Evidence of horizontal gene transfer between human maternal microbiome and infant gut microbiome

 Researchers have discovered a new mode of vertical mother-to-infant microbiome transmission, where microbes in the maternal gut shared genes with microbes in the infant gut during the perinatal period starting immediately before birth and extending thought the first few weeks after birth. This horizontal gene transfer allowed maternal microbial strains to influence the functional capacity of the infant microbiome, in the absence of persistent transmission of the microbial strains themselves. Such a large-scale integrative analysis, presented December 22 in the journal Cell, provides a series of high-resolution snapshots of gut colonization dynamics that influence infant development both before and after birth.

"This is the first study to describe the transfer of mobile genetic elements between maternal and infant microbiomes," says senior study author Ramnik Xavier of the Broad Institute of MIT and Harvard. "Our study also, for the first time, integrated gut microbiome and metabolomic profiles from both mothers and infants and discovered links between gut metabolites, bacteria and breastmilk substrates. This investigation represents a unique perspective into the co-development of infant gut microbiomes and metabolomes under the influence of known maternal and dietary factors."

Gut bacteria promote the maturation of the immune system in part through the production of microbial metabolites. The development of the infant gut microbiome follows predictable patterns, starting with transmission of microbes from the mother at birth. In addition to immune system maturation, microbial metabolites also influence early cognitive development. The perinatal period represents a critical window for cognitive and immune system development, promoted by maternal and infant gut microbiota and their metabolites. Nevertheless, the co-development of microbiomes and metabolomes during the perinatal period and the determinants of this process are not well understood.

To address this knowledge gap, Xavier and his colleagues tracked the co-development of microbiomes and metabolomes from late pregnancy to one year of age using longitudinal multi-omics data from a cohort of 70 mother-infant dyads. They discovered large-scale mother-to-infant interspecies transfer of mobile genetic elements, frequently involving genes associated with diet-related adaptations. Infant gut metabolomes were less diverse than maternal metabolomes but featured hundreds of unique metabolites and microbe-metabolite associations not detected in mothers. Metabolomes and serum cytokine signatures of infants who received regular, but not extensively hydrolyzed, formula were distinct from those of exclusively breastfed infants.

"The infant gut harbored thousands of unique metabolites, many of which were likely modified from breastmilk substrates by gut bacteria," says Tommi Vatanen, co-first author on the study along with Karolina Jabbar, both of the Broad Institute of MIT and Harvard. "Many of these metabolites likely impact immune system and cognitive development."

Pregnancy was associated with an increase in steroid compounds, including gonadal hormone derivatives and intermediates of bile acid biosynthesis, several of which were independently linked to impaired glucose tolerance. Although infant gut metabolomes were less diverse than maternal metabolomes, the researchers detected more than 2,500 infant-unique metabolomic features. Moreover, they identified numerous infant-specific associations of bacterial species and fecal metabolites, including neurotransmitters and immune modulators.

"We were surprised to find that maternal gut bacteria that were rarely observed in infants contributed to the infant gut microbiome structure," says Xavier "We also found evidence that prophages -- dormant bacteriophages, or viruses that reside on bacterial genomes -- contribute to the exchange of mobile genetic elements between maternal and infant microbiomes."

The authors say that the maternal microbiome may shape the infant gut microbiome through horizontal gene transfer, apart from classical vertical transmission of strains and species. Moreover, the identification of distinctive metabolomic profiles and microbe-metabolite interactions in the infant gut constitutes a platform for further study of microbial contributions to infant development.

One study limitation was that the researchers did not consider changes in diet and lifestyle between pregnancy and the postpartum period, which may have affected microbiome and metabolome alterations. In future studies, they plan to further explore linkages between bacteria and metabolites and investigate strain-specific bacterial metabolic output using isolated bacteria in vitro.

"Taken together, our integrative analysis expands the concept of vertical transmission of the gut microbiome and provides new insights into the development of maternal and infant microbiomes and metabolomes during late pregnancy and early life," Xavier says.

This work was funded by the National Institutes of Health, the Juvenile Diabetes Research Foundation, the Center for Microbiome Informatics and Therapeutics, and the Wallenberg Foundations. Xavier is co-founder of Jnana Therapeutics and Celsius Therapeutics, Board Director at MoonLake Immunotherapeutics, and consultant to Nestlé; these organizations had no role in the study. All other authors declare no competing interests.

Source: Science Daily

Cystic fibrosis drug could help treat pneumonia

 Pathogens such as SARS-CoV-2 and pneumococcus can cause severe pneumonia. If the airways then fill with fluid, the patient risks developing acute respiratory distress syndrome. Researchers at Charité -- Universitätsmedizin Berlin have now discovered the molecular mechanisms that trigger fluid accumulation in the lungs. This also led them to discover a potential new therapy: A cystic fibrosis drug proved effective in their laboratory experiments, raising hope that this could be used to treat pneumonia regardless of the pathogen that caused it. The study has been published in the journal Science Translational Medicine.

