Publisher Health

Inadequate pollination has led to a 3-5% loss of fruit, vegetable, and nut production and an estimated 427,000 excess deaths annually from lost healthy food consumption and associated diseases, including heart disease, stroke, diabetes, and certain cancers, according to research led by Harvard T.H. Chan School of Public Health. It is the first study to quantify the human health toll of insufficient wild (animal) pollinators on human health.
“A critical missing piece in the biodiversity discussion has been a lack of direct linkages to human health. This research establishes that loss of pollinators is already impacting health on a scale with other global health risk factors, such as prostate cancer or substance use disorders,” said Samuel Myers, principal research scientist, planetary health, Department of Environmental Health and senior author of the study.
The study will be published December 14, 2022 in Environmental Health Perspectives.
Increasing human pressure on natural systems is causing alarming losses in biodiversity, the topic of the COP 15 UN Biodiversity Conference currently taking place in Montreal. This includes 1-2% annual declines of insect populations, leading some to warn of an impending “insect apocalypse” in the coming decades. Key among insect species are pollinators, which increase yields of three-fourths of crop varieties and are critical to growing healthy foods like fruits, vegetables, and nuts. Changes in land-use, use of harmful pesticides, and advancing climate change threaten wild pollinators, imperiling human supply of healthy foods.
The researchers used a model framework, which included empirical evidence from a network of hundreds of experimental farms across Asia, Africa, Europe and Latin America, that looked at “pollinator yield gaps” for the most important pollinator-dependent crops, to show how much crop loss was due to insufficient pollination. They then used a global risk-disease model to estimate the health impacts the changes in pollination could have on dietary risks and mortality by country. Additionally, they calculated the loss of economic value from lost pollination in three case study countries.
The results showed that lost food production was concentrated in lower-income countries but that the health burden was greater in middle- and higher-income countries, where rates of non-communicable diseases are higher. The geographic distribution was somewhat unusual in that generally the health effects from global environmental change are centered among the poorest populations in regions such as South Asia and Sub-Saharan Africa. Here, middle-income countries with large populations — China, India, Indonesia, and Russia — suffered the greatest burden.
The analysis also showed that lower-income countries lost significant agricultural income due to insufficient pollination and lower yields, potentially 10-30% of total agricultural value.
“The results might seem surprising, but they reflect the complex dynamics of factors behind food systems and human populations around the world. Only with this type of interdisciplinary modeling can we get a better fix on the magnitude and impact of the problem,” said co-author Timothy Sulser, senior scientist, International Food Policy Research Institute.
Strategies to protect wild pollinators are not just an environmental issue, but a health and economic one as well. “This study shows that doing too little to help pollinators does not just harm nature, but human health as well,” said lead author Matthew Smith, research scientist, Department of Environmental Health.
Support for the study was provided by grants from the Gordon & Betty Moore Foundation, Weston Foods Inc., Fifth Generation Inc., and the CGIAR Research Program on Policies, Institutions, and Markets.

