intervene now and help children and teens build the foundation for a long, healthy life.”

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Food as medicine? It’s not as simple as it sounds.

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Ever since I was a doctor fresh out of residency, I have prescribed food to my patients to prevent and treat chronic health problems, such as diabetes and heart disease. But health insurance had never covered the cost of a healthy meal, which means some patients cannot afford the healthy diet I’ve given them.

That has recently changed in California and a handful of other states, where Medicaid now covers some food targeting patients with diet-related conditions. As a result, I now prescribe “Medically Supportive Food,” or MSF, for some patients — a weekly bag of groceries, or up to three daily meals — paid for by insurance as if it were a medication.

This move to embrace “food as medicine” is bolstered by research showing that food prescriptions by medical professionals can cut health-care costs and improve well-being, especially for those who do not have the resources to access healthy food.

In a recent study, researchers estimated that offering a nationwide “medically tailored meal” benefit to individuals with such conditions as heart disease, cancer and diabetes could save $185.1 billion in medical costs and avert more than 18 million hospitalizations over a 10-year period.

For those who see food as an integral part of healing, this is a monumental step forward. But prescribing food is not as straightforward as it sounds.

Food is more complex than any pill. This makes it difficult for doctors and patients to know which medically tailored foods are the best medicine and which suppliers can best deliver these edible therapies.

First, there’s a real challenge in identifying which suppliers provide the most nutritious food. A pharmaceutical drug, whether it is generic or brand name, has a near-identical makeup regardless of who makes it. But food varies dramatically in nutrient content depending on seed, season, farming and processing method, and how long it was stored before it was eaten. Combine foods to make a meal and the nutrient variability gets even greater.

The lack of standardization made it hard, for instance, for Dennis Hsieh, a physician and chief medical officer of the Contra Costa Health Plan based in California, to choose among the food vendors bidding to fill the food prescriptions for his plan’s enrollees.

Hsieh has extensive experience contracting with medical supply companies for drugs and other health-care products, but this is his first foray into the food sector. He said he received little guidance from California’s Department of Health Care Services about what he should be buying. Its policy guide merely suggests he offer “appropriate dietary therapies based on evidence-based nutritional practice guidelines.”

“At the end of the day, my basic criteria [for vendors] is that they get the food to patients and that they are not giving them McDonald’s and charging us for it,” he said.

Ultimately, Hsieh contracted with six vendors. He said he hopes these vendors will offer meals and groceries that reproduce the cost savings and health benefits of the “food is medicine” studies, but he doesn’t “have the experience” to judge which vendors will accomplish this.

Michelle Kuppich, a registered dietitian and director of the California Food Is Medicine Coalition, is also concerned about the quality of some of the food entering this growing medical marketplace.

“There are many new companies coming into this space because there is money involved and people want the health-care dollars,” Kuppich said. She said she suspects that some of them “started off selling prepared meals for weight loss and then rebranded.”

Kuppich has found it challenging to get information about the nutritional value of some of the food being sold. “There is a lack of transparency in terms of ingredients,” she said.

Some of the vendors are offering food that is just as ultra-processed as fast-food meals that Hsieh hopes to avoid. Ultra-processed foods have been linked with chronic diseases and a higher risk of early death.

What are ultra-processed foods? What should I eat instead?

For example, GA Foods, a Florida-based vendor of medically supportive food, offers over 50 “nutritionally balanced” meals that contain additives, including corn syrup and other sweeteners, food coloring, flavor additives, hydrolyzed protein and preservatives. “We follow guidelines from the top organizations around each disease state and update guidelines as they are released,” said Mary O’Hara, senior marketing manager for GA Foods. “Our medically tailored meal portfolio continuously evolves to meet patient needs and new innovations around health and wellness.”

And Tracy Smith, vice president of marketing for Mom’s Meals, an Iowa-based company that serves over a million meals per week nationwide, said some of their meals include a micronutrient blend of magnesium, zinc, iron, calcium, and vitamins C, B1 and B6 to “ensure that the meal fully meets one-third of a person’s Dietary Reference Intake. We do that instead of including additional servings of food that would then take that meal above recommended calories, sodium or carbohydrates per serving, for example.”

