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Some parents avoid giving their kids fruit juice, for fear that it might rot their teeth.

But the bad effects of juice on a child’s oral health could be short-lived, thanks to the remarkable properties of saliva, according to a new study.

Saliva protects teeth and gums from bacteria by creating a slippery film on teeth, and also can help repair early damage to tooth enamel, researchers said.

Sipping some apple juice temporarily disrupts this protection, but the effect begins to wear off within 10 minutes, researchers reported Sept. 3 in the journal PLOS One.

In fact, researchers found that water causes greater initial disruption to saliva’s protective properties, although recovery is much faster.

“We were genuinely surprised by these results,” lead researcher Mahdi Mutahar said in a news release. He’s a senior lecturer in dentistry with the University of Portsmouth’s School of Dental, Health and Care Professions in the United Kingdom.

“It’s long been believed that apple juice, like other acidic drinks, immediately harms our oral health, including the teeth,” he said. “However, our research shows that saliva plays a vital role in protecting and quickly repairing the mouth to prevent lasting damage.”

There’s a “but,” however.

“But it’s important to point out that long-exposure to apple juice — by repeatedly drinking it or not washing your mouth out with water after taking a sip — can have a long-term negative effect on our oral hygiene,” Mutahar added.

For the study, researchers asked 32 healthy college students and staff to rinse their mouths with apple juice for one minute, then repeat the process with tap water.

The team used cutting-edge lab techniques to measure how slippery and protective saliva is before and after drinking both beverages.

Results showed that key proteins found in saliva are affected when a person drinks apple juice, but that mucins — spit’s main lubricating proteins — remain stable.

After one swig of apple juice, lubrication returns to normal as mucins resume their slippery protective work, researchers said.

“The biggest shock though was discovering that rinsing mouths with tap water actually caused more friction and disruption than apple juice,” Mutahar said.

Portsmouth tap water contains high concentrations of sodium, potassium and magnesium, which interfered with mucins, lab tests revealed.

“The Portsmouth water we used contains minerals that seem to interfere with saliva’s lubricating proteins, more than the fruit juice did,” Mutahar said.

These results suggest that drinking fruit juice now and then might not be immediately damaging, thanks to how saliva works.

But chugging fruit juice throughout the day could overwhelm the natural defense provided by saliva, affecting oral health, researchers warned.

“Think of it like a cut on your skin,” Mutahar said. “Your body can heal small, occasional damage quite well, but if you keep reopening the wound, it becomes a problem. The same principle applies here.”

Researchers recommend that children and adults who want to drink some fruit juice should:

Drink the juice quickly, rather than sipping slowly.

Rinse with water immediately afterward, to remove lingering acids and sugars.

Use a straw to reduce contact between the juice and teeth.

Give your mouth time to recover between juice drinks.

The research team is now exploring what happens if people drink juice several times a day. Future research could look at whether adding protective proteins like mucins to everyday drinks could protect people’s teeth and gums.

More information

The University of Pennsylvania has more on juice and tooth health.

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Backed by NOK 50 million (~USD 5 million) from the Mohn Foundation in partnership with the University of Bergen (UiB) and Haukeland University Hospital, the Center will unite clinicians, neuroscientists, and data experts to understand who is at risk, how disease begins, and how to protect the brain before irreversible damage occurs. 

A cornerstone of the Center is research on REM sleep behavior disorder (RBD) – a sleep condition in which people act out their dreams. Many individuals with RBD already have very early, so called prodromal, disease changes in their brain and a substantially increased risk of later developing full blown PD, DLB or MSA. This creates a rare opportunity to understand early mechanisms driving these disease and, crucially, to test strategies that might delay or prevent disease progression.

What the Center will do

• Build a national RBD cohort as a platform for world-class clinical research.
• Develop and validate biomarkers (digital, molecular, imaging) to detect early disease, monitor change over short intervals, and measure treatment effects.
• Design and run pioneering preventive trials in at-risk populations, testing whether early interventions can meaningfully alter disease trajectories.
• Leverage artificial intelligence to discover patterns that signal risk even earlier – potentially before symptoms emerge.

“TMF has supported high-quality research in Bergen for over two decades. We are pleased to support the research environment led by Professor Tzoulis at UiB and Haukeland University Hospital. We have high expectations that this initiative will significantly advance understanding of Parkinson’s disease and related disorders”, says Nicholas Nunn, Managing Director, Trond Mohn Research Foundation.