An autopsy in New York showed that the journalist had a tear in the ascending aorta, a large vessel that carries blood from the heart.Grant Wahl, the celebrated soccer journalist who died suddenly last week at the World Cup in Qatar, had a rupture in a blood vessel leading from the heart, his family announced on Wednesday.His death resulted from a weakness in an artery wall called an aneurysm, which may balloon outward and then tear open. An autopsy conducted in New York revealed that Mr. Wahl, 49, experienced a catastrophic rupture in the ascending aorta, which carries oxygenated blood from the heart.The autopsy puts an end to rampant speculation that followed Mr. Wahl’s death. Posts on social media hinted at links to Covid vaccines or retaliation by the Qatari government for an article Mr. Wahl had written about immigrant deaths.Mr. Wahl’s wife, Dr. Celine Gounder, is a leading infectious disease physician who rose to prominence during the coronavirus pandemic and advised President Biden’s transition team on Covid-19. She and the rest of the family rejected, in particular, the speculation linking his death to vaccines, saying that it was especially insulting because of her work.He probably died instantly and did not feel pain, Dr. Gounder said in an interview on Tuesday. “I really do feel some relief in knowing what it was,” she said.Mr. Wahl had been sick with a cold for several days before collapsing, and had written in his newsletter and on Twitter that he felt his body was breaking down after weeks of poor sleep and long days covering the games.He had just turned 49 and was quite healthy, making his death even more of a shock to his friends, family and readers. The sniffles and other cold symptoms he had were most likely unrelated to the aneurysm, Dr. Gounder said.Until the autopsy, Dr. Gounder said, she had been worried that perhaps she could have prevented his death if they had talked more often while he was in Qatar or if she had been there with him.Mr. Wahl’s brother, Eric Wahl, initially said on social media that he suspected foul play and later suggested that his brother might have experienced a blood clot in his lungs. On Tuesday, Eric Wahl said that he no longer believed those were factors in his brother’s death.The autopsy found that Mr. Wahl had an ascending thoracic aortic aneurysm, a weakening of the blood vessel that often goes undetected. As the aneurysm grows, it may produce a cough, shortness of breath or chest pain, some of which the doctors consulted by Mr. Wahl in Qatar might have attributed to his cold and a possible case of bronchitis.In rare cases, the aneurysm can rupture and lead to death. Doctors are now exploring whether Mr. Wahl had Marfan syndrome, a risk factor for this type of aneurysm. He was tall and thin and had long arms, all of which can be signs of the genetic syndrome.Mr. Wahl joined Sports Illustrated in 1996 as a fact checker, a traditional entry route for young journalists, and wrote hundreds of articles on a variety of sports for the magazine over the next two decades.One early profile, a cover story on a teenage LeBron James in 2002, remained a touchstone for both writer and subject 20 years later. Mr. Wahl would occasionally reminisce about it to his 850,000 followers on Twitter, and Mr. James spoke about its meaning to him and his family while eulogizing the writer at a news conference and on social media over the weekend.But Mr. Wahl was best known for writing about soccer, which he began covering while he was a student reporter at Princeton University in the early 1990s. Through his books, tweets, podcasts and magazine articles, he became a guide of sorts for a generation of fans and readers just learning the game.He also used his profile and social-media megaphone to highlight the growth of women’s soccer, the breadth of corruption in soccer, human rights violations and gay rights.Mr. Wahl had worked at Sports Illustrated for more than 23 years when the magazine’s publisher abruptly fired him over a dispute about pandemic-related pay cuts. But he had a large following by then, and started an email newsletter and podcast that quickly became successful.In Qatar, Mr. Wahl was covering his eighth World Cup. He was in the press box in the closing minutes of the quarterfinal match between Argentina and the Netherlands when he collapsed.According to two New York Times journalists who were present, medical personnel tried to revive Mr. Wahl for about 20 minutes before he was transported to a hospital in Doha. He was pronounced dead at the hospital.Dr. Gounder’s relationships with the Biden administration and public health agencies, including the New York City health department, helped her bring the unembalmed body to the United States for the autopsy.Dr. Gounder said she wanted to ascertain the circumstances of her husband’s death in part to quell online speculation. “I wanted to make sure the conspiracy theories about his death were put to rest,” she said.