Pneumonia is the most common cause of fluid buildup in the lungs. This condition, known as pulmonary edema, results in parts of the airspaces filling with fluid instead of air, which prevents them from doing their job of exchanging gases. Patients struggle to breath and their body can't get enough oxygen. The diagnosis is acute respiratory distress syndrome, or ARDS. "Despite cutting-edge medical procedures, roughly 40 percent of patients with ARDS die in intensive care. The problem is that antibiotics, antivirals, and immune modulating therapies rarely work well enough," says study leader Prof. Dr. Wolfgang Kuebler, Director of the Institute of Physiology at Charité. "That's why we took a very different approach in our study. Instead of focusing on the pathogen, we focused on strengthening the barrier function of the blood vessels in the lungs." This makes sense, as they are the source of the fluid in pulmonary edema. The lung vessels become permeable, allowing fluid from the blood to flow into the surrounding tissue -- and thereby flood the airspaces.

But what actually causes this? What are the underlying molecular mechanisms? A Charité research team led by Prof. Kuebler set out to answer these questions. They performed experiments using cells, lung tissue, and isolated lungs. The study centered on the CFTR chloride channel, which scientists know is mainly found in the mucosal cells of our airways. There, it plays a major role in keeping our mucus thin so it can drain away easily. The researchers have now shown for the first time that cells in the blood vessels of the lungs also have CFTR and that its presence is drastically reduced in pneumonia.

To find out what role CFTR plays in the pulmonary vessels and what is happening at the molecular level when the chloride channel is lost, the researchers blocked the channel with an inhibitor and dictated the number of chloride ions in the cells. They then used a special imaging technique known as immunofluorescence imaging: "We saw that inhibiting CFTR triggered a molecular cascade that ultimately causes the lung's blood vessels to begin leaking," says Dr. Lasti Erfinanda, who also works at the Institute of Physiology and is the study's lead author. "So CFTR actually does play a very key role in the development of pulmonary edema."

The study findings indicate that the loss of CFTR causes chloride to accumulate in the cells because it stops being transported out of them. The excess chloride triggers signaling that ends with an uncontrolled flow of calcium into the cells via a calcium channel. "The increased calcium concentration then causes the vascular cells to contract -- much like the effect that calcium has on muscle cells," explains Prof. Kuebler. "This results in gaps between the cells -- which allows fluid to spill out of the blood vessels. Chloride channels are therefore crucial in maintaining the barrier function of the pulmonary vessels."

The research team then addressed another question: How could they attenuate or prevent the pneumonia-induced loss of chloride channels in the pulmonary vessels? To answer this, the researchers used a therapeutic agent that is classed as a CFTR modulator and currently used to treat cystic fibrosis. In cystic fibrosis patients, a genetic mutation prevents the CFTR chloride channel from working properly in the mucosal cells of the airways, resulting in very viscous mucus. "Ivacaftor is a drug that increases the chances of the chloride channel opening, which helps the mucus to flow through the airways," says Dr. Erfinanda. "We wanted to see if it would also have a positive effect on the cells in the blood vessels of the lungs."

Ivacaftor did make the chloride channels more stable: it led to less degradation in the channels than that typically caused by the lung's inflammatory processes. Experiments on animal models showed the same effect: treatment with ivacaftor increased the probability of surviving severe pneumonia, reduced lung injury, and resulted in much milder symptoms and a much better general condition than without the drug. "We really weren't expecting it to work so well," says Prof. Kuebler. "We hope our findings will pave the way for clinical trials to test the efficacy of CFTR modulators in pneumonia patients. If this promising, pathogen-independent therapy finds its way into clinical practice, it could benefit a huge number of patients and prevent pneumonia from becoming life-threatening -- even in the case of unknown pathogens."

Prof. Kuebler and his team are now planning research projects aimed at developing other potential therapies based on the CFTR signaling pathway. They are also going to research which patients have an elevated risk of developing ARDS, so they can provide these patients with preventive, personalized treatment.

Source: SciencDaily

COVID-19 booster increases durability of antibody response, research shows

 New research from the University of Virginia School of Medicine speaks to the benefits of a COVID-19 booster.

The new findings shed light on how mRNA boosters -- both Pfizer and Moderna -- affect the durability of our antibodies to COVID-19. A booster, the researchers report, made for longer-lasting antibodies for all recipients, even those who have recovered from a COVID-19 infection.

