4) FACIAL AGE SCAN

Biometric Markers reflect strength attributes or physical attributes that can be measured by a device designed to do so, or a picture of your face in the instance of age determination by facial scan. These indicators have a large body of statically significant, correlating data. validating their use as components of age regressive, monitoring protocols.

Determining your age by scanning your face and then having an artificial intellengence system make an accurate determination of your biological age may seem like science fiction. Actually this research began fifty years ago. Several research groups are currently researching what information can accurately be extracted from such scans. Incredibly that list now includes the fellowing: Age, Sex, Emotional State, Political Affiliation and Sexual preference. The Relevant References provided below support this biometric marker as being highly correlated with BASP. Several commercial companies currently offer this ability. Most of them are demonstrations for paid services like Visage Technologies demo show on the right. Click on the Image and you can try it yourself now.

Click [√] to Enlarge

A 2014 Washington Post article succinctly described how the process determines your biological age using data from an image of your face. Click on the info graphic one the right to enlarge and review the process.

ARC is in contact with several research groups and we are attempting to offer this biometric marker of aging on this site in the near future.

We would advise that the hallmarks of aging, as reflected in key landmarks of facial changes would be somewhat resistant to quickly reflecting changes in your biological age as we move the BASP backwards. This is because many of the age related changes are keyed to increased cartilage growth and the reduction of these landmarks, such as nose and ear size, would be very slow to occur or will not change at all. Those research biometric landmarks are highly accurate in reflecting the normal aging process, but may not have a high correlation or provide meaningful insights when attempting to measure the regression of a persons age. Many of the hallmarks that determine age from a facial scan do not rely on these artifacts. The accuracy of these indicators is currently +/- 3 years. Changes in your age over time provided by these AI scans will however provide you with a simple, quasi indication of your current BASP in a free and relevant manor. No one scan-age will be as important as determining a trend from multiple scans over time.

Highlighted excerpts from an article that reviewed and discussed one such research groups progress in 2015 is provided below. The techniques described in that article have been improved upon in the seven years since it was published.

◉ Scientists have created a 3D imaging system they claim can reliably predict a person’s biological age from the look of their face alone.

◉ The researchers believe the technology could be used to judge whether proposed anti-ageing treatments have any effect, and to help doctors fine-tune advice and therapies for their patients.

◉ From young adulthood to old age, the images captured the process of steady decline. Mouths become wider, noses larger. The corners of the eyes droop. The face loses its smoothness, becomes plump with subcutaneous fat, and the whole lot sags as gravity triumphs over the collagen and elastin fabric of the skin. [1]

When this work was accomplished in 2015 the standard deviation from actual age was about 6 years. That has improved since then to around 3 years.

Virtually no ones biological age is the same as their chronological age. This is true for AI Facial Scan Age. The most important thing you can do to turn face scanning resources into a useful BASP tracking tool is to fellow the fellowing rules each time you capture your age when scanning your face.

PhotoAgeClock has improved this error rate to less than 2.3 years in a sample of 8414 individuals ranging in age from 20 to 80. [2]

TIPS ON OPTOMIZING ACURATE AGE RESULTS

1) Always use the same biometric resource.

2) Us the same facial expression. You need to think of the same thing, such a pleasant experience each time.

3) Smiling or frowning creates wrinkles in you face and will increase you age from these facial scans.

4) Remove your glasses as these can also degrade the results.

5) Take your facial age scan at the same time of day.

6) Use the same lighting conditions.

7) Maintain the same distance from the camera each time.

8) Maintain a record or diary of all of your BASP markers and organize them by the dates they were captured.

Facial Age Recognition Resources Available Online:

Both of these links are free to use as a non-commercial, consumer oriented resources.

◉ Visage Technologies Facial Recognition

◉ Young.AI a division of Deep Longevity

Cited References:

[[1] [2015] Scan allows scientists to determine biological age from the face alone

[2] [2018] PhotoAgeClock- deep learning algorithms for development of non-invasive visual biomarkers of aging

Relevant References:

[2014] Recognizing Age-Separated Face Images- Humans and Machines

[2022] Fair and accurate age prediction using distribution aware data curation and augmentation

[2022] Applying Artificial Intelligence for Age Estimation in Digital Forensic Investigations

[2015] Age and Gender Classification using Convolutional Neural Networks

[2018] Age Estimation of Face Images Based on CNN and Divide-and-Rule Strategy

[2015] Three-dimensional human facial morphologies as robust aging markers

[2018] Face Recognition Vendor Test (FRVT)

[2018] Age estimation via face images- a survey

[2019] Improved graph-based SFA- information preservation complements the slowness principle

[2016] Apparent Age Estimation from Face Images Combining General and Children-Specialized Deep Learning Models

[2020] Deep learning approach for facial age classification: a survey of the state-of-the-art

[2022] Daily steps and all-cause mortality: a meta-analysis of 15 international cohorts

As we have advocated several times on this site, that your primary care physician should be an active participant in this endeavor. Many of the labs we target below requires your physician to provide script to the laboratory in order to draw them.

