What’s Hot: December 2019

What’s Hot: December 2019

News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.


  • Chronic inflammation “a substantial public health crisis”
  • Study suggests benefit for luteolin against prostate cancer
  • Boosting NAD+ extends lifespan in models of accelerated aging
  • Markers of immune status, inflammation associated with premature mortality


    Chronic inflammation “a substantial public health crisis”

    Chronic inflammation a substantial public health crisis December 9, 2019. An article appearing on December 5, 2019 in the journal Nature Medicine indicts systemic chronic inflammation as the factor behind diseases that represent the world’s leading causes of disability and mortality, including cardiovascular disease, cancer, diabetes, chronic kidney disease, nonalcoholic fatty liver disease, and neurodegenerative and autoimmune disorders.

    While short-term, acute inflammation is a natural and necessary response to infection and illness, inflammation that becomes chronic increases the risk of disease. In fact, authors David Furman of the Buck Institute for Research on Aging and colleagues estimate that diseases related to inflammation are behind half of all deaths worldwide. They list several risk factors that promote “this health-damaging phenotype,” which include poor diet, physical inactivity, psychological stress, infections and exposure to industrial and environmental toxins. "Chronic inflammation is influenced by many social, environmental and lifestyle factors," commented senior author George Slavich, who is the director of the UCLA Laboratory for Stress Assessment and a research scientist at the Norman Cousins Center for Psychoneuroimmunology at UCLA. "If we make people aware of these risk factors, our hope is that individuals will reduce the factors that apply to them."

    The authors of the article recommend the identification of new biomarkers in the body that improve the ability to screen for, diagnose and treat chronic inflammation. Currently, only a few are known, including C-reactive protein (CRP).

    "It's also important to recognize that inflammation is a contributor not just to physical health problems, but also mental health problems such as anxiety disorders, depression, post-traumatic stress disorder, schizophrenia, self-harm and suicide," Dr Slavich added. "This is a substantial public health crisis."

    —D Dye



    Study suggests benefit for luteolin against prostate cancer

    Study suggests benefit for luteolin against prostate cancer December 6, 2019. Research reported on December 5, 2019 in the journal Carcinogenesis indicates a role for the antioxidant flavonoid luteolin against prostate cancer, including castration-resistant disease. While prostate cancer is dependent upon male hormones during its initial stages, castration-resistant prostate cancer (CRPC) refers to disease that no longer responds to androgen-blocking therapy, making it more difficult to treat. Existing therapies for CRPC have demonstrated limited success.

    For the current study, Aya Naiki-Ito of Nagoya City University and colleagues investigated the effects of luteolin in a rat model of prostate cancer and found that the flavonoid induced apoptosis (programmed cell death), thereby inhibiting the cancer’s progression. Luteolin also induced apoptosis in rat and human castration-resistant prostate cancer cells and dose-dependently decreased cell proliferation.

    In castrated mice that received implanted rat and human prostate cancer tumors, oral administration of luteolin also enhanced apoptosis as well as inhibited angiogenesis, which is the formation of new blood vessels that helps facilitate a tumor’s growth. Luteolin was shown to block the expression of androgen receptor splice variant 7 (AR-V7), which is a contributor to cell proliferation and treatment resistance in castration-resistant disease.

    Genetic analysis identified MiR-8080 as a gene that is upregulated by luteolin. In human castration-resistant prostate cancer cells that received the gene, AR-V7 expression level was lowered and apoptosis induced. Conversely, knocking out the gene blocked luteolin’s ability to decrease AR-V7 and cell proliferation in human castration-resistant prostate cancer cells.

    When luteolin was added to the chemotherapy enzalutamide in mice that received the human castration-resistant prostate cancer grafts, AR-V7 was downregulated and the drug’s action was enhanced.

    “These results indicate luteolin inhibits castration-resistant prostate cancer by AR-V7 suppression through miR-8080, highlighting luteolin and miR-8080 as promising therapeutic agents for this disease,” the authors concluded.

    —D Dye



    Boosting NAD+ extends lifespan in models of accelerated aging

    Boosting NAD+ extends lifespan in models of accelerated aging December 4, 2019. Research reported on November 21, 2019 in Nature Communications revealedthat the metabolic cofactor nicotinamide adenine dinucleotide (NAD+) is depleted in Werner syndrome, a premature aging disease characterized by metabolic dysfunction. It was determined that the disease is caused by faults in a cleanup process known as mitophagy, which breaks down defective mitochondria that produce energy within the cells.

    “We are showing for the first time that Werner Syndrome is due to errors in the clean-up process,” announced Vilhelm A. Bohr of the Center for Healthy Aging at the University of Copenhagen and the National Institute on Aging.

    Dr Bohr and associates studied mitophagy in blood samples derived from Werner syndrome patients and in fly and worm models of the disease. Boosting NAD+ levels by administering the NAD+ precursors nicotinamide riboside and nicotinamide mononucleotide improved faulty mitophagy and delayed accelerated aging, including stem cell dysfunction. “It strongly reinforces our findings that the clean-up process seems to be important in both human cells and across different animals,” he stated. “And then it is encouraging that in living animals, we can improve lifespan and delay the aging processes which are the key symptoms of Werner Syndrome.”

    “Our findings suggest that accelerated aging in Werner syndrome is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts Werner syndrome phenotypes,” the authors conclude.

    “Our results are so promising that we have received inquiries from Japan with a view to performing clinical studies of patients with Werner Syndrome,” Dr Bohr added. “We very much hope that the studies will point in the same direction so that patients can live longer and with a higher quality of life.”

    —D Dye



    Markers of immune status, inflammation associated with premature mortality

    Markers of immune status, inflammation associated with premature mortality December 2, 2019. A study published on December 2, 2019 in JAMA Network Open found an association between a greater risk of premature mortality and markers of inflammation and immune function.

    Researchers analyzed information collected upon the enrollment of 31,178 participants in the National Health and Nutrition Examination Survey (NHANES) who were recruited during 1999 to 2010. The team found that having lymphopenia, which is a reduction in white blood cells known as lymphocytes (indicating impaired immune function), was associated with a 30% greater risk of mortality during 12 years of follow-up in comparison with those who did not have the condition. Increases in red blood cell distribution width (a measure of the body's ability to maintain a healthy red blood cell population) and C-reactive protein (CRP), a marker of inflammation, were additionally associated with greater mortality risk. Subjects who had the highest scores of immunohematologic status, indicating severe lymphopenia, high red blood cell distribution width (indicative of bone marrow dysregulation) and high CRP levels, experienced the greatest mortality ten-year mortality risk. Conversely, participants who did not have lymphopenia and whose red blood cell distribution width and CRP levels were among the lowest one-third of the study population had the lowest mortality risk.

    "Scientists have gone to great lengths and expense to develop novel biomarkers to identify people at the highest risk for death and disease," commented senior author Jarrod Dalton, PhD. "Here we have taken a more pragmatic approach - investigating the predictive power of components of a patient's white blood cell count, which is collected as part of routine blood work during standard health exams. The complete blood count test is convenient, inexpensive and, as our findings suggest, may be used to help physicians screen for and prevent disease and disease-related mortality."

    —D Dye


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