"These results fit with other recent reports and indicate that booster shots enhance the durability of vaccine-elicited antibodies," said senior researcher Jeffrey Wilson, MD, PhD, of UVA Health's Division of Asthma, Allergy and Immunology.

Tracking COVID-19 antibodies

Wilson and his collaborators looked at antibody levels following a booster in 117 UVA employee volunteers and compared those results with the levels seen in 228 volunteers after their primary vaccination series. Antibody levels one week to 31 days after the primary series and booster were similar, but the boosted antibodies stuck around longer regardless of whether the person had had COVID-19.

"Our initial thought was that that boosters would lead to higher antibody levels than the primary vaccine series, but that was not what we found," said researcher Samuel Ailsworth, the first author of a new scientific paper outlining the findings. "Instead, we found that the booster led to longer lasting antibodies."

Antibody levels naturally decline over time after an infection or after vaccination, but higher levels are thought to be more protective. Thus, longer-lasting antibodies would be expected to provide more sustained immunity against severe COVID-19.

The researchers found that the antibodies generated by the Moderna booster proved longer lasting than those generated by the Pfizer booster. Moderna's antibody levels exceeded Pfizer's out to five months, the end of the study period. Although the findings were statistically significant, Wilson notes that both mRNA vaccine boosters provide enhanced and fairly similar levels of protection against COVID-19 in recently published large epidemiologic studies.

Because the frequency of COVID-19 infections in the community was relatively high when the boosters were being given, the authors also studied the effect of COVID-19 infection on antibody levels. The findings suggest that the "enhanced antibody durability observed after booster vaccination was not explained by hybrid immunity," the researchers report in their paper.

The new results are the latest from Wilson's team tracking the antibody response to the COVID-19 vaccines over time. The researchers previously found that after the primary vaccination series the antibodies generated by Pfizer's COVID-19 vaccine rose more slowly and declined more quickly than those generated by the Moderna vaccine. That study also found that older recipients of the Pfizer vaccine generated fewer antibodies than did younger recipients -- but this wasn't the case for Moderna, where age did not appear to be a factor.

In the latest results, younger booster recipients initially generated more antibodies than did older recipients, but this difference disappeared with time.

Wilson notes that this study adds to the accumulating evidence that boosters are an important of protecting the community from COVID-19. "Although only about half of the U.S. population that is eligible for a booster has received one, it is increasingly clear that boosters enhance the protection that is conferred by the primary series mRNA vaccines alone," he said.

Findings Published

The researchers have published their latest findings in the scientific journal Annals of Allergy, Asthma & Immunology. The team consisted of Samuel M. Ailsworth, Behnam Keshavarz, Nathan E. Richards, Lisa J. Workman, Deborah D. Murphy, Michael R. Nelson, Thomas A.E. Platts-Mills and Wilson. The researchers reported no financial interests in the work.

The research was supported by the UVA Manning COVID-19 Research Fund, an American Academy of Allergy, Asthma & Immunology Faculty Development Award and National Institutes of Health grant R37-AI20565.

Source: ScienceDaily

Common food dye can trigger inflammatory bowel diseases, animal study suggests

 Long-term consumption of Allura Red food dye can be a potential trigger of inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, says McMaster University's Waliul Khan. Researchers using experimental animal models of IBD found that continual exposure to Allura Red AC harms gut health and promotes inflammation.

The dye directly disrupts gut barrier function and increases the production of serotonin, a hormone/neurotransmitter found in the gut, which subsequently alters gut microbiota composition leading to increased susceptibility to colitis.

Khan said Allura Red (also called FD&C Red 40 and Food Red 17), is a common ingredient in candies, soft drinks, dairy products and some cereals. The dye is used to add colour and texture to foodstuffs, often to attract children.

The use of synthetic food dyes such as Allura Red has increased significantly over the last several decades, but there has been little earlier study of these dyes' effects on gut health. Khan and his team published their findings in Nature Communications. Yun Han (Eric) Kwon, who recently completed PhD in Khan's laboratory, is first author.

"This study demonstrates significant harmful effects of Allura Red on gut health and identifies gut serotonin as a critical factor mediating these effects. These findings have important implication in the prevention and management of gut inflammation," said Khan, the study's senior author, a professor of the Department of Pathology and Molecular Medicine and a principal investigator of Farncombe Family Digestive Health Research Institute.

"What we have found is striking and alarming, as this common synthetic food dye is a possible dietary trigger for IBDs. This research is a significant advance in alerting the public on the potential harms of food dyes that we consume daily," he said.

"The literature suggests that the consumption of Allura Red also affects certain allergies, immune disorders and behavioural problems in children, such as attention deficit hyperactivity disorder."