Fortifying foods with vitamins and minerals can prevent anemia and other diseases linked to deficiencies of specific nutrients, but it cannot reproduce the more complete nutrition offered in a whole food. A carrot, for example, has all the nutrients in a Mom’s Meals blend, plus dozens of additional disease-fighting compounds, which work together to influence our health.

Cathryn Couch, founder and chief executive of Ceres Community Project, a nonprofit MSF supplier based in Sonoma County, Calif., said, “We use high-quality, nutrient-dense food and we don’t need to add anything to meet the nutrient requirements for our clients.” Couch said sourcing food regionally and limiting storage and transit time helps ensure higher nutritional quality. (It also can help support the local economy and diminish the environmental footprint.)

Health-care providers also face a challenge of identifying which vendors offer food that appeals to the taste buds — and the soul.

“None of these food interventions work if the people don’t want to eat the food,” said Seth Berkowitz, a researcher who led some food is medicine pilot studies and is now an associate professor in general medicine and clinical epidemiology at the University of North Carolina School of Medicine. He described food as offering gastronomic pleasure, cultural connection and family memories.

Berkowitz said national vendors offer “an economy of scale” that keeps costs down, but the pilot studies he was involved with in Boston that showed positive results had received their food from a nonprofit group that says it serves “scratch-made” meals and buys from local farmers.

“Mission-driven organizations may offer benefits,” Berkowitz said. “It remains to be seen whether the secret sauce that made those small efforts work can be scaled.”

Nutrition and lifestyle coaching

Beyond supplying food, MSF vendors in California are expected to offer nutrition and lifestyle coaching to their clients, since research shows that coupling food assistance with education is more likely to promote healthy eating patterns.

As with the food, these services vary. Some vendors give enrollees access to a brief nutrition consultation or a healthy eating app, while others provide real-time cooking and shopping classes.

“The number one thing I hear from our clients is ‘I learned how to use a knife,’” said Sarah Nelson, executive director of 18 Reasons, an MSF provider in the San Francisco Bay area. She has discovered that her clients are more likely to try new vegetables if they are given a recipe and practice prepping them in a group setting.

“Nutrition education and counseling is as important as the food, so that people can prepare healthy meals once their prescription ends,” Kuppich said.

How it works in a doctor’s office

Recently, I wrote a food prescription for a 50-year-old woman with poorly controlled Type 2 diabetes. She was enrolled in MediCal, California’s health insurance program for children and adults with limited income and resources.

I tried my best to direct her to the vendor that would deliver the tastiest, most nutrient-dense, culturally relevant food. But even with my nutrition know-how, I found it challenging to figure out which one that might be.

She ultimately chose a nonprofit group that sources most of its food locally and delivered meals to her doorstep. Two months into her prescription, her blood sugars improved, and I called her to give her the good news. I asked her what she thought of the meals. “They are so nice, it is really good to see them,” she said.

It took me a moment to realize she was referring to the delivery person, not the food.

Her comment left me wondering what had produced the positive change in blood sugar. Was it the food? The social connection? Both?

Regardless, it was a bracing reminder that food is not a pill, it’s a much more complicated medicine.

At any age, a healthy diet can extend your life

Daphne Miller is a family physician and clinical professor at the University of California at San Francisco, and a research scientist at the University of California Berkeley School of Public Health. She is also founder of the Health From the Soil Up Initiative.

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Would You Sell Your Extra Kidney?

When we were teenagers, my brother and I received kidney transplants six days apart. It wasn’t supposed to be that way. He, two years older, was scheduled to receive my dad’s kidney in April of 1998. Twenty-four hours before the surgery, the transplant team performed its final blood panel and discovered a tissue incompatibility that all the previous testing had somehow missed. My brother was pushed onto “the list,” where he’d wait, who knows how long, for the kidney of somebody who had died and possessed the generous foresight to be a donor after death. I was next in line for my dad’s kidney. We matched, and the date was set for August 28. Then my parents got a call early in the morning on August 22. There had been a car crash. A kidney was available. As with many things in life, my brother went first and I followed.