Parkinson’s is the world’s fastest-growing brain disease, and there is still no treatment that can slow or prevent progression,” says Professor Charalampos (Haris) Tzoulis, Head of the Mohn Research Center for Neuroprotection, Professor of Neurology and Neurogenetics at UiB and Consultant Neurologist at Haukeland University Hospital. “By identifying risk earlier and developing scalable tools to monitor change, we can finally test prevention – moving from reacting after irreversible damage has occurred to protecting the brain at a very early stage.”

Professor Tzoulis also leads the K.G. Jebsen Center for Parkinson’s Disease and directs the Neuro-SysMed Center for Clinical Treatment Research in Neurology, providing a strong clinical and research foundation for the new Center.

Why it matters

The Mohn Research Center offers new hope to affected individuals and a promise to reduce the enormous societal burden these diseases represent, bringing us closer to a new era of prevention-driven brain medicine.

A new report shows that certain mental health conditions escalate the risk of developing heart disease by 50-100%—and adverse outcomes from existing heart conditions by 60-170%.

Every 34 seconds, someone in the United States dies from heart disease. As nearly half of the country suffers from some form of cardiovascular disease (CVD), another 1 in 4 adults experience a mental health disorder in their lifetime, signaling an inevitable overlap.

The new report in The Lancet Regional Health-Europe summarizes cardiovascular health disparities among those diagnosed with depression, anxiety, schizophrenia, bipolar and post-traumatic stress disorders (PTSD). The article is part of a series aiming to raise awareness around disparities in CVD health in four populations: women, the elderly, racial minorities, and those with mental health conditions.

Emory University professor Viola Vaccarino led this metareview linking mental health conditions to CVD, along with coauthors Amit Shah and Douglas Bremner, also Emory professors.

The report associated the following conditions and their corresponding risks of developing CVD:

• Major depression, 72%
• PTSD, 57%
• Bipolar disorder, 61%
• Panic disorder, 50%
• Phobic anxiety, 70%
• Schizophrenia, nearly 100%

The research also shows that these conditions are associated with a poorer prognosis, greater risk for readmission, and higher mortality from existing heart conditions. For example, major depression more than doubles the mortality rate in those with existing CVD.

Additionally, the report emphasizes a bidirectional relationship. “More than 40% of those with cardiovascular disease also have a mental health condition,” adds Vaccarino.

According to the report, a well-documented relationship exists among depression, schizophrenia, PTSD, and abnormal stress responses in the autonomic nervous system (ANS) and hypothalamic-pituitary adrenal axis (HPA).

The former allows the brain to manage involuntary responses, such as functions of the liver, heart, sweat glands, and eye muscles. The ANS also manages both acceleration and deceleration of these functions, regulating inflammatory responses. Since most major organs have ANS nerve endings, this system affects most bodily functions.

The HPA also influences immune response and metabolism, which can affect cardiovascular function.

According to the report, dysregulation of these systems creates “adverse downstream effects that can affect cardiovascular risk chronically, including increased inflammation, metabolic abnormalities, high blood pressure, enhanced systemic vascular resistance, and autonomic inflexibility.”

Inflammation has also been implicated in both the development of heart disease and mental health conditions.

The role of social determinants of health in CVD disparities is critical. Those with mental health conditions may face disruptions and barriers in the continuum of care, such as affordability and accessibility. Compromised health literacy or communication can also impede access to health screenings and treatment.

Clinicians could also be challenged to care for patients with certain mental conditions, which can be compounded by stigma and existing models that fragment mental and physical health care. Stigmas are also present in the field of clinical research, where having a mental health condition is often an exclusionary criterion in randomized trials.

Moreover, according to the report, current prediction models don’t account for mental health disorders when forecasting the risk of developing heart disease.

To address the disparities of CVD among people with mental health disorders, the authors recommend an integrated approach with interdisciplinary care encompassing behavioral, mental and cardiovascular health.

“The tight connection between cardiovascular and psychological health warrants changes in the health care system that are more amenable to patients with comorbidities,” says Vaccarino.

“A clinical team would be ideal for the care of these patients—a team of specialists, social workers, and nursing staff who work in collaboration to provide multidisciplinary care and resources.”

The report concludes that closing the health disparity gap upholds the rights of those living with a mental health condition to achieve the highest level of health and fully participate in society.