Khan said that IBDs are serious chronic inflammatory conditions of the human bowel that affect millions of people worldwide. While their exact causes are still not fully understood, studies have shown that dysregulated immune responses, genetic factors, gut microbiota imbalances, and environmental factors can trigger these conditions.

In recent years there has been significant progress in identifying susceptibility genes and understanding the role of the immune system and host microbiota in the pathogenesis of IBDs. However, similar advances in defining environmental risk factors have lagged, he said.

Khan said that environmental triggers for IBDs include the typical Western diet, which includes processed fats, red and processed meats, sugar and a lack of fibre. He added that the Western diet and processed food also includes large amounts of various additives and dyes.

He added that the study suggests a link between a commonly used food dye and IBDs and warrants further exploration between food dyes and IBDs at experimental, epidemiological and clinical levels.

The study was funded by the Canadian Institutes of Health Research.

Source: Science Daily

Scientists find key reason why loss of smell occurs in long COVID-19

 The reason some people fail to recover their sense of smell after COVID-19 is linked to an ongoing immune assault on olfactory nerve cells and an associated decline in the number of those cells, a team of scientists led by Duke Health report.

The finding, publishing online Dec. 21 in the journal Science Translational Medicine, provides an important insight into a vexing problem that has plagued millions who have not fully recovered their sense of smell after COVID-19.

While focusing on the loss smell, the finding also sheds light on the possible underlying causes of other long COVID-19 symptoms -- including generalized fatigue, shortness of breath, and brain fog -- that might be triggered by similar biological mechanisms.

"One of the first symptoms that has typically been associated with COVID-19 infection is loss of smell," said senior author Bradley Goldstein, M.D., Ph.D., associate professor in Duke's Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology.

"Fortunately, many people who have an altered sense of smell during the acute phase of viral infection will recover smell within the next one to two weeks, but some do not," Goldstein said. "We need to better understand why this subset of people will go on to have persistent smell loss for months to years after being infected with SARS-CoV2."

In the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analyzed olfactory epithelial samples collected from 24 biopsies, including nine patients suffering from long-term smell loss following COVID-19.

This biopsy-based approach -- using sophisticated single-cell analyses in collaboration with Sandeep Datta, M.D., Ph.D., at Harvard University -- revealed widespread infiltration of T-cells engaged in an inflammatory response in the olfactory epithelium, the tissue in the nose where smell nerve cells are located. This unique inflammation process persisted despite the absence of detectable SARS-CoV-2 levels.

Additionally, the number of olfactory sensory neurons were diminished, possibly due to damage of the delicate tissue from the ongoing inflammation.

"The findings are striking," Goldstein said. "It's almost resembling a sort of autoimmune-like process in the nose."

Goldstein said learning what sites are damaged and what cell types are involved is a key step toward beginning to design treatments. He said the researchers were encouraged that neurons appeared to maintain some ability to repair even after the long-term immune onslaught.

"We are hopeful that modulating the abnormal immune response or repair processes within the nose of these patients could help to at least partially restore a sense of smell," Goldstein said, noting this work is currently underway in his lab.

He said the findings from this study could also inform additional research into other long-COVID-19 symptoms that might be undergoing similar inflammatory processes.

In addition to Goldstein and Datta, study authors include John B. Finlay, David H. Brann, Ralph Abi-Hachem, David W. Jang, Allison D. Oliva, Tiffany Ko, Rupali Gupta, Sebastian A. Wellford, E. Ashley Moseman, Sophie S. Jang, Carol H. Yan, Hiroaki Matusnami, and Tatsuya Tsukahara.

The study received funding support from the National Institutes of Health (DC018371, DC016859, AG074324, DC019956) and the Duke Department of Head and Neck Surgery & Communication Sciences.

Source: ScienceDaily

Infant gene therapy is a breakthrough for Artemis-SCID patients

 Ten young children born without functioning immune systems and lacking the ability to fight infections are on track for healthier lives thanks to a new gene therapy treatment pioneered at UC San Francisco, reports a Dec. 22 study in the New England Journal of Medicine.

The children have Artemis-SCID, a very rare genetic disorder that is typically treated with a bone marrow transplant from a healthy donor, ideally a matched brother or sister. The new gene therapy allows researchers to treat newly diagnosed babies with their own cells -- adding a healthy copy of the Artemis gene to the baby's harvested marrow stem cells, then infusing the corrected stem cells back into their bodies -- in hopes of avoiding many of the short- and long-term complications of the standard treatment, including death.

The children in the trial -- all under the age of 5 -- are living at home with their families, attending daycare and preschool, playing outside, and living normal lives, said Mort Cowan, MD, UCSF pediatrics professor and the trial's lead investigator.

