Precision Nutrition, Epigenetics & Practitioner-Led Longevity Care — Dr. Chris Oswald — Head of Medical Affairs, Pure Encapsulations, Nestlé Health Science.
Dr. Chris Oswald, DC, CNS, is Head of Medical Affairs for Pure Encapsulations (https://www.pureencapsulations.com/), part of Nestlé Health Science family. He is a chiropractor, certified nutrition specialist and certified functional medicine practitioner and has been treating patients since 2007.
At Pure Encapsulations, Dr. Oswald leads medical education, scientific strategy, and innovation across well-known professional brands including Pure Encapsulations, Douglas Labs, Klean Athlete, Genestra, and others. In this role, he sits at the intersection of clinical science, practitioner education, and product innovation — translating complex evidence into practical tools that help healthcare professionals practice more confident, personalized nutritional medicine.
Dr. Oswald’s clinical work, in combination with his work in professional dietary supplement companies, gives him unique insight into the creation of clinically useful tools and education to support the unique needs of clinicians and patients in functional, integrative and natural health.
Before joining Pure Encapsulations, Dr. Oswald held senior leadership roles across the nutraceutical and health tech landscape, including Chief Science Officer, Head of Product Innovation and R&D, Head of Operations, Interim Head of Sales, and VP of Nutraceuticals at companies like January AI and Further Food. Across those roles, he’s led everything from supply chain and regulatory strategy to product development, claims substantiation, and national practitioner education.
The study, published in Genomic Psychiatry, identified how stress hormones activate specific RNA molecules called long noncoding RNAs, or IncRNAs, that interact with the gene-silencing complex PRC2, turning off genes that are vital to communication between neurons. In essence, these IncRNAs act like “switches,” turning off functionality for more than 3,000 genes, many of which support neurotransmitter signaling and other processes that are essential for healthy brain functioning. The study specifically discovered 79 IncRNAs that were significantly altered under stress conditions.
While scientists have long understood that stress hormones send signals to the brain that affect gene functionality, it was previously unknown as to exactly how these signals create long-lasting changes inside cells. The study, led by Yogesh Dwivedi, Ph.D., Distinguished Professor and Elesabeth Ridgely Shook Endowed Chair in the Department of Psychiatry and Behavioral Neurobiology, and co-director of UAB Depression and Suicide Center, uncovers how lncRNAs associate with a molecule called polycomb repressive complex 2, or PRC2, to modify chromatin following activation of the glucocorticoid receptor, or GR — the cell’s master regulator of stress response. Chromatin is important in relaying messages from the external environment, including stressful conditions, to alter the genetic composition, a process known as epigenetics.
“As chronic stress is a major risk factor for conditions like major depressive disorder, this newly uncovered link between stress hormones and IncRNA gene silencing could potentially lead to more targeted mental health treatments,” Dwivedi said. “In fact, stress-induced changes in chromatin structure have been implicated in a range of psychiatric and neurodegenerative conditions.”
IncRNAs act like “switches,” turning off functionality for more than 3,000 genes that are essential for healthy brain functioning. A recent groundbreaking study from researchers at the University of Alabama at Birmingham highlights the discovery of a molecular link between stress hormones and changes in brain cell communication, which could open the door for new treatments to address depression and other psychiatric conditions.
DNA can be thought of as a vast library that stores all genetic information. Cells do not use this information all at once. Instead, they copy only the necessary parts into RNA, which is then used to produce proteins—the essential building blocks of life. This copying process is called transcription, and it is carried out by a molecule known as RNA polymerase II.
When RNA polymerase II begins actively transcribing DNA, a specific site called Ser2 on its tail region is marked with a small chemical group known as a phosphate. This phosphate acts as a sign that transcription is in progress. Until now, observing this sign required stopping cellular activity and chemically treating the cells to visualize the phosphate. As a result, it was impossible to see how transcription changes dynamically in living cells.
To overcome this limitation, a research team led by Professor Hiroshi Kimura at Institute of Science Tokyo (Science Tokyo) chose a different approach. Instead of freezing cells at a single moment, they aimed to track transcription continuously without stopping cellular activity.
The metabolites associated with type 2 diabetes were also found to be genetically linked to clinical traits and tissue types that are relevant to the disease. Furthermore, the team developed a unique signature of 44 metabolites that improved prediction of future risk of type 2 diabetes. ScienceMission sciencenewshighlights.
Diabetes, a metabolic disease, is on the rise worldwide, and over 90 percent of cases are type 2 diabetes, where the body does not effectively respond to insulin. Researchers identified metabolites (small molecules found in blood generated through metabolism associated with risk of developing type 2 diabetes in the future and revealed genetic and lifestyle factors that may influence these metabolites. They also developed a metabolomic signature that predicts future risk of type 2 diabetes beyond traditional risk factors. Their results are published in Nature Medicine.
In this study, researchers tracked 23,634 individuals with diverse ethnic backgrounds across 10 prospective cohorts with up to 26 years of follow-up. These individuals were initially free of type 2 diabetes. The team analyzed 469 metabolites in blood samples, as well as genetic, diet, and lifestyle data, to see how they relate to risk of developing type 2 diabetes. Of the metabolites examined, 235 were found to be associated with a higher or lower risk of developing type 2 diabetes, 67 of which were new discoveries.
“Interestingly, we found that diet and lifestyle factors may have a stronger influence on metabolites linked to type 2 diabetes than on metabolites not associated with the disease,” said first and co-corresponding author. “This is especially true for obesity, physical activity, and intake of certain foods and beverages such as red meat, vegetables, sugary drinks, and coffee or tea. Increasing evidence suggests that these dietary and lifestyle factors are associated with greater or lower risk of type 2 diabetes. Our study revealed that specific metabolites may act as potential mediators, linking these factors with type 2 diabetes risk.”
Although DNA is tightly packed and protected within the cell nucleus, it is constantly threatened by damage from normal metabolic processes or external stressors such as radiation or chemical substances. To counteract this, cells rely on an elaborate network of repair mechanisms. When these systems fail, DNA damage can accumulate, impair cellular function, and contribute to cancer, aging, and degenerative diseases.
One particularly severe form of DNA damage are the so-called DNA–protein crosslinks (DPCs), in which proteins become attached to DNA. DPCs can arise from alcohol consumption, exposure to substances such as formaldehyde or other aldehydes, or from errors made by enzymes involved in DNA replication and repair. Because DPCs can cause serious errors during cell division by stalling DNA replication, DNA–protein crosslinks pose a serious threat to genome integrity.
The enzyme SPRTN removes DPCs by cleaving the DNA-protein crosslinks. SPRTN malfunctions, for example as a result of mutations, may predispose individuals to developing bone deformities and liver cancer in their teenage years. This rare genetic disorder is known as Ruijs-Aalfs syndrome. Its underlying mechanism remains poorly understood, and there are no specific therapies.
Plants display a wide range of life spans and aging rates. Although dynamic changes to DNA methylation are a hallmark of aging in mammals, it is unclear whether similar molecular signatures reflect rates of aging and organism life span in plants. In this work, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, which causes DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging can be manipulated by extending or curtailing life span and that shoot apical meristems are protected from these epigenetic changes. We demonstrate that a program of transcriptional repression suppresses DNA methylation maintenance pathways during aging and that mutants of this program display a complete absence of epigenetic decay while physical aging remains unaffected.