The tally is less than 1 percent of all deaths linked to the coronavirus, but it shows that it is possible to die from lingering symptoms after infection.Long Covid has caused or contributed to at least 3,500 deaths in the United States, an analysis of death certificates by the Centers for Disease Control and Prevention found.The study, published on Wednesday, is believed to be the first nationwide examination of whether long Covid or related terms appear in official American death records. While it found that such phrases were recorded in only a tiny proportion of the more than a million deaths tied to infection with the coronavirus, the researchers and other experts said the results added to growing recognition of how serious long-term post-Covid medical problems can be.“It’s not one of the leading causes of death, but, considering that this is the first time that we’ve looked at it and that long Covid is an illness that we’re learning more about day after day, the major takeaway is that it is possible for somebody to die and for long Covid to have played a part in their death,” said Farida Ahmad, a health scientist at the National Center for Health Statistics at the C.D.C. who led the study.Long Covid is a complex constellation of symptoms that can last for months or longer and can affect virtually every organ system. Some of the most debilitating post-Covid symptoms are breathing problems, heart issues, extreme fatigue and cognitive and neurological issues.The researchers looked at death certificates in every state and Washington, D.C., dated from Jan. 1, 2020 to June 30, 2022. They found 1,021,487 certificates that included a diagnostic code for Covid-19 as an underlying or contributing cause of death. Of those, 3,544 — or 0.3 percent of the total — listed long Covid or terms like post-Covid syndrome, chronic Covid or long-haul Covid. Ms. Ahmad and experts not involved in the research said the number of deaths related to long Covid in the study was almost certainly an underestimate. It has taken time for the condition to be recognized and identified by doctors and other medical providers. And the study was not able to include a new diagnostic code for long Covid because it was not yet being used in reporting of deaths in the United States, the researchers said.“This new research is important in raising a concern, but it should be followed with more definitive work,” said Dr. Jeffrey Martin, chief of the division of clinical epidemiology in the department of epidemiology and biostatistics at the University of California, San Francisco, who was not involved in the research.“Historically, death certificates have been incomplete in explaining how a person died,” said Dr. Martin, who suggested that future research should include interviewing patients’ doctors and family members and evaluating their medical records.The study found that more death certificates mentioned long Covid after 2020 and that the condition was more likely to be listed on death certificates in the weeks or months after a peak of Covid cases, Ms. Ahmad said.The study found that some of the long Covid patterns related to age, sex, race and ethnicity differed from those seen in deaths caused by the initial infection. For example, while Black and Hispanic people had higher death rates from the initial coronavirus infection than non-Hispanic whites, those groups did not have higher death rates related to long Covid, the study found.The researchers suggested that the difference might be partly because of systemic disparities that have resulted in less access to health care for Black and Hispanic patients, who might not have received appropriate long-Covid diagnoses. The study said it was also possible that, because Black and Hispanic patients died at higher rates from the initial illness than white patients, they might have “fewer Covid-19 survivors left to experience long-Covid conditions.”Nearly 57 percent of deaths related to long Covid were in people 75 and older. Nearly a third of the death certificates that mentioned long Covid listed the underlying or main cause of death as a non-Covid condition such as heart disease, cancer or Alzheimer’s.“This is just scratching the surface — this is a first look,” said David Putrino, the director of rehabilitation innovation for the Mount Sinai Health System in New York, who was not involved in the study.He said the study appeared to be primarily capturing deaths of people who experienced serious initial infection with the coronavirus and who survived that phase but went on to have organ damage and other severe complications. He said other deaths related to long Covid should be studied, including deaths by suicide of people who had devastating post-Covid symptoms.Another report published on Wednesday, by the Documenting Covid-19 project, offered a snapshot of deaths related to long Covid by looking at death certificates in 2020 and 2021 in Minnesota, New Mexico and a few other locations. That report, conducted by the Brown Institute for Media Innovation at Columbia University and MuckRock, a public records foundation, found that 18 of the 28 deaths associated with long Covid in Minnesota during those years were in people over 80 years old and that most of the patients had worked in blue-collar jobs and lacked a college degree. In New Mexico, about a third of the 13 deaths related to long Covid were in people under 60, and some were frontline or essential workers, the report said.Experts evaluating the C.D.C. study cautioned that it was both an incomplete picture of mortality linked to long Covid and of the larger toll of the condition, which has been estimated by the Government Accountability Office to have affected 7.7 million to 23 million people in the United States.“This is an important thing to explore and study, but it shouldn’t be used as a proxy for saying, Oh, well, long Covid isn’t that severe because look how few deaths there are,” Dr. Putrino said. “We should not be measuring the damage that long Covid does by deaths alone.”

Researchers have characterised prostate cancer cell dynamics at a single-cell resolution across the timespan of the disease — from its beginning to the point of androgen independence, where the tumour no longer responds to hormone deprivation therapy.
Their study in mice, published today in eLife, reveals an expansion of intermediate cells that occurs in prostate cancer, which correlates with resistance to treatment and poor clinical outcomes in humans. These cells are castration-resistant, meaning they continue to grow in the absence of testosterone and could explain how prostate tumours become resistant to hormone-related treatments.
Prostate cancer is the most diagnosed form of cancer, and the second-leading cause of cancer-related deaths in males from the US. This is in large part due to an incomplete knowledge of the cellular drivers behind the disease’s progression and the risk of progressing to castration resistant prostate cancer (CRPC).