"Already, the course of their illness is so much better than with the typical treatment," said Cowan, who has treated more than 30 children with Artemis-SCID using standard bone marrow transplants. "I've never seen results like this in any of the other kids. It's amazing."

Gene correction has been used before in patients with other genetic forms of SCID, but its use in Artemis-SCID is significant because these patients usually respond more poorly to standard bone marrow transplants. Complications can include rejecting the marrow graft, graft-vs.-host disease -- in which the donor T cells attack the recipient's tissues -- chronic infections leading to organ damage, stunted growth, and premature death.

Signs of Stronger Immunity

The first outcome of the Phase I/II trial involved the safe transfusion of gene-corrected cells that would differentiate into white blood cells by 42 days after infusion. Researchers theorized patients would need less chemotherapy to prepare their marrow for transfusion when their own cells were being used; thus only 25% of a full dose of busulfan was administered. The second outcome was T-cell reconstitution at 12 months, a measurement of the strength of the immune system.

All 10 patients were safely transfused with their own gene-corrected stem cells that gave rise to corrected peripheral blood cells within 42 days. All 10 were growing their own T cells and B cells by 12 weeks, and four of nine (excluding a patient who received a second treatment) achieved full T-cell immune reconstitution by 12 months. Four of nine also achieved full B cell immunity by 24 months, allowing them to discontinue immunoglobulin replacement and receive standard childhood vaccinations. An additional three patients, who were followed for fewer than 24 months, had promising B cell development when compared to previous outcomes for donor-transplanted patients.

One child required a second infusion of gene-corrected bone marrow due to a persistent infection with cytomegalovirus prior to gene therapy but is now infection free with good T- and B-cell immunity. "All of the results are better than those previously seen with Artemis-SCID patients who received donor bone marrow transplants," noted Jennifer Puck, MD, UCSF pediatrics professor and co-lead investigator in the study.

"Having patients in the trial achieve full T-cell immunity is outstanding. B-cell recovery takes longer, but so far it looks as if the patients also have a far better chance for B-cell reconstitution than they would with a regular bone marrow transplant," Puck said. "Successfully using less chemotherapy is also a big win, minimizing the harmful side effects of full dose busulfan in small infants."

Better B-cell immunity could help avoid issues such as chronic lung disease that often develop later in childhood for Artemis-SCID patients who receive a standard bone marrow transplant, Cowan added.

The children in the trial are currently between the ages of 18 months and 4.5 years; nine were born in the U.S. and were diagnosed following newborn screening for SCID; one was born in Canada and diagnosed at five months of age with clinical illness. Four patients are of Navajo/Apache Native American descent, where the Artemis-SCID mutation is more common. Median follow-up was 31.2 months. At the time of study publication, six patients had been followed for at least 24 months.

"We're pioneering gene therapy in this very rare disease right now, but we are using techniques that can be exported to other situations and can help many other conditions worldwide," said Puck. "Every new innovation happens one patient at a time."

Co-authors: Also contributing to this research from UCSF were: Jason Yu, PhD; Carol Fraser-Browne, BA; Ukina Sanford, MS; Misako Kawahara, BA; Wendy Chan, BS; Shivali Chag, MS; and Robert Currier, PhD, of the UCSF Department of Pediatrics; Jess Oh, MS, of the UCSF Benioff Children's Hospital San Francisco; Jasmeen Dara, MD; Janelle Facchino, NP; Christopher Dvorak, MD, of the UCSF Department of Pediatrics and UCSF Benioff Children's Hospital San Francisco; Joan Hilton, DSc, MPH, of the UCSF Department of Epidemiology and Biostatistics; and Janel Long-Boyle, PharmD, PhD, of UCSF's Department of Pediatrics, School of Pharmacy and UCSF Benioff Children's Hospital San Francisco. Please refer to the paper for additional co-authors.

Source: ScienceDaily

Researchers use 3D bioprinting to create eye tissue

 Scientists used patient stem cells and 3D bioprinting to produce eye tissue that will advance understanding of the mechanisms of blinding diseases. The research team from the National Eye Institute (NEI), part of the National Institutes of Health, printed a combination of cells that form the outer blood-retina barrier -- eye tissue that supports the retina's light-sensing photoreceptors. The technique provides a theoretically unlimited supply of patient-derived tissue to study degenerative retinal diseases such as age-related macular degeneration (AMD).

"We know that AMD starts in the outer blood-retina barrier," said Kapil Bharti, Ph.D., who heads the NEI Section on Ocular and Stem Cell Translational Research. "However, mechanisms of AMD initiation and progression to advanced dry and wet stages remain poorly understood due to the lack of physiologically relevant human models."