His operation went smoothly. Six days later, it was my turn. I remember visiting the doctor shortly before the transplant, feeling the pinprick and stinging flush of local anesthetic, then a blunted tugging, the nauseating and strange sensation of a dialysis catheter withdrawn from below my collarbone. I remember, later, the tranquil fog of midazolam as I was rolled to the OR. 

I remember waking from great depths after surgery under bright lights and shivering violently, then falling back asleep. I remember lying naked under blankets in the ICU, mildly delirious from morphine while watching a movie about a plane crash in the Alaskan wilderness, with Anthony Hopkins and Alec Baldwin fleeing a giant grizzly bear. I remember friends visiting me on the recovery floor, and how it hurt to laugh.

But now that 24 years have passed, all in relatively good health, I can recognize how much I’ve forgotten. I forget the short leash of dialysis from the months before my transplant: those oversize recliners deep inside the taupe core of a hospital building where, three times a week, machines drained and recycled my blood. I forget the plainness of a low-potassium, low-phosphorus, low-salt diet. I forget how bizarre it is that a few pills in the morning and a few at night keep the foreign organ in my lower abdomen alive—keep me alive. I, regrettably, lose sight of the supreme gift I’ve been given, this indefinite allowance of extra time, while 90,000 other Americans wait for this same gift, often on dialysis for years. Roughly 4 percent will die every year still waiting, and another 4 percent will become too sick to undergo major surgery. But here I am, forgetting this grace.

Five years ago, my brother’s kidney began to fail, and all of these buried memories resurfaced. His blood tests returned erratic levels, and nephrologists fretted. He was in and out of the hospital with recurring viral infections. A biopsy revealed necrotic tissue perforating half his kidney, webbed throughout like the tunnels of an ant colony. Finally, in May of 2018, he sent an email to family and friends, distilling the two borrowed decades during which he had attended concerts, hiked the Pacific Northwest, fallen in love, gotten married, started a family. All of these details were offered with a kind of chummy lightheartedness, but, as every reader knew, they barreled toward the inevitable and awkward conclusion. He was 37 years old and back in the hunt for a kidney. Would you be so kind as to consider … ?

The first successful kidney transplant took place in Boston in 1954 between a deliriously ill Richard Herrick and his identical twin brother, Ronald. Eight years later, his new kidney still doing its job, Richard died of a heart attack. Scattered attempts had come before then. In Ukraine, in 1933, the kidney of a 60-year-old man with type B blood who’d been dead for six hours was transplanted into a 26-year-old woman with type O blood who’d lost kidney function after poisoning herself. The recipient survived for two more days, which is miraculous considering the technology, circumstances, and general knowledge at the time. A transplant recipient in Chicago, in 1950, had some additional kidney function for a few months. Paris became a hotbed of experimentation in the early ’50s. Then came the Herricks.

Their story was technically dazzling but left unsolved the central biological puzzle of transplantation: how to tame the immune system. In most cases, our bodies recognize foreign tissue and send a battery of B and T cells to kill it. As identical twins with identical-enough tissue types, the Herricks sidestepped this problem. But doctors would need a solution to our innate immune response if kidney transplants were ever to become a mainstream procedure. Early efforts subjected patients to full-body preoperative blasts of X-ray radiation at borderline-lethal doses. The intent was to crush the immune system, then let it rebuild with the new kidney in place. This was sometimes accompanied by an injection of bone marrow. Most patients died from organ rejection, graft-versus-host disease, or both. The field of transplant surgery grew insular and desperate. Citing the fundamental precept of avoiding unnecessary harm, the more conservative medical practitioners of the day vilified the practice. Around this time, one detractor wondered, “When will our colleagues give up this game of experimenting on human beings? And when will they realize that dying, too, can be a mercy?”