Obviously, we want to see the markers move in the opposite direction that historical values normally move. (See: “Correlates of Aging”) If a marker historically increases as we age, we want to see a small but noticeable decrease between our last lab draw and the most recent one. You should note that many of them peak between 65-80 years of age and then begin to decline again. This can produce the false impression that things are improving, when in fact your are seeing the results of normal aging. You should also be aware that many uncontrollable factors can impact these markers. Environmental contaminants; (dust, cigaret smoke, recreational drugs, alcohol, pesticides) emotional state including stress, sleep, mild to severe infections and changes in medications can all cause changes in any or all of the biomarkers we want to monitor. This makes it important that you monitoring protocol is maintained for as long as you are implementing aging interventions.

BASP is the difference between your chronological age, which is intransigent and inevitable, and the physiological / biological age of your immunological systems including organs, cells and chronokines. Clinical and laboratory biological markers are utilized to determine your current BASP.

Environmental factors like pollution, cigarets, alcohol, poor diet and any diseases process will move your BASP higher (older age). Exercise, good diet, meditation, sleep, socialization, friends, lovers, and family moves your BASP down (younger age).

Obviously targeted, biologically active, interventional modalities hold the potential to also regress you BASP. This site is dedicated to finding and optimizing the interventional strategies that safely allow for the reduction of your BASP. Targets of opportunity and agents that effectively and safely regress your BASP are emerging daily.

We have identified a minimal, yet effective set of markers and clinical observations that will provide you with relevant feedback on your progress in regressing you BASP score.

(1) ARC-BASP CORE BIOMARKERS

Expanding this core set of markers to include more expensive and more difficult to obtain BASP markers is of course desirable. The more information you have to guide and make decisions the more effective your path to effectively reducing your BASP will be.

We have provided five sets of markers that allow you to select and expand the amount of information you want or are able to obtain. Each marker is ranked as to its ease and expense of obtaining it and its relevance to effectively determine your BASP score.

The “E-Score,” is basically an ease of obtaining each biomarker and is scored on a scale of between 1 and 3. The system was adopted from the paper titled: “Ranking Biomarkers of Aging by Citation Profiling and Effort Scoring,” They describe this criteria as:

• A low e-score (1) describes a potential biomarker which is easy to sample, to handle and to process (usually automated fast and reliable measurements are available from known sources). For example, blood counts from venous blood qualify, since such blood can be sampled easily, the plasma/serum can be stored at room temperature (up to3 h for many analytes) or in a standard freezer (≥3 month for most analytes) and be processed by equipment that is regularly available in a standard diagnostic/clinical unit or research laboratory. The costs are low to moderate (≤10 €).

• A moderate e-score (2) is assigned if one step (sampling, handling, or processing) is associated with substantial extra effort for routine laboratories. This includes sampling under special conditions, a requirement for prompt sample handling, or the need for elaborate validation.

• A high e-score (3) implies elaborate sampling (e.g., biopsy, lumbar puncture, etc.), handling (e.g., storage in liquid nitrogen) and/or processing (e.g., non-routine nucleotide or protein sequencing). The financial costs are usually high.

Click [√] to Enlarge Image

This same group also attempted to provide a relevance score for each marker. This is simply a citation search of all published peer reviewed articles that contained the search criteria shown on the right. The field is moving so fast that some of the scores this process has generated no longer accurately reflect some indicators actual relevance. The authors freely admit that all of their scores are somewhat subjective.

These search results were then further divided into sub-categories. We have produced an excel spreadsheet that contains all of these markers including their RC-Scores and E-Scores that you can download by clicking on the “Excel” link below. We have annotated and added to the indicators provided and in some cases introducing new categories such as age determination by facial recognition. Finally we added our own ranking to denote the most effective and least expensive clinical/biomarkers of aging. Screenshots of each spreadsheet are available by clicking on the icon at the right of each biomarker category.

(1) Clinical, Physical Capability and Organ Function Biomarkers

(2) Routine Laboratory Biomarkers

(3) Research Laboratory Biomarkers (Non-epigenetic)

(4) Research Laboratory Biomarkers based on Epigenetic Measurements

(5) Visual Facial Age Recognition by AI

Complete Excel BioMarkers Spreadsheet is available by clicking on this image: > > >

Horvath’s DNA Methylation BASP Indicators

DNA methylation is a biological process by which methyl groups are added to the DNA molecule. Recent research efforts provided compelling evidence of genome-wide DNA methylation alterations in aging and age-related disease. It is currently well established that DNA methylation biomarkers can determine biological age of any tissue across the entire human lifespan, even during development. [1]

Steve Horvath’s group, using large scale validation data from thousands of individuals, we demonstrate that DNA methylation GrimAge stands out among existing epigenetic clocks in terms of its predictive ability for time-to-death, time-to-coronary heart disease, time-to-cancer, its strong relationship with computed tomography data for fatty liver/excess visceral fat, and age-at-menopause. [2]

DNA methylation has also been suggested as a target in a regressive paradyme. If increased methylation is an indication of age, would a targeted therapy that reduces that methylation levels be an anti-aging intervention?

