Healthy diet with less sugar is linked to younger biological age

Researchers at UC San Francisco have found a link between following a diet that is rich in vitamins and minerals, especially one without much added sugar, and having a younger biological age at the cellular level.  


 
They looked at how three different measures of healthy eating affected an “epigenetic clock” – a biochemical test that can approximate both health and lifespan – and found that the better people ate, the younger their cells looked. Even when people ate healthy diets, each gram of added sugar they consumed was associated with an increase in their epigenetic age. 


 
“The diets we examined align with existing recommendations for preventing disease and promoting health, and they highlight the potency of antioxidant and anti-inflammatory nutrients in particular,” said Dorothy Chiu, PhD, a postdoctoral scholar at the UCSF Osher Center for Integrative Health and first author of the study, “From a lifestyle medicine standpoint, it is empowering to see how heeding these recommendations may promote a younger cellular age relative to chronological age.” 
 
The study is one of the first to show a link between added sugar and epigenetic aging, and the first to examine this link in a heterogenous group of women – both Black and white – in midlife. Most studies on the topic have involved older white participants.   
 
The study helps deepen our understanding of why sugar is so detrimental to health, added study co-senior author Elissa Epel, PhD, a UCSF professor in the Department of Psychiatry and Behavioral Sciences. 
 
“We knew that high levels of added sugars are linked to worsened metabolic health and early disease, possibly more than any other dietary factor,” Epel said. “Now we know that accelerated epigenetic aging is underlying this relationship, and this is likely one of many ways that excessive sugar intake limits healthy longevity.” 
 
Women in the study reported consuming an average of 61.5 grams of added sugar per day, though the range was large: from 2.7 to 316 grams of added sugar daily. A bar of milk chocolate has about 25 grams of added sugar, while a 12-ounce can of cola has about 39 grams. The U.S. Food and Drug Administration recommends adults consume no more than 50 grams of added sugar per day. 
 
 A nutrient-based approach 
 
For the cross-sectional study, researchers analyzed food records from 342 Black and white women with a mean age of 39 years from Northern California. Then, they compared their diets with epigenetic clock measures, which were derived from saliva samples.  
 
Researchers scored the women’s diets to see how they compared to a Mediterranean-style diet rich in anti-inflammatory and antioxidant foods and then to a diet linked to lower risk for chronic disease.  
 
Finally, they scored the women’s diets against a measure they created called the “Epigenetic Nutrient Index (ENI)”, which is based on nutrients (not foods) that have been linked to anti-oxidative or anti-inflammatory processes and DNA maintenance and repair. These include Vitamins A, C, B12 and E, folate, selenium, magnesium, dietary fiber and isoflavones.  
 
Adherence to any of the diets was significantly associated with lower epigenetic age, with the Mediterranean diet having the strongest association.  
  
The researchers examined sugar intake separately and found that consuming foods with added sugar was associated with accelerated biological aging, even in the presence of an otherwise healthy diet.  
 
“Given that epigenetic patterns appear to be reversible, it may be that eliminating 10 grams of added sugar per day is akin to turning back the biological clock by 2.4 months, if sustained over time,” said co-senior author Barbara Laraia, PhD, RD, a UC Berkeley professor in the Food, Nutrition and Population Health program. “Focusing on foods that are high in key nutrients and low in added sugars may be a new way to help motivate people to eat well for longevity.”  

Can a computer tell patients how their multiple sclerosis will progress?

AI MS

Machine learning models can reliably inform clinicians about the disability progression of multiple sclerosis, according to a new study published this week in the open-access journal PLOS Digital Health by Edward De Brouwer of KU Leuven, Belgium, and colleagues.

Multiple sclerosis (MS) is a chronic progressive autoimmune disease that leads to severe disability over time through a complex pattern of progression, recovery, and relapse. Its global prevalence has increased by more than 30% over the last decade. Yet there are few tools that can predict the progression of MS to help clinicians and patients make life planning and treatment decision-making. 

In the new study, De Brouwer and colleagues used data on 15,240 adults with at least three years of MS history who were being treated at 146 MS centers in 40 countries. Data on two years of each patient’s disease progression was used to train state-of-the-art machine learning models to predict the probability of disease progression over the subsequent months and years. The models were trained and validated using strict clinical guidelines, promoting applicability of the models in clinical practice. While individual models varied in performance across different patient subgroups, the models had an average area under the ROC curve (ROC-AUC) of 0.71 ± 0.01. The study found that the history of disability progression was more predictive for future disability progression than treatment or relapse history.

The authors conclude that the models developed in the study have the potential to greatly enhance planning for individuals with MS and could be evaluated in a clinical impact study.

De Brouwer adds: “Using the clinical history of more than 15,000 people with multiple sclerosis, we trained a machine learning model capable of reliably predicting the probability of disability progression in the next two years. The model only uses routinely collected clinical variables, which makes it widely applicable. Our rigorous benchmarking and external validation support the vast potential of machine learning models for helping patients planning their lives and clinicians optimizing treatment strategies.”