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Why Armored CAR T Therapy Is Our Best Shot at Curing Cancer

Immune therapies have rewritten the game when it comes to cancer treatment, earning the “fifth pillar” label next to more tried and true treatments like radiation therapy, surgery, and chemotherapy. And no immunotherapy has garnered quite the same excitement as CAR T-cell therapy, first approved in 2017 by the Food and Drug Administration to treat a form of acute lymphoblastic leukemia. At the time, then-FDA Commissioner Scott Gottlieb called the approval “a new frontier in medical innovation,” and it seemed like the possibilities for CAR T were near-endless.

Flash-forward almost six years, and six therapies have been approved for blood cancers, including lymphomas, leukemia, and multiple myeloma. There’s no question that when CAR T works, it works incredibly well. But why it doesn’t work for the majority of patients or cancer types has befuddled researchers.

“We have patients who, several years ago would have no options and because of this new therapy they are now in long-term remissions,” Jakub Svoboda, an oncologist at the University of Pennsylvania, told The Daily Beast. “But with all of that, what I see in my clinic is that the number of patients who greatly benefit from this treatment is still well under 50 percent” as a third-line treatment for a type of lymphoma, he added.

CAR T therapies also haven’t yet been expanded to treat solid tumors, which make up the majority of cancers. The immune therapy hasn’t been able to crack physical barriers, idiosyncratic tumor cells, and a suppressive microenvironment that characterize these cancers. But a new generation of CAR T therapies are emerging, equipped with highly effective small molecules that scientists hope will solve their low success rate for both blood cancers and solid tumors. Known as “armored CAR T,” these infusions have been boosted with additional layers of protection and cancer-fighting proteins. Early research shows that the armored flavor of CAR T might have what it takes for immunotherapy to go the extra mile.

“We’re making these cells and sending them on this really difficult adventure through different terrains and different problems—so we need to give them a set of tools,” Wendell Lim, a cellular and molecular pharmacology researcher at the University of California, San Francisco, told The Daily Beast.

Briefly, immunotherapy can boost or restore the body’s immune system by lowering cancer cells’ defenses, priming the immune system’s T cells to destroy tumors, or—in the case of CAR T-cell therapy— genetically editing a patient’s T cells. Scientists do this by isolating a patient’s T cells from their blood and inserting a gene for a chimeric antigen receptor—a type of synthetic protein that has been specially made to bind to another protein present on the surface of that patient’s cancer cells. Then, upon infusing these modified T cells back into a patient, the immune fighters will recognize and destroy the tumor cells when the patient’s normal T cells have failed.

That, at least, is the idea. But when CAR T doesn’t work, a few factors could be at play. One, Lim said, is the tumor microenvironment, the set of chemicals and structures present in solid cancers that naturally suppress pushback from the body’s immune system. Tumor heterogeneity is also a factor—depending on the type and stage of cancer, tumor cells may not express the protein that the CAR T cells’ receptors have been designed to recognize, blocking the ability of the CAR T cells to attack the cancer Finally, there are physical barriers on the outside of a solid tumor that can even prevent the T cells from entering inside to destroy the cancer.

Armored CAR T is meant to overcome these difficulties. With this form of therapy, not only are T cells engineered to express a tumor cell’s surface protein, they are also given potent cargo often in the form of small proteins called cytokines. If deployed on their own, such molecules can be toxic—but pairing them with T cells designed to release them at the tumor site and nowhere else represents a promising new strategy.

Svodoba is helping to lead a clinical trial using armored CAR T-cell therapy to treat patients with non-Hodgkin lymphoma for whom previous CAR T therapy has failed. Last month, he presented findings that the first seven patients treated with this therapy all responded to it and were alive eight months after receiving it. Svoboda said an important additional finding was that toxicities experienced by the patients—a concern with cytokines—were comparable to those from traditional CAR T therapy.

Lim’s team is also working on an armored CAR-T therapy, with the potential for it to be used to treat solid tumors. In a paper published in Science on Dec. 16, he and his colleagues designed T cells to release a cytokine directly to the tumors of mice with pancreatic cancer and melanoma. In the study, they wrote that these cancers are “nearly completely resistant” to treatment with traditional CAR T, but releasing a cytokine allowed the engineered T cells to get past the tumor microenvironment—effectively solving one of the issues that has set the therapy back.

