Scientists have recently developed an effective means of slowing the aging of mice. When researchers increased levels of NAD+ (nicotinamide adenine dinucleotide), older muscle cells began functioning more like those from younger animals.
They discovered that treated mice had epigenetic patterns more closely matching those seen in younger animals, suggesting that manipulating transcription factors might be an effective strategy for combatting aging in humans.
Fecal Transplants from Young Mice
Researchers have devised a breakthrough way of slowing the aging process of mice. By giving old ones fecal transplants from young ones, researchers saw remarkable results – old mice that received transplants looked and behaved much younger than their counterparts who hadn’t. Furthermore, this treatment improved health conditions such as inflammation levels and mitochondrial function in addition to increasing grip strength significantly.
On May 30, their research was published in mSystems journal. Their investigation involved using an innovative gene therapy technique called ICE, or inducible changes to epigenome, that uses short cuts in DNA that alter how it folds temporarily but heal quickly; these cuts mimic lifestyle and environmental factors which contribute to premature aging.
By administering an ICE cocktail to mice, researchers were able to alter how their DNA folded, leading to changes in gene expression that reset their epigenetic patterns and made them look and act much younger than before.
Resetting of epigenetic patterns was no mere temporary change; researchers observed that when they exposed animals to ICE for longer, they displayed signs of reversed aging processes in both their kidneys and skin – specifically kidney epigenetic patterns that resembled those found in younger mice; similarly, skin epigenetic patterns of treated mice demonstrated less cell proliferation and greater scarring as opposed to similar findings among older animals.
Scientists attributed this reversal of aging to the young microbiome’s positive influence on gut-brain and gut-retina axes as well as its ability to boost immunity and metabolism, while simultaneously improving cognitive and synaptic plasticity of mice that had received fecal transplants as well as its capacity for changing composition of gut microbiota; those receiving these transplants were found to be rich with bacteria that promoted fatty acid digestion and heterolactic fermentation while those that hadn’t were more likely to produce methane and butane from carbohydrates than aged mice that received transplants.
RNA Molecules
Although genetic mutations were once thought to cause aging, recent research indicates that changes in gene expression rather than DNA sequence may actually accelerate it. This phenomenon, known as epigenetics, can be affected by lifestyle factors like diet, exercise, stress and environmental toxins – with scientists having demonstrated how manipulating gene expression could reverse aging processes altogether.
Transcription factors, or chemical “switches”, allow scientists to turn genes on or off by acting like switches. When the scientists injected old mice with transcription factors, their cells began acting more like those of younger animals; when examined closer, their kidneys and skin also revealed epigenetic patterns similar to younger animals’ kidneys and skin tissues.
Ribonucleic acid (RNA), a small biological molecule with similar structures to DNA, differs by having single stranded backbone composed of alternating phosphate groups and the sugar ribose instead of deoxyribose; furthermore it contains bases Adenine, Thymine, Cytosine and Guanine as well as the nitrogenous base uracil as replacements; this nucleic acid controls gene expression while providing information from genome to regions in cells where proteins are made by carrying information between genome and other cells where proteins are made.
RNA molecules also possess many non-coding functions, such as catalyzing reactions, regulating gene expression and providing templates for adding telomere repeats during cell division. Finally, dying cells release them and act as biomarkers of disease states.
RNA has played an indispensable role in human evolution, yet its function is even more critical in today’s world of infectious diseases and other health concerns. For instance, HIV and cold virus use RNA to destroy naive T cells, leading to acquired immune deficiency syndrome. Manipulating RNA provides powerful tools for discovering ways to prevent or treat diseases more effectively.
Vitamin D3
Vitamin D3 is often referred to as “the calcium vitamin”, yet its benefits extend far beyond bone health. Vitamin D3 plays an integral part in metabolic processes that support muscle, insulin production and nervous system health as well as helping to regulate mood, protect from autoimmune and seasonal disorders and even slow cell aging processes. Studies indicate this as being true.
Vitamin D3 is produced naturally when exposed to sunlight and ultraviolet (UVB) radiation from sunlight, becoming active by exposure to sunlight and UVB rays in sunlight-exposed skin cells. UVB radiation converts previtamin D3 (7-dehydrocholesterol) to provitamin D3, then previtamin D3 becomes previtamin D3, before finally being converted to active (1a,25-dihydroxycholecalciferol). Once active (1a,25-dihydroxycholecalciferol), activated vitamin D3 can binds VDR and stop expression of TNF-a thus preventing chronic inflammation while slowing ageing effects.
Recent research conducted on white blood cell telomere length in participants receiving 2,000 IU of vitamin D3 daily for four years as opposed to taking a placebo showed that participants who took vitamin D’s telomeres were longer; losing an average of 140 base pairs less over four years–roughly equivalent to three less years of cellular aging.
This research marks the first time lifestyle factors were directly demonstrated to impact telomere length. Telomeres tend to shorten in individuals who consume high-fat diets, smoke cigarettes and experience stress.
Research supports the hypothesis that diet and supplementation with vitamins D3 and NAD+ could aid cellular metabolism and delay biological aging; however, more studies must be conducted in order to pinpoint exactly how these nutrients influence telomere length and other key cellular processes.
Sun exposure or eating foods rich in vitamin D are effective means of supplementation, such as eggs, fortified milk products, fish, cod liver oil and green leafy vegetables. To further minimize oxidative damage and inflammation responses it is advised to consume low glycemic index foods and limit saturated fat intake – these will also help preserve telomere length – as we age, our telomeres shorten which leads to cancerous transformation and other illnesses; keeping vitamin D levels up alongside an anti-inflammatory diet rich in phytochemicals can reverse these processes of accelerated aging processes.
NAD+
NAD+, also known as Nicotinamide Adenine Dinucleotide, plays an essential role in human cellular metabolism and age-related diseases1,2. Recent studies indicate that declining levels of NAD+ may contribute to ageing and age-related illnesses1,2. Increasing NAD+ levels can be achieved either by decreasing enzyme activity that consume it or supplementation with its precursors.
NAD+ serves as a substrate for over 300 enzyme reactions that regulate key cellular functions and metabolic pathways, such as cell death regulation, controlling the balance between oxidized and reduced forms of NAD+ known as its redox state, protecting DNA to ensure genomic stability, autophagy (cellular recycling mechanism)3,4 etc.
The NAD+/NADH ratio is essential to controlling oxidative enzyme activities that balance prooxidative and reductive reactions in cells, thus maintaining their proper functions and providing energy for growth and repair processes. Under normal circumstances, its ratio should typically range from 700:1 up to 700:1, providing energy for both growth and repair processes. As we age however, this balance diminishes significantly leading to impaired cell functions as well as leading to disease associated with ageing and associated with advanced age.
Researchers found that increasing NAD+ in blood stem cells reversed the high glucose metabolism associated with aging in mice. They administered nicotine to increase concentration of the precursor of NAD+ (nicotinamide mononucleotide; NMN), thus increasing survival, differentiation and number of blood stem cells; furthermore this also significantly decreased high glucose uptake by brain, heart and other organ cells restoring more youthful levels of metabolism for these organs of mice.
The research team also examined cells from skeletal muscle and found that both NMN and apigenin, another NAD+ precursor, increased both the number and differentiation of stem cells found there. This result suggests that using similar strategies – decreasing activity of enzymes that consume NAD+ while supplementing with either NMN or apigenin – might help humans live longer, healthier lives.