The prostate gland epithelium — a type of body tissue that forms the surface of glands and organs — is typically composed of two types of epithelial cells: basal cells and highly-differentiated luminal cells (cells which have altered in form). However, a more stem-like, castration-resistant intermediate of the luminal cells has previously been proposed.
“It has been suggested that normal luminal cells are able to transition into these progenitor cells under castrate conditions,” says lead author Alexandre Germanos, a PhD candidate in Molecular and Cellular Biology at the University of Washington, US, and a graduate student at the Division of Human Biology, Fred Hutchinson Cancer Center, US. “There is evidence that these cells contribute to the initial development of tumours in the prostate and resistance to treatment in advanced cancers, although this is yet to be confirmed in other models of CRPC.”
To study this further, Germanos and colleagues used a mouse model of CRPC to create an ‘atlas of prostate cellular composition and evolution’ through the course of the disease.

Many Americans think of gout as a disease from a bygone era, akin to rickets or scurvy. The condition commonly afflicted the rich and royal, including American historical figures such as Benjamin Franklin and Thomas Jefferson.
Gout is indeed one of the earliest known diseases, first identified by the ancient Egyptians around 2640 BC. But the disease is more prevalent now than ever, affecting more than 10 million people in the United States or approximately 5 percent of the adult population.
Gout is the most common form of inflammatory arthritis, in which urate (a byproduct of purine-rich foods like meat and alcohol) builds up in the body and forms needle-shaped crystals in and around the joints, usually starting in the foot. The crystal deposits lead to flares of severe pain, joint swelling and tenderness, and can progress to chronic joint damage that limits patients’ movement and quality of life.
Excess urate circulating in the blood (known as hyperuricemia) has long been considered the major cause of gout, but counterintuitively, most people with high urate levels do not actually develop the disease. In fact, asymptomatic hyperuricemia is approximately four times more prevalent than gout. Gout patients also show mysteriously higher levels of urate in their joint fluid compared to their blood. Thus hyperuricemia must not be the only thing stimulating urate crystal deposition in the joints. So what else could be causing the disease?
In a new study published online on December 1, 2022 in Arthritis & Rheumatology, an international research team led by University of California San Diego School of Medicine identified a novel molecular pathway that causes gout and its progression to joint tissue erosion. The findings position lubricin, a protein found in joint fluid, as a novel therapeutic target for both the prevention and treatment of the disease.
The scientists were interested in exploring the genetic factors that lead not to high levels of circulating urate, but specifically to urate production and crystal deposition within joints. To do this, they studied a rare case of gout in which the patient had developed urate crystal deposits and erosion in her joints but did not show high levels of urate in her blood.
“This naturally occurring and extremely unusual disorder provided a unique opportunity to look at gouty arthritis through a different lens, and understand what molecular processes contribute to the disease independent of hyperuricemia,” said senior author Robert Terkeltaub, MD, professor at UC San Diego School of Medicine and section chief of Rheumatology at the Veterans Affairs San Diego Healthcare System.
Using whole genome sequencing, RNA-sequencing and quantitative proteomic methods, the researchers were able to identify a major molecular pathway that was disrupted in the patient, centering on a significant reduction in lubricin. The mucinous protein provides essential lubrication and protection to joint tissues, and regulates the function of a specific type of white blood cell that promotes inflammation in the joint.
Additional experiments confirmed that under healthy conditions, lubricin suppresses the secretion of urate and xanthine oxidase (an enzyme that produces urate) by activated white blood cells, and also blocks urate from crystallizing in the joint. The researchers then assessed several patients with the common form of gout and confirmed that they too had markedly decreased levels of lubricin.
The authors suggest that whether or not a hyperacemia patient goes on to develop gout may thus be influenced by which gene variants they have for lubricin and other molecules that control its production or degradation in the joint.
“Our findings show that lubricin may be a new biomarker for tracing patients’ risk of developing gout, and that new drugs to maintain and increase lubricin could limit the incidence and progression of gouty arthritis,” said Terkeltaub.