Utilizing Food as Medicine: A Modern Exploration of an Old Practice

Maintaining prediabetic status after diagnosis reduces risk of death decades later

This idea may have been typical centuries ago, but today, many societies are dealing with overfeeding and undernourishment, resulting in widespread health problems. Returning to fundamental principles could be a significant part of the solution.

“We’ve all heard the saying ‘you are what you eat,’ often used to describe the negative health effects of an unhealthy diet. However, this concept can also work in a positive way. Researchers are revisiting the ancient idea of using food to treat ailments, taking advantage of modern knowledge about genetics and metabolism to reintroduce the teachings of Yinshan Zhengyao to the public.”

Yinshan Zhengyao is the world’s first authoritative nutritional treatise, compiled by Hu Sihui, a dietitian of the Yuan dynasty. This work embodies the traditional Chinese medicinal concept of

‘homology of food and medicine,’ rich in the cultural heritage of the Chinese nation,” said, Min-Hui Li, researcher and author of the study. Yinshan Zhengyao comprises 174 medicinal plants across 55 unique plant families and 111 genera. These plants are indispensable to the culture of traditional Chinese medicine (TCM). Another highly important piece of this traditional Chinese text is the power of the mind and mood over the human body. Cheerfulness and tranquility are aspects that are emphasized in Yinshan Zhengyao, as the mind-body connection can be as important as the fuel taken in by an individual.

“In Yinshan Zhengyao, dietary therapies are particularly interesting for their effects on regulating digestion, respiration, endocrine, and nervous system functions, as well as protecting and regulating various organs,” said Li. The foundation of this text is to provide treatment (and prevention) for chronic diseases through the use of plants, as well as to instil the importance of quality food in society. By viewing food as medicine, greater emphasis and care are put into preparing and consuming food by “putting the food to work” not only as a source of energy but as a source of longevity.

In Traditional Chinese Medicine (TCM), diseases are thought to result from imbalances in the body. For instance, the kidneys are considered to be closely linked with the reproductive system and the regulation of fluid metabolism. Recent research has revealed that, apart from their role in the urinary system, the kidneys are also involved in maintaining fluid balance and endocrine function. Treating a specific part of the body can have unexpected effects elsewhere, such as lower back pain or weakness in the limbs due to kidney issues.

“With the Yinshan Zhengyao text dating back to the early 14th century, modern medicine and therapies can be used in conjunction with the plant and diet information available from this early work on diet, health, and nutrition. Professor Min-Hui Li and his team propose integrating modern information to explore and analyze the healthcare use of medicine and parallel food sources.”

By studying modern applications of health and medicine, such as the human genome, metabolism, regulatory networks, and their relationships, researchers aim to continue enhancing human health and promoting the concept of food as medicine in a broader, more contemporary context.

A new therapeutic target offers a promising pathway for multiple sclerosis treatment

Researchers find that blocking an overproduced channel protein could significantly improve symptoms in an animal model of multiple sclerosis.
Researchers find that blocking an overproduced channel protein could significantly improve symptoms in an animal model of multiple sclerosis.

Researchers from Kyushu University have identified a potential therapeutic target for the treatment of advanced multiple sclerosis (MS), a potentially disabling condition associated with the central nervous system. In their latest study, conducted using an experimental mouse model of MS, they explored the role of connexin 43 (Cx43), a protein involved in cellular communication and cardiac function, and examined whether targeting this protein with specific blockers could improve MS symptoms.

Like most neurodegenerative diseases, MS has very limited treatment options, more so once it reaches the chronic stage. To add to this, MS affects nearly three million people worldwide, making it a massively challenging neurological disease. Though our understanding of the precise nature of MS is limited, researchers have established that MS is caused by the patient’s own immune system wreaking havoc on their central nervous system. Specifically, the immune system attacks the protective myelin sheath surrounding nerve fibers in the brain and spinal cord, causing demyelination and creating areas of scarring and damage called lesions.

In a 2013 study, researchers from Kyushu University, including Associate Professor Ryo Yamasaki from the Faculty of Medical Sciences, found that the production of Cx43 was increased in supportive cells called astroglia, near chronic MS lesions. As mentioned earlier, Cx43 is essential for cell-to-cell signaling and plays a key role in modulating the immune system. The researchers therefore hypothesized that Cx43 could play a pivotal role in promoting neuroinflammation—a process where the immune response is triggered to fight off infection or heal damaged tissue—in the context of MS, ultimately leading to demyelination.

Now, a recent study published in Scientific Reports on May 13, 2024, by Yamasaki, in collaboration with researchers from the International University of Health and Welfare, adds further support to the hypothesis that Cx43 plays a key role in causing MS.  Their study has revealed that a drug called INI-0602, which effectively ‘plugs’ and blocks Cx43 channels, markedly improved MS symptoms in experimental mice.

The researchers conducted an extensive series of experiments in an experimental mouse model of MS and in cultured astroglia cells from the mouse model, to understand the effects of Cx43 blockade. The results of these tests and analyses were quite consistent, suggesting that INI-0602 could not only suppress the overproduction of Cx43 in astroglia, but also mitigate many of the hallmark features of MS, including demyelination and excessive immune cell infiltration into the nervous system.