The outer blood-retina barrier consists of the retinal pigment epithelium (RPE), separated by Bruch's membrane from the blood-vessel rich choriocapillaris. Bruch's membrane regulates the exchange of nutrients and waste between the choriocapillaris and the RPE. In AMD, lipoprotein deposits called drusen form outside Bruch's membrane, impeding its function. Over time, the RPE break down leading to photoreceptor degeneration and vision loss.

Bharti and colleagues combined three immature choroidal cell types in a hydrogel: pericytes and endothelial cells, which are key components of capillaries; and fibroblasts, which give tissues structure. The scientists then printed the gel on a biodegradable scaffold. Within days, the cells began to mature into a dense capillary network.

On day nine, the scientists seeded retinal pigment epithelial cells on the flip side of the scaffold. The printed tissue reached full maturity on day 42. Tissue analyses and genetic and functional testing showed that the printed tissue looked and behaved similarly to native outer blood-retina barrier. Under induced stress, printed tissue exhibited patterns of early AMD such as drusen deposits underneath the RPE and progression to late dry stage AMD, where tissue degradation was observed. Low oxygen induced wet AMD-like appearance, with hyperproliferation of choroidal vessels that migrated into the sub-RPE zone. Anti-VEGF drugs, used to treat AMD suppressed this vessel overgrowth and migration and restored tissue morphology.

"By printing cells, we're facilitating the exchange of cellular cues that are necessary for normal outer blood-retina barrier anatomy," said Bharti. "For example, presence of RPE cells induces gene expression changes in fibroblasts that contribute to the formation of Bruch's membrane -- something that was suggested many years ago but wasn't proven until our model."

Among the technical challenges that Bharti's team addressed were generating a suitable biodegradable scaffold and achieving a consistent printing pattern through the development of a temperature-sensitive hydrogel that achieved distinct rows when cold but that dissolved when the gel warmed. Good row consistency enabled a more precise system of quantifying tissue structures. They also optimized the cell mixture ratio of pericytes, endothelial cells, and fibroblasts.

Co-author Marc Ferrer, Ph.D., director of the 3D Tissue Bioprinting Laboratory at NIH's National Center for Advancing Translational Sciences, and his team provided expertise for the biofabrication of the outer blood-retina barrier tissues "in-a-well," along with analytical measurements to enable drug screening.

"Our collaborative efforts have resulted in very relevant retina tissue models of degenerative eye diseases," Ferrer said. "Such tissue models have many potential uses in translational applications, including therapeutics development."

Bharti and collaborators are using printed blood-retina barrier models to study AMD, and they are experimenting with adding additional cell types to the printing process, such as immune cells, to better recapitulate native tissue.

Source: ScienceDaily

Does sex provide health benefits?

Sex may give a boost to certain aspects of people’s well-being and physical health, some research suggests. However, several studies on the subject are now outdated, and not all potential benefits apply to everyone.

Scientific research has highlighted several possible benefits besides procreation that come with sexual intercourse. These pluses include preserving heart health in some people, reducing blood pressure, and boosting immunity.

Sex can also improve mood, relationships, and mental well-being.

In this article, we look at the possible health benefits of sex and highlight relevant research, focusing on the physical rather than emotional aspects.

Helping heart health

Partnered sex appears to have some protective effect on cardiovascular health, especially in women.

A 2016 study looked at the potential health benefits of sexual activity with a regular partner.

This research foundTrusted Source that sexually active women have a lower risk of cardiac events later in life.

However, the study also concluded that high levels of sexual activity might increase the risk of cardiovascular events in men. This conclusion contradicts most earlier research, and further studies are necessary to verify this risk.

Males and females with heart problems should ask a doctor about how much sex is safe for them. They should also be specific about the regularity and intensity with which they have sex, as this may affect the potential strain on the heart.

Reducing blood pressure

The same 2016 study also measured blood pressure as one of the markers of heart health. The researchers found that older women who expressed satisfaction with their sex lives were less likely to have high blood pressure.

However, the study authors did not find the same results in older men.

According to the American Heart Association (AHA), high blood pressure can affect both libido and a man’s ability to achieve and maintain an erection.

Medication for high blood pressure can also reduce libidoTrusted Source and cause erectile dysfunction.

While this does not confirm a benefit, it may show a link between blood pressure and sexual health.

Many people with high blood pressure, or hypertension, have safety concerns when it comes to sexual intercourse.

While it is always important to speak with a doctor, it is usually safe for people with high blood pressure to have sex.

If hypertension medication is causing sexual difficulties, a person can talk to their doctor who may be able to prescribe a different medication or dosage to relieve the adverse effects.

Boosting the immune system

Some early research found that regular sex increased the effectiveness of the immune system.

Researchers found that people who had frequent sex, which they defined as one to two times per week, had more immunoglobin A (IgA) in their system than others. IgA is an antibody that lives in the mucosal tissue, such as the salivary glands, nose, and vaginal tissue.