Co-authors include: Leigh-Ana Rossitto, Ru LiuBryan, Majid Ghassemian, Anaamika Campeau and David J. Gonzalez at UC San Diego; Marin Miner at Veterans Affairs San Diego Healthcare System; Khaled Elsaid and Sandy Elsayed at Chapman University; Amanda Phipps-Green, Tony R. Merriman and Murray Cadzow at University of Otago; Jacob Karsh at University of Ottawa; Gregory D. Jay at Rhode Island Hospital; Marwa Qadri at Jazan University; Talia J. Dambruoso at Brown University; Tannin Schmidt at University of Connecticut Health Center; Nicola Dalbet and Ashika Chhana at University of Auckland; Jennifer Höglund at University of Gothenburg; Nancy Maltez at Ottawa Riverside Hospital; and Niclas G. Karlsson at Oslo Metropolitan University.
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Materials provided by University of California – San Diego. Original written by Nicole Mlynaryk. Note: Content may be edited for style and length.

A new study has found that young Brits would be willing to change to a more sustainable diet, but a lack of understanding about what that actually means is preventing many from doing so.
Many people are also uncertain about what changes they should make.
Sustainable diets are defined by the UN as “diets with low environmental impacts which contribute to food and nutrition security and to healthy life for present and future generations.”
Previous research has suggested that 20-30% of environmental impacts in Europe and the UK originate from our diets, including impacts from food production, processing and retail. It is also now widely accepted that the consumption of meat and animal products typically has a higher environmental impact than plant-based foods.
“When thinking about how to live more sustainably, people seem to understand that this can mean taking fewer flights, using the car less, recycling more, but it seems that not everyone is aware of the difference that changing their diet can make as well,” explained Katherine Appleton, Professor of Psychology at Bournemouth University, who led the study.
For this new study, researchers from Bournemouth University interviewed twenty-one mostly young adults from a range of households and with different cooking responsibilities — from cooking for everyone in the house, to living with others who do all the cooking for them.

In a global study, researchers have identified that most reservoirs of rodent-borne diseases tend to live exclusively or occasionally in or near human dwellings, show large fluctuations in their numbers, and/or are hunted for meat or fur.
The COVID-19 pandemic has stressed the need to better understand the transmission routes of animal-spread diseases. The study demonstrates how the risk of pathogen transmission from animals to humans is driven by the interplay between natural and human-caused factors.
Rodents’ “fast life” with sexual maturity at early age, many litters per year and numerous young per litter is an important explanation why rodents are important reservoirs for pathogens. But why do humans get infected by rodent-borne pathogens?
“Most rodents that spread zoonotic pathogens, meaning pathogens spreading between animals and humans, show large population fluctuations, move at least occasionally indoors, or are hunted for meat or fur. Our results were consistent among pathogen types i.e., virus, bacteria, fungi, and parasites. And with transmission modes, i.e., intermediate, involvement of vectors or non-close and close contact, with close contact including inhalation of contaminated aerosols,” says Frauke Ecke, project leader and Professor at University of Helsinki, Finland and senior lecturer at Swedish University of Agricultural Sciences (SLU).
Global study on 436 rodent species
In the study published in Nature Communications, researchers from SLU, University of Helsinki and Cary Institute of Ecosystem Studies, USA, performed a global quantitative study based on data collected from research papers and databases. The study includes 436 rodent species of which 282 are all known reservoirs of zoonotic pathogens. The researchers studied the linkage among the rodents’ choice of environment, variation in numbers i.e., population fluctuations, humans’ hunting of rodents, and the status of rodents as reservoirs.
“It is remarkable how consistent the results are among continents, disease systems and rodent species,” says Rick Ostfeld, co-leader of the study.
Some areas of the world are more risky to get zoonoses from rodents
In addition, the researchers have identified regions where transmission risk between rodents and humans is high. Large parts of Europe, especially central and northern Europe, a wide stretch extending from eastern Europe to eastern Asia, eastern China, parts of South America, south-east Australia, and eastern regions in North America are at high risk.
“If people encounter a rodent in these regions, there is a high risk that this rodent carries zoonotic pathogens,” says Ecke.