By delving further into the mechanisms underlying these results, the team found that INI-0602 led to improved symptoms by regulating immune processes. More specifically, treatment with this compound reduced the levels of pro-inflammatory cytokines—proteins produced by immune cells that trigger the immune system—and increased those of anti-inflammatory cytokines in the cerebrospinal fluid. The drug also altered calcium signaling in astroglia, limiting their ability to promote inflammation. Together, these effects reduced disease severity in experimental mouse model. 

Overall, the findings of this study have important implications for future MS therapies. “Targeting Cx43 channels with specific blockers like INI-0602 could serve as a novel therapeutic strategy for chronic MS. This, in turn, could facilitate the development of new treatments for patients with MS,” highlights Yamasaki. He adds, “Our findings also challenge a critical issue in MS treatment, that of limiting disease progression in chronic stages by targeting Cx43, where current treatments are found to be less effective.”

Large study confirms: Siblings of autistic children have 20% chance of autism

Research finds sex of first autistic child, number of autistic children and other factors influence likelihood of autism
Research finds sex of first autistic child, number of autistic children and other factors influence likelihood of autism

Siblings of autistic children have a 20% chance of being autistic themselves — about seven times higher than the rate in infants with no autistic siblings.

That’s the key finding of a new paper by UC Davis MIND Institute researcher Sally Ozonoff and the Baby Siblings Research Consortium. The consortium is a collection of more than 20 research groups at universities worldwide.

The new study is based on a large, diverse group of families at research sites across the United States, Canada, and the United Kingdom. It confirms the same research group’s 2011 findings about the likelihood of autism in siblings.

Increasing autism rates prompt new study

“The rate of autism diagnosis in the general community has been steadily increasing since our previous paper was published,” Ozonoff explained. 

The latest estimates from the Centers for Disease Control and Prevention show that about 1 in 36 children has autism. In 2011, the estimate was 1 in 68.

Ozonoff noted that there have also been changes in autism diagnostic criteria over the past decade. In addition, there is a growing awareness of autism in girls.

“So, it was important to understand if these had any impact on the likelihood of autism recurrence within a family,” she said.  

The 2011 paper found a recurrence rate of 18.7%, while the new paper found a rate of 20.2% — a small but not significant increase.

“This should reassure providers who are counseling families and monitoring development. It should also help families plan for and support future children,” Ozonoff said.

A larger, more diverse study

The new study included data from 1,605 infants at 18 research sites. All infants had an older autistic sibling.

“This study was much larger than the first and included more racially diverse participants,” Ozonoff said. The original study included 664 children.

Researchers followed the children from as early as 6 months of age for up to seven visits. Trained clinicians assessed the children for autism at age 3 using the Autism Diagnostic Observation Schedule (ADOS-2), a well-validated tool. The data were gathered from 2010 to 2019.

Sex of first autistic child, multiple autistic siblings key factors

Researchers found that the sex of the first autistic child influenced the likelihood that autism would recur within a family.

“If a family’s first autistic child was a girl, they were 50% more likely to have another child with autism than if their first autistic child was a boy,” Ozonoff said. “This points to genetic differences that increase recurrence likelihood in families who have an autistic daughter.”  

The researchers also found that a child with multiple autistic siblings has a higher chance of autism (37%) than a child with only one sibling on the spectrum (21%).

The sex of the infant was also associated with the likelihood of familial recurrence. If the later-born infant was a boy, they were almost twice as likely as a girl to be diagnosed themselves.

“The familial recurrence rate if the new baby was a boy was 25%, whereas it was 13% if the new baby was a girl,” Ozonoff explained. “This is in line with the fact that boys are diagnosed with autism about four times as often as girls in general.”

Race, maternal education level influence recurrence

The researchers found that race and the mother’s education level were likely factors as well. In non-white families, the recurrence rate was 25%. In white families, the recurrence rate was about 18%. In families where the mother had a high school education or less, recurrence was 32%. With some college, the rate was 25.5%, and with a college degree the rate was 19.7%. When the mother had a graduate degree, it dropped to 16.9%.

“These findings are new — and critical to replicate,” Ozonoff explained. “They do mirror the recent CDC findings that autism is more prevalent in children of historically underrepresented groups.” She noted that this reversed a longtime trend of lower prevalence in those groups.

Most importantly, said Ozonoff, if these findings are replicated, they may indicate that there are social determinants of health that may lead to higher rates of autism in families. She emphasized that this study was not designed to answer those critical questions, and more research is needed.

Tracking outcomes

Unlike the first study, the researchers also tracked families who dropped out of the three-year study to see if their outcomes differed from those who did. “We wondered whether families who stayed in the study may have had children who were more affected — making them more worried about their development,” she explained.

That could have biased the estimates of recurrence to be higher than they really were. The current study showed that was not the case.

“So, now we have two large, independent studies that report familial recurrence in the same range,” Ozonoff said. “This reinforces how important it is that providers closely monitor the siblings of autistic children for delays in social development or communication. This is especially true in families who have reduced access to care, because early diagnosis and intervention are critical.”