 Is there any correlation between longevity, a college education, and racial identity? Find out by sticking around for this story, plus we'll have other stories in this episode of Lifespan News. Welcome to Lifespan News on X10, your source for longevity science updates. I'm your host, Brent Nalley. If you missed our last episode, then you can watch it by clicking the card above. We encourage you to check the description below for links to these stories. Continuing with our first story, researchers in the United States have shown that there's a longevity advantage of having a bachelor's degree, and this advantage has increased in the US over the past three decades. Well at the same time, the racial gap in life expectancy has decreased, using data from the National Vital Statistical System to analyze mortality rates for 48.9 million adults. The researchers made a 1990 to 2018 time series of mortality rates and expectancy years lived from 25 to 75. Those with a BA made continuous progress between 1990 and 2018 and could expect to live 48.2 years between the ages of 25 years and 75 years by 2018. By contrast, those without a BA showed a decline after 2010 and could expect to live only 45.1 years between the ages of 25 years and 75 years by 2018. There was little increase in adult life expectancy for whites, but substantial gains among blacks until 2012, narrowing the racial gap by 70%. The researchers state, quote, currently adult longevity is more strongly linked to a BA than a racial identity, in contrast to the situation in 1990, end quote. For our next story, a Spanish team discovers how telomere involvement in tumor generation is regulated. The telomeres and telomerase group led by Spanish National Cancer Research Center director Maria Blasco is making more progress in understanding the role of telomeres in cancer development. Telomeres are known to function as protective caps at the end of chromosomes, preventing the strands from fraying or accidentally fusing with each other. Telomeres also regulate cellular aging, in that when telomeres become too short as a consequence of cell division, cells stop dividing. This mechanism is thought to be one of the ways the body prevents tumor formation. The group was among the first to suggest that shelter ends, which is a type of protein complex wrapped around telomeres to protect them, could be viable targets for cancer therapies. Recently the researchers had previously showed that eliminating a particular shelter in TRF1 prevented the initiation and progression of deadly cancers, such as lung cancer and glioblastoma and mice. Recently the group found out how telomeres can be regulated from signals from outside the cells, and how these signals may induce abnormal cell proliferation. The researchers found a link between the aforementioned shelter in TRF1 and the AKT signaling pathway. By genetically modifying TRF1 to be unresponsive to AKT, the researchers observed that telomeres in the modified cells shortened and accumulated more damage, which made them unable to form tumors. The next step will be to generate genetically modified mice with telomeres that are invisible to AKT to see if this will make the mice more cancer resistant as the researchers expect. By the way, Lifespan News is released every Tuesday at noon Eastern time, while our other Science and Advocacy X10 videos are released every other Monday also at noon Eastern time. We encourage you to subscribe to our X10 YouTube channel. Once you're subscribed, be sure to click the notification bell and select all notifications to ensure you don't miss any videos. Now back to the news. A new delivery method based on nanoparticles could improve the efficiency of NMN and Metformin in the liver. Nanotechnology holds significant promise for medicine, offering the possibility of using nanomaterials to carry drugs or control their release. One challenge is that nanomedicines are taken up more by the liver than other tissues. The research team at the University of Sydney decided to take advantage of this to deliver medicines that target metabolic conditions in the liver. The researchers created quantum dots, or QD, 7 nanometers in size as a drug delivery vehicle. These QDs accumulate in the liver and are then rapidly cleared from the body. The team attached Metformin and nicotinamide mononucleotide, or NMM, to the QDs and added these to the drinking water of mice. The researchers showed that the use of QDs made the Metformin as effective as a dose 100 times stronger. And for NMM, the difference was about 1,000 fold. The researchers also showed that QD NMM was able to improve glucose tolerance and reduce fasting insulin and insulin resistance in 18 and 24 month old mice. NMM did not have the same effect, even at doses 100 times greater. It will be interesting to see if follow-up research is able to repeat these results, determine these mechanisms at play and eventually translate the findings to humans. Moving on, a major health-related data project secures funding in the United Kingdom. In the UK, the All-Party Parliamentary Group, or APPG, for longevity has secured funding for its OpenLife data project, which aims to create a framework for effective and ethical collection of health-related data on a national level. The OpenLife data framework, or OLDF, is described as, quote, a collaborative ecosystem to stimulate social and business model innovation using ethical data models, end quote. U.P.G. co-founder Tina Woods highlighted the importance of including non-health data, such as, quote, the data gathered by wearables and smartphone apps, but also shopping purchases, social media, and banking transactions, end quote. Tina cites the importance of cataloging, quote, the complex environmental exposures we are subjected to throughout our lives, including our diet, lifestyle factors, and social influences, and our body's responses to these challenges, end quote. Wearables can be used to collect both health data and non-health data. A major issue is privacy concerns, which make people reluctant to share their data. To that end, one of the goals of the OLDF is to, quote, build public trust in the use of data for individual and collective health and social care purposes, end quote. The authors of the framework also address questions of inequality, noting that the COVID pandemic has underscored the vast differences in overall health and health outcomes among groups divided by race, gender, and income. According to the authors, gathering more data will help scientists, physicians, and governing bodies better understand and address those differences. Effective and safe ways of gathering, sharing, and using such data can revolutionize health care. The work of APPG for longevity and the OLDF in particular provide an encouraging example of the governmental involvement needed to implement these changes. To find out more, check out our interview of Tina Woods and our review of Tina's recent book in the description below. For our final story, a new study links proteins associated with Alzheimer's disease with a common loss of sight. New research has revealed a link between amyloid beta, or AB, which is a protein associated with Alzheimer's disease, or AD, and age-related macular degeneration, or AMD, which is one of the most common causes of vision loss with age. AB is known to accumulate not only in the brains of AD patients, but also in the retina of the eye as people get older. This is evident in donor eyes from patients who suffered from AMD. In particular, a new study published in cells investigated the effect of AB exposure on retina cells of normal mouse eyes. According to their findings, the resulting pathology was strikingly similar to human AMD. According to the researchers, AB proteins collected in the lysosomes of retinal cells. The lysosome's job is to clear unwanted waste from the cell. But the lysosomes were unable to break down AB, so up to 85% of AB remained within these cells. This also meant that fewer lysosomes were available to perform other routine waste breakdown. The researchers hope that one of the next steps in their research might be the repurposing of Alzheimer's drugs to break down amyloids in the retina. That's all the news for this video. Before you go, there's a few quick, free, and simple things that you can do to help us solve the human aging problem. If you haven't already, please make sure to like this video, share this video on your social media, make sure that you're subscribed with a bell turned to all notifications to ensure you don't miss any videos. Is there a recent life extension story that you think we should have included in one of our recent videos but haven't yet? In which of the stories from this video excited you the most, let us know what you think in the comments below. We really appreciate it, and we look forward to seeing you in the next video, at least as healthy as you are now.