Examples of such pathogen carrying rodents include the bank vole in Europe, the North American deer mouse, and Azara’s Grass Mouse in South America. These species show large population fluctuations and can also move indoors.
“It is especially the large population fluctuations together with the disturbance of the rodents’ natural habitat that can explain why rodents move nearby and into human dwellings. This movement behaviour is typical for so-called generalists, which are species that can cope with many different environments. These generalists are the most important reservoirs of pathogens,” explains Ecke.

Wearable fitness devices offer new insights into the relationship between physical activity and type 2 diabetes, according to a new analysis of the National Institutes of Health’s All of Us Research Program data published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
Type 2 diabetes is the most common form of the disease, affecting 90% to 95% of people with diabetes. In type 2 diabetes, the body is resistant to the action of insulin, meaning it cannot use insulin properly, so it cannot carry sugar into the cells. Type 2 diabetes most often develops in people over age 45, but more and more children, teens and young adults are being diagnosed.
“We investigated the relationship between physical activity and type 2 diabetes with an innovative approach using data from wearable devices linked to electronic health records in a real-world population,” said Andrew S. Perry, M.D., of Vanderbilt University Medical Center in Nashville, Tenn. “We found that people who spent more time in any type of physical activity had a lower risk of developing type 2 diabetes. Our data shows the importance of moving your body every day to lower your risk of diabetes.”
The researchers analyzed Fitbit data and type 2 diabetes rates from 5,677 participants included in the NIH’s All of Us Research Program between 2010-2021. All of Us is part of an effort to advance individualized health care by enrolling one million or more participants to contribute their health data over many years. About 75% of the participants that the researchers studied were female.
They found 97 new cases of diabetes over a follow-up of 4 years in the data set. People with an average daily step count of 10,700 were 44% less likely to develop type 2 diabetes than those with 6,000 steps.
“We hope to study more diverse populations in future studies to confirm the generalizability of these findings,” Perry said.
The other authors of this study are Jeffrey Annis, Hiral Master, Aymone Kouame, Kayla Marginean, Ravi Shah and Evan Brittain of Vanderbilt University School of Medicine in Nashville, Tenn.; Matthew Nayor of Boston University School of Medicine in Boston, Mass.; Andrew Hughes and Dan M. Roden of Vanderbilt University Medical Center; Paul A. Harris of Vanderbilt University School of Medicine and Vanderbilt University Medical Center; Karthik Natarajan of Columbia University in New York, N.Y.; and Venkatesh Murthy of the University of Michigan in Ann Arbor, Mich.
The study received funding from the NIH.
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Materials provided by The Endocrine Society. Note: Content may be edited for style and length.

A large study that focused on whether exercise and mindfulness training could boost cognitive function in older adults found no such improvement following either intervention. Researchers at Washington University School of Medicine in St. Louis and the University of California, San Diego, studied the cognitive effects of exercise, mindfulness training or both for up to 18 months in older adults who reported age-related changes in memory but had not been diagnosed with any form of dementia.
The findings are published Dec. 13 in JAMA.
“We know beyond any doubt that exercise is good for older adults, that it can lower risk for cardiac problems, strengthen bones, improve mood and have other beneficial effects — and there has been some thought that it also might improve cognitive function,” said the study’s first author, Eric J. Lenze, MD, the Wallace and Lucille Renard Professor and head of the Department of Psychiatry at Washington University. “Likewise, mindfulness training is beneficial because it reduces stress, and stress can be bad for your brain. Therefore, we hypothesized that if older adults exercised regularly, practiced mindfulness or did both there might be cognitive benefits — but that’s not what we found.”
Lenze and his colleagues still want to see whether there may be some cognitive effects over a longer time period, so they plan to continue studying this group of older adults to learn whether exercise and mindfulness might help prevent future cognitive declines. In this study, however, the practices did not boost cognitive function.
“So many older adults are concerned about memory,” said senior author Julie Wetherell, PhD, a professor of psychiatry at UC San Diego. “It’s important for studies like ours to develop and test behavioral interventions to try to provide them with neuroprotection and stress reduction as well as general health benefits.”
The researchers studied 585 adults ages 65 through 84. None had been diagnosed with dementia, but all had concerns about minor memory problems and other age-related cognitive declines.