“The way to think about the future of CAR T-cell therapies is developing reliable tools that solve certain problems and coupling them together in one package,” Lim said. The researchers hope to begin patient trials of an armored CAR T therapy within the next two years.

Getting these treatments to the clinic won’t be a speedy process—more trials will be needed to make sure that armored CAR T can be effective while reducing toxicity as much as possible. Personalized immunotherapy can also take time to produce—time that cancer patients may not always have—and are often expensive. Still, Svodoba said that efforts are underway to make therapies more accessible, and that the cost may be worth it if armored CAR T can be effective in the long run.

“If one infusion of an expensive product can result in long-term remission or a cure, investing in that type of product makes a lot of sense to me.”

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Why Do You Get Sick in the Winter? Blame Your Nose

To figure out what exactly was causing this antiviral capability, the scientists then incubated the vesicles with the viruses and imaged them under a microscope. They found that the viruses got stuck to receptors on the vesicles’ surface—trapping them and rendering them incapable of infecting cells. In other words, the vesicles were acting as a kind of decoy. “Because the same receptors are on the vesicles as are on the cells, most of the viruses get bound to the vesicle and killed before they ever get to the cells,” Bleier says. 

In addition, the scientists also found that the stimulated vesicles contained higher quantities of microRNA—small strands of RNA—previously known to have antiviral activity.

Finally, the scientists wanted to see how a small temperature change might affect the quality and quantity of the secreted vesicles. To create a dish-based mimic of the human nose, they used small pieces of mucosal tissue extracted from a few patients’ noses and placed those little tissues, known as explants, into cell culture. Then they lowered the temperature from 37 to 32 degrees Celsius, stimulated the tissue to upregulate TLR3, and collected the secreted vesicles.

They found that the cold caused a 42 percent drop in the tissues’ ability to secrete vesicles, and those vesicles had 77 percent fewer of the receptors that would let them bind to and neutralize a virus. “Even in that 5-degree drop for 15 minutes, it resulted in a really dramatic difference,” Amiji says. 

Noam Cohen, an otorhinolaryngologist at the University of Pennsylvania, says that this work sheds light on the mechanics of how viruses spread more easily in cold weather. (Cohen was unaffiliated with this work, but previously mentored Bleier when he was a medical student.) “What this paper is demonstrating is that viruses, even though they’re incredibly simplistic, are incredibly crafty,” he says. “They’ve optimized a cooler temperature to replicate.”  

Jennifer Bomberger, a microbiologist and immunologist at Dartmouth College, says that one of the study’s interesting points was how the “vesicles weren’t just immune-education,” meaning they weren’t just ferrying immune system instructions. Instead, she continues, “they were actually carrying out some of the actual antiviral effects themselves by binding to the virus.” She notes, though, that looking at mucus from patients with real infections (rather than using a virus-mimic) might provide additional insights into how these vesicles work.

The behavior of these vesicles isn’t the only reason why upper respiratory infections peak during the wintertime. Previous work has shown that colder temperatures also diminish the work of immune system antiviral molecules called interferons. Viruses also tend to spread as people move indoors. Social distancing during the pandemic has also potentially left people with less built-up immunity to the viruses that cause the flu and RSV, both part of the “tripledemic” that emerged this winter.  

Still, Amiji says that understanding exactly how the vesicles change could lead to some interesting ideas for therapies—because perhaps scientists can control those changes. He visualizes it as “hacking” the vesicle “tweets.” “How can we increase the content of these antiviral mRNAs or other molecules to have a positive effect?” he asks.

In light of the Covid-19 pandemic, the team notes that there’s already a practical real-world way to help your nose defend you in cold weather: Masking. Noses can stay snug and cozy under a mask—as any glasses-wearer whose lenses have fogged from their warm breath can attest. “Wearing masks may have a dual protective role,” says Bleier. “One is certainly preventing physical inhalation of the [viral] particles, but also by maintaining local temperatures, at least at a relatively higher level than the outside environment.”

And here’s one more idea to consider: Maybe it’s just time for a vacation somewhere warm.

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