Laboratory Markers correlating with BASP

Multiple common laboratory markers included in studies like complete blood cell counts and blood chemistry panels also have demonstrated stistcically significant correlations with your BASP vs chronological ages. [3]

Multiple elements of facial recognition age determination. Skin is the largest human organ. Its visibility and accessibility make it a good BASP marker from facial images. There are several biomarkers associated with your eyes that also can contribute to an accurate estimate of your age. AI analysis of your face can produce an accurate indication of your BASP. [4]

[1] DNA Methylation Biomarkers in Aging and Age-Related Diseases

[2] DNA methylation GrimAge strongly predicts lifespan and healthspan

[3] 2021 Correlation analyses between age and indices in routine blood laboratory tests suggest potential aging biomarkers, Annals of Blood

[4]

•••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••••

The primary addressable, interventional BASP targets are detailed in the following paragraph. It would represent the ultimate hubris to assume that this list in any way represents the final word, in both 1) an optimal list of targets, 2) most effective dosage; 3) most effective time of administration; 4) most effective interval of administration; 5) and/or the most effective interventional molecules.

On a personal note I can provide limited (N of 2) feedback on what is described at this point in time. Much like the mice in the Conboy study we have experienced improvements in energy, gastral intestinal function and comfort, memory, concentration and sleep. Our mental outlook has dramatically improved and the feeling of heading toward a cliff that many older individuals experience has abated. Total quality of life is at leat 50% better than prior to implementing this protocol. Activities of daily living have become much easier to accomplish. This work will continue for many years fine tuning the optimal age-regression protocol. You own contribution to this information is critical.

If the word is bolded and underscored it is included in our inventory of supplemental interventions.

1) Increasing levels of TGF-beta-1 are correlated with increasing age[4]. The Conboys in the referenced paper describe it as: “age-related elevation in the intensity of this pathway may contribute to diminished stem cell regeneration in the hippocampal niche, which combined with our prior results with the skeletal muscle stem cell niche would demonstrate conservation of signal transduction changes with age.” ALK5 provides an effective and very druggable target that results in the downregulation or inhibition of TGF-beta-1 signaling. Supplements able to inhibit ALK5 include EGEC, Fiesten, Qcertain, and Curcumin. Resveratrol [1] an Petrostilbene[] inhibit the signaling downstream from ALK5 at pSmad 2,3.

2) Levels of the hormone Oxytocin decline with age.

Oxytocin can be up-regulated by the administration of several forms of Oxytocin now available online.

Oxytocin can be up-regulated by multiple supplements including:

3) AKG is a required intermediary in the Krebs cycle. It also facilitates the assembly and transportation of many of the bodies building blocks; amino-acids. Multiple studies in multiple animal models have documented an increased life-span resulting from AKG supplementation.

4) Glutathione is an important component of cellular metabolism and energy production. A recent paper described how the supplementation with N-acetylcysteine (NAC), and Glycine increased intercellular glutathione, producing dramatic and sustained improvements in multiple measurements, leading to an improved quality of life. This included improved glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition. [2] Another research group accomplished similar results providing only Lyophilized Glutathione as the interventional supplementation [3]. 5) Leucine has demonstrated in multiple studies a longevity benefit [4]. Dehydroepiandrosterone (DHEA). Vitamin D is expected to be a primary anti-aging medicine in the near future due to its numerous positive effects in the elderly population.

5) Down regulation of IL-6.

IL-6, perhaps considered one of the first aging biomarkers, was described as “a cytokine for gerontologists” (Ershler, 1993). IL-6 is the best characterized biomarker for “inflammaging,” a chronic low-grade inflammation that develops with advanced age and contributes to the pathogenesis of age-related diseases and most recently has been recognized as a core element of the secretome produced by senescent cells (Lopez-Otin et al., 2013; Ferrucci and Fabbri, 2018; Franceschi et al., 2018). High circulating levels of proinflammatory cytokines, such as IL-6 have been associated both cross-sectionally and prospectively with major age-related chronic diseases as well as with disability and frailty (Maggio et al., 2013). Insulin-like Growth Factor-1 (IGF-1 (IGF 1), which contributes to the decline of muscle strength with aging (Maggio et al., 2013; Johnson et al., 2020; Moaddel et al., 2021)

As the age increased by 1 year, IL-6 values increased by 0.05 pg/ml (95% CI: 0.02, 0.09; p < .01) [5].

