This paper aims to perform a scoping review of existing published literature and determine inconsistencies versus consistencies, if any.The methodology here was to examine multiple published papers regarding nicotinamide adenine dinucleotide (NAD) synthesis, and from there data was extrapolated to evidence the ability of nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide (NAM), nicotinamide mononucleotide (NMNH), and dihydronicotinamide riboside (DNR) as NAD precursors. This scoping
Cardiovascular disease (CVD) is one of the greatest disease burdens and takes the lives of many each year. There are many risk factors both modifiable and non-modifiable which contribute to the onset and progression of the disease. Trimethylamine N-oxide (TMAO) in recent years has been found to have a correlation with CVD onset. Those with increased levels of the metabolite have a markedly increased risk of future development of cardiometabolic disorders.This literature review aimed to critique past studies undertaken to find a consensus of the significance of the interrelationship between TMAO and cardiovascular risk. A definite link between TMAO levels and a CVD outcome was found. The majority of the literature stated the relationship with evidence; however, there is still some uncertainty as to why and how the correlation occurs. Further study needs to be done to further dissect and understand the relationship between TMAO and CVD risk.
As humans age multiple forms of biological decay ensue, and many aspects of human biology can be measured to determine how far biological machinery has drifted from homeostasis. Research has led to aging clocks being developed that claim to predict biological age as opposed to chronological age. Aging could be regarded as a measured loss of homeostatic biological equilibrium that augments biological decay in fully developed tissues. Measuring aspects of how far various elements of biology have drifted from a youthful state may allow us to make determinations on a subject's health but also make informed predictions on their biological age. As we see across human physiology, many facets that maintain human health taper off such as nicotinamide adenine dinucleotide, glutathione, catalase, super oxide dismutase, and more.Extracellular vesicle density also tapers off during age combined with epigenetic drift, telomere attrition, and stem cell exhaustion, whilst genomic instability and biological insults from environment and lifestyle factors increase. Measuring these types of biomarkers with aging clocks may allow subjects to understand their own health more accurately and enable subjects to better focus on their efforts in the pursuit of longevity and, in addition, allow healthcare practitioners to deliver better health advice.
Epigenetic drift causes modification in gene expression during aging and a myriad of physiological changes that are mostly undesirable, remove youthful phenotype and are related to biological decay and disease onset. The epigenome is considered a stable regulator of genetic expression. Moreover, evidence is now accumulating that commonly available compounds found in foods can influence the epigenome to embrace a more youthful and therefore, more disease resistant state. Here we explore the correlation between nutriment and the epigenetic regulation through various types of alimentation. The aim is not to discuss specific chemicals involved in disease onset. Instead, we offer a brief glance at pathogens and offer a practical pathway into epigenetic regulation, hypothesizing that epigenetic drift might be attenuated by several foods able to drive a more youthful and disease resistant phenotype.
The longevity industry is vastly different than the health industry.Health foods and health products may deliver health benefits, but these benefits are mostly only available if you are deficient in a vitamin or mineral, but no health product has been shown to profoundly extend lifespan (if at all). 1 The study by Khan et al. 2019 conducted nine systematic reviews, and four randomized control trials were chosen that embodied a total of 277 trials, 24 interventions, with a total of 992,129 participants. These data from John Hopkins Medicine support the idea that an avid user of health products will still age and experience biological decay at their natural rate of aging. John Hopkins did find minor health benefits from low-salt diet, omega-3 fatty acids supplements, and possibly folic acid supplements in some people.Lifespan and health-span remain separate challenges, as lifespan simply denotes the duration of a person's life, whereas health-span refers to the time a human can remain fit, vibrant, and healthy. The onset of biological decay and the elimination of health-span appears to be the origin of where suffering, disease, and death emanate from.
As longevity companies emerge with new products and the fields of anti-aging research develop new cutting-edge therapies, three distinct classes of longevity methodologies emerge. This discussion finds that there are three clear classes (Tiers) of longevity systems that are currently under development, and all three will be paramount to achieve biological escape velocity (where tissues can be repaired faster than aging can damage them). These classes are referred to as Tier 1, Tier 2, and Tier 3 treatments and are described in detail below. These three Tiers are required for easy identification for pharmaceutical companies and research companies to determine the type of therapy they may choose to deliver being noninvasive, invasive, time consuming, or simple end user products. Specific targets and goals need to be defined clearly from an early perspective in the development of these technologies for future precision medicines. This allows consumers of future anti-aging technologies to consider which Tier a particular therapy may be, delivering a more informed choice.
This scoping review aims to perform a brief but comprehensive assessment of existing peer‐reviewed literature and determine whether raising nicotinamide adenine dinucleotide can prevent or promote tumorigenesis. The examination of extensive peer‐reviewed data regarding the synthesis of nicotinamide adenine dinucleotide has been performed with a focus on nuclear dynamics and the deoxyribose nucleic acid repair pathway. Various enzymatic protective functions have been identified from nicotinamide adenine dinucleotide levels, as well as the threat role that is also explored. Nicotinamide adenine dinucleotide precursors and sirtuin‐activating compounds are becoming ubiquitous in the commercial market. Further research into whether elevating levels of nicotinamide adenine dinucleotide or overexpression of sirtuins can increase the potential for neoplasm or other age‐related pathophysiology is warranted due to the high energy requirements of certain diseases such as cancer.
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