Source: Emory University

Breast cancers frequently spread to the bone, establishing tumors that are largely impervious to treatment and are associated with poor patient prognoses. A deficiency in the oxygen-carrying capacity of the blood, or anemia, is among the most common complications of these common metastases. Though such anemia was thought to stem from the tumor’s disruption of bone marrow-the body’s manufacturing hub for all blood cells, including its oxygen-bearing red blood cells-its precise underlying causes were a mystery.

No longer. In exploring the niche in bone marrow where such tumors take root, researchers led by Yibin Kang and Yujiao Han of the Princeton Branch of the Ludwig Institute for Cancer Research uncovered a pair of canny strategies breast cancer cells employ to access the metabolic support essential to their survival and proliferation in the oxygen-poor microenvironment of bone marrow. These adaptations, they report in the current issue of Cell, directly disrupt the function of specialized bone marrow cells that produce red blood cells, causing the anemia that accompanies bone metastasis.

Targeting these metabolic transactions between cancer cells and specialized cells of the bone marrow microenvironment could lead to novel therapies that disrupt tumor growth while preserving bone marrow function and alleviating anemia, a frequently overlooked but debilitating complication for women living with metastatic breast cancer.”

Yibin Kang, Ludwig Institute for Cancer Research

Metastasis is a tall order for the average cancer cell. Only a select few in any given tumor evolve the full suite of skills and capabilities required to sally forth and take root in other organs. These venturesome cells must not only survive a dangerous migration, through inhospitable terrain, to distant sites but also adapt extensively to the unfamiliar and frequently hostile microenvironments of alien tissues to establish a tumor. The latter feat often entails mimicking some properties of local cells to better handle the metabolic demands of their new home. It also typically involves the manipulation of noncancerous cells in the vicinity to furnish, among other things, the nutrients essential to cancer cell proliferation.

Iron is a case in point. Though bone marrow has healthy reserves of this essential mineral, it is not readily available to invading cancer cells. So Han, Kang and colleagues took note when they discovered that a highly specialized type of iron-recycling immune cell-the erythroblast island (EBI) macrophage-was noticeably abundant in the metastatic niche and seemed to cluster around cancer cells.

In healthy bone marrow, EBI-macrophages serve as nurse cells, providing iron to erythroblasts, the precursors of red blood cells. Erythroblasts need the mineral to make functional hemoglobin molecules, which red blood cells use to capture oxygen for dissemination throughout the body.

“We found that EBI-macrophages are hijacked by metastatic breast tumor cells to acquire iron, depriving erythroblasts of a mineral essential to the production of red blood cells,” said Han. “Depleting these macrophages in mice impaired bone metastasis of breast cancer.”

The researchers show that similar iron-handling macrophages are found in human bone metastases not only from breast cancer, but also from lung and kidney tumors. This suggests that the hijacking of iron-recycling macrophages might be a common phenomenon in cancers that metastasize to the bone.

The researchers also discovered that with a dedicated source of iron now available to them, the cancer cells begin to mimic erythroblasts, expressing a component of hemoglobin-β-globin-to better survive the hypoxic environment in the bone marrow. And, again, this mimicry was reflected in human tumors: elevated β-globin expression in tumor cells, they show, is associated with an increased risk of bone metastasis.

The two adaptations have synergistic effects. By coopting EBI-macrophages, cancer cells corner the local market for iron in bone marrow, disrupting the generation of new red blood cells. They then use that iron to support their own survival and proliferation, which further compromises erythroblast function.

“We’ve uncovered a novel axis of tumor-immune-metabolic crosstalk that promotes both metastatic progression and cancer-associated anemia,” said Kang. “Our work illustrates the remarkable plasticity of metastatic cells that grow in the bone and identifies a potential mechanism underlying the anemia caused by such metastases. These findings can be exploited for the development of therapies that could improve both the survival and the quality of life of cancer patients.”

This work was supported by the Ludwig Institute for Cancer Research, the American Cancer Society, the Charles H. Revson Foundation, the Brewster Foundation, the Breast Cancer Research Foundation and the Susan G. Komen Foundation.

Aside from his post as a Member of the Princeton Branch of the Ludwig Institute for Cancer Research, Yibin Kang is Warner-Lambert/Parke-Davis Professor of Molecular Biology at Princeton University and an Associate Director of Rutgers Cancer Institute of New Jersey.