However, it is important to recognize that this study appeared in 2004, and researchers have not repeated it since. A new study might yield different results.

A more recent study looked at a small group of women to see if there were differences between the immune activity of those who were sexually active and those who are not.

The study examined their immune system’s ability to kill different infectious pathogens at various points in the menstrual cycle.

While the results suggest that there might be some differences between the groups, the authors say more research is necessary before drawing any conclusions.

Reducing prostate cancer risk

An early study, again from 2004, found that high frequency of ejaculation may reduce the risk of prostate cancer.

The study investigated almost 30,000 malesTrusted Source, looking at how often they ejaculated at different points in their life.

They concluded that those who ejaculated more than 21 times per month had a lower risk of prostate cancer than men who only ejaculated 4–7 times per month.

In 2016, the researchers extended this study for an additional 10 yearsTrusted Source to continue their research on the participants’ risk for developing prostate cancer.

This follow-up confirmed the initial findings. The males who ejaculated most frequently had a lower risk for prostate cancer those who ejaculated less often.

Relieving stress

Sex can serve as a natural way to relieve stress. A 2019 study looked at the effect that intimacy with a partner had on cortisol levels. Cortisol is a steroid hormone that circulates the body in response to stress.

The researchers found that expressions of intimacy, whether sexual or not, helped to bring cortisol levels in both males and female back within normal range.

Sex triggers the release of oxytocin, endorphins, and other “feel-good” hormones, which may be responsible for this stress reducing effect.

Here, learn more about stress.

Improving sleep

The National Sleep Foundation suggest that sexual activity has hormonal benefits for sleep.

The same hormones that reduce stress and anxiety are also responsible for inducing sleepiness. Sex leads to the release of oxytocin, dopamine, and endorphins throughout the body.

After a person has an orgasm, another hormone called prolactin starts to circulate. Prolactin induces feelings of satisfaction and relaxation.

Precautions

While sex can be a pleasurable and potentially healthful activity, it is essential to remember that sex without protection can pose a risk to overall health.

People who have sex without using contraceptives have a risk of sexually transmitted infections (STIs) and unplanned pregnancies. Using a condom or other contraceptive method can reduce the risk of these outcomes.

If a person has multiple partners, they can bring down the risk by reducing the number of people with whom they have sexual contact.

If sex becomes painful or causes bleeding, a person should talk to a healthcare professional.

Q:

Is sex addiction a real disease and can too much sex cause it?

A:

The American Association of Sexuality Educators, Counselors and Therapists (AASECT)
do not find sufficient empirical evidence to support the classification of sex addiction as a mental health disorder.

If you are feeling troubled by sexual urges, thoughts or behaviors that feel out of control, your relationships are being impacted, or any area of your life is being negatively affected, then it is best to seek professional help.

Trusted Source Answers represent the opinions of our medical experts. All content is strictly informational and should not be considered medical advice.

How does sex affect your brain?

Having sex can flavor our nights, and days, with sweet pleasure and excitement, relieving stress and worry. And, of course, sex has been key to ensuring that the human race lives on. In this article, we ask, “How does sex impact what happens in the brain?”

Sexual intercourse is known to impact the way in which the rest of our body functions.

Recent studies have shown that it can have an effect on how much we eat, and how well the heart functions.

As we have reported on Medical News Today, sex has been cited as an effective method of burning calories, with scientists noting that appetite is reduced in the aftermath.

Also, a study published in the Journal of Health and Social Behavior in 2016 found that women who have satisfying sex later in life might be better protected against the risk of high blood pressure.

Many of the effects of sex on the body are actually tied to the way in which this pastime influences brain activity and the release of hormones in the central nervous system.

Here, we explain what happens in the brain when we are sexually stimulated, and we look at how this activity can lead to changes in mood, metabolism, and the perception of pain.

Brain activity and sexual stimulation

For both men and women, sexual stimulation and satisfaction have been demonstrated to increase the activity of brain networks related to pain and emotional states, as well as to the reward system.

This led some researchers to liken sex to other stimulants from which we expect an instant “high,” such as drugs and alcohol.

The brain and penile stimulation

A 2005 studyTrusted Source by researchers at the University Medical Center Groningen in the Netherlands used positron emission tomography scans to monitor the cerebral blood flow of male participants while their genitals were being stimulated by their female partners.

The scans demonstrated that stimulating the erect penis increased blood flow in the posterior insula and the secondary somatosensory cortex in the right hemisphere of the brain, while decreasing it in the right amygdala.

The insulaTrusted Source is a part of the brain that has been tied to processing emotions, as well as to sensations of pain and warmth. Similarly, the secondary somatosensory cortexTrusted Source is thought to play an important role in encoding sensations of pain.

As for the amygdala, it is known to be involved in the regulation of emotions, and dysregulations of its activityTrusted Source have been tied to the development of anxiety disorders.

An older study from the same university — which focused on brain regions that were activated at the time of ejaculation — found that there was an increase in blood flow to the cerebellum, which also plays a key role in the processing of emotions.

The researchers liken the activation of the cerebellum during ejaculation to the pleasure rush caused by other activities that stimulate the brain’s reward system.

“Our results correspond with reports of cerebellar activation during heroin rush, sexual arousal, listening to pleasurable music, and monetary reward.”

The brain and the female orgasm

In a study of the female orgasm that was conducted last year, scientists from Rutgers University in Newark, NJ, monitored the brain activity of 10 female participants as they achieved the peak of their pleasure — either by self-stimulation or by being stimulated by their partners.

The regions that were “significantly activated” during orgasm, the team found, included part of the prefrontal cortex, the orbitofrontal cortex, the insula, the cingulate gyrus, and the cerebellum.

These brain regions are variously involved in the processing of emotions and sensations of pain, as well as in the regulation of some metabolic processes and decision-making.

Another study previously covered on MNT suggested that the rhythmic and pleasurable stimulation associated with orgasm puts the brain in a trance-like state. Study author Adam Safron compares the effect of female orgasms on the brain to that induced by dancing or listening to music.

“Music and dance may be the only things that come close to sexual interaction in their power to entrain neural rhythms and produce sensory absorption and trance,” he writes.

“That is,” he adds, “the reasons we enjoy sexual experiences may overlap heavily with the reasons we enjoy musical experience, both in terms of proximate (i.e. neural entrainment and induction of trance-like states) and ultimate (i.e. mate choice and bonding) levels of causation.”

Sex and hormonal activity

So what does this all mean? In essence, it means that sex can impact our mood — normally for the better, but sometimes for the worse.

Having sex has repeatedly been associated with improved moods and psychological, as well as physiological, relaxation.

The reason behind why we may feel that stress impacts us less after a session between the sheets is due to a brain region called the hypothalamus.

The hypothalamus dictates the release of a hormone called oxytocin.

Higher levels of oxytocin can make us feel more relaxed, as studies have noted that it can offset the effects of cortisolTrusted Source, the hormone linked with an increased state of stress.

Not only does oxytocin make us calmer, but it also dampens our sense of pain. A study from 2013 found that this hormone could relieve headachesTrusted Source in individuals living with them as a chronic condition.

Another study from 2013 suggested that a different set of hormones that are released during sexual intercourse — called endorphins — can also relieve the pain associated with cluster headaches.

Can sex also make us feel down?

The answer to that, unfortunately, is “yes.” While sex is generally hailed as a great natural remedy for the blues, a small segment of the population actually report an instant down rather than an instant high after engaging in this activity.

This condition is known as “postcoital dysphoria,” and its causes remain largely unknown. One study conducted in 2010 interviewed 222 female university students to better understand its effects.

Of these participants, 32.9 percent said that they had experienced negative moods after sex.

The team noted that a lifelong prevalence of this condition could be down to past traumatic events. In most cases, however, its causes remained unclear and a biological predisposition could not be eliminated.

“This draws attention to the unique nature of [postcoital dysphoria], where the melancholy is limited only to the period following sexual intercourse and the individual cannot explain why the dysphoria occurs,” the authors write.

Sex may lead to better sleep

Studies have shown that sexual intercourse can also improve sleep. After an orgasm, the body also releases higher levels of a hormone called prolactinTrusted Source, which is known to play a key roleTrusted Source in sleep.

Researchers from Central Queensland University in Australia also hypothesized that the release of oxytocin during sex may act as a sedative, leading to a better night’s sleep.

In the case of men, ejaculation has been found to reduce activity in the prefrontal cortex, which is a brain region known to benefit particularly from a good night’s sleep.

In sleep, the prefrontal cortex exhibits the slowest brainwave activity compared with other brain regions, which supports the proper execution of cognitive functions during the daytime.

Researchers say that sex may lead to better cognitive functioning in older age, protecting people from memory loss and other cognitive impairments. Studies have shown that “older men who are sexually active […] have increased levels of general cognitive function.”

For women, being sexually active later in life appears to sustain memory recall, specifically. These effects may be due to the action of hormones such as testosterone and oxytocin, which are influenced by intercourse.

So, next time you’re about to slip between the sheets with that special someone, just know that this moment of passion will spark a whole neural firework show, releasing a special hormonal cocktail that will, at its best, charge a whole set of biological batteries.

Source - Medical News Today