REFERENCES:

[1] 2014 Activation of SIRT3 by resveratrol ameliorates cardiac fibrosis and improvescardiac function via the TGF-!/Smad3 pathway

[2] 2021 Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition: Results of a pilot clinical trial

[3] 2018 Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function

[4] 2011 Low-dose lithium uptake promotes longevity in humans and metazoans

[5] 2021 Defining IL-6 levels in healthy individuals: A meta-analysis

Basic Monitoring Protocol (BMP)

Interval: Every three months

CLINICAL:

Height, Weight, Temperature, Blood Pressure,

Grip strength, Measurement around waist.

Facial Image age analysis

LABORATORY DRAWS:

View fullsize

Basic Monitoring Protocol (BMP) Click [√] to Enlarge

Macrophages are monocytes that have finished their tasks in the bloodstream, and have moved to other organs or tissues in the body and matured.

The two types of cell are similar: both monocytes and macrophages are both responsible for destroying harmful substances. The key differences are that macrophages are about double the size of monocytes. Macrophages stay stationary in extracellular fluid, but monocytes move through the bloodstream.

Advanced Monitoring Protocol (AMP)

Now is the time

Epigenetic Monitoring Protocol (EMP)

Now is the time

CLINICAL LABRATORY MARKERS

Now is the time

CHEMISTRY AND BOOD CELL MARKERS

Laboratory markers derived from blood increase or decrease with age depending on six factors: 1) your environment; 2) your disease state; 3) mental health; 4) your current chronological age; 5) your sex; and 6) your race. Tables exists that will allow you to determine your best comparison group[1].

EPIGENETIC DNA METHYLATION MARKERS

Within this frame, there is growing interest around biomarkers of biological age. Biological age is intended as a synthetic index constituted by a single marker or the combination of few biological markers which, alone or integrated with functional markers, not only correlates with chronological age but is/are capable of identifying individuals “younger” or “older” than their chronological age in the same demographic cohorts.

With such biomarkers, it should be possible to obtain trajectories of aging, where the “accelerated” ones would predict unhealthy aging and diseases, while the “decelerated” ones would be associated with healthy aging and longevity. The pos- sibility to draw trajectories of aging is a fascinating, far-reaching perspective, especially in consideration of the abovementioned long incubation preclinical period that characterizes most of the major age-related chronic diseases, and is considered the critical time window for effective treatments. Biomarkers of biological age could greatly contribute to identify the subjects characterized by higher risk to develop overt clinical diseases who would have a major benefit from tailored preventive treatments. However, these biomarkers are apparently informative about the status of deep molecular mechanisms (the seven pillars) underpinning the age-related decline which predisposes to ARDs but do not tell us which specific disease people characterized by acceler- ated biological age are predisposed to. Accordingly, a major biomedical aim is to identify the subjects at higher risk for each specific ARD at very early stage. At present, the combination of the new generation of effective biomarkers, capable of assess- ing the deep biological age, with the classical and innovative biochemical and functional disease-specific ones represents the best strategy to identify disease-specific aging trajectories. Within this perspective, particular attention has to be devoted to the genetics of each individual which is the complex result of the interaction between nuclear and mitochondrial genetics (stable with the exception of somatic mutations) and microbiomes’s genetics (malleable and adaptative to the environment), focus- ing on GM for its capability to be modified by basic habits such as nutrition. In particular, we predict that it will be useful to combine the abovementioned integrated biomarkers’ assess- ment with established and new genetic risk factors for ARDs, taking into account some criticalities related to population genetics and demographic birth cohorts (225).

To date, there are no clinically validated markers of biological age; however, a number of promising candidates have been proposed in the last years. We will discuss three of them: (i) DNA methylation markers, (ii) N-glycan markers, and (iii) GM biomarkers. [1]

VISUTAL MEMORY TEST

https://humanbenchmark.com/tests/memory

Biological Markers of Aging provide both a feedback mechanism, measuring your progress in regressing your Biological Age Set Point (BASP). This comprehensive list is divided into four categories. The first are relevant markers that are readably available, inexpensive and insightful. These markers also have a strong, stistcically significant age/maker/BASP correlation. The second group consists of laboratory, epigenetic and clinical markers that will require lab/blood draws, or collection and transportation of the biological sample to a remote laboratory. These markers are obviously more expensive and difficult to obtain and often require a prescription from your physician. The third group of markers can provide you with a direct indication of your BASP. This includes epigenetic clocks and multiple complete BASP age analysis provided by various online sites. The cost of obtaining this information can be high. Some of the sites provide access to these markers if you are buying a supplement that they also sell on there site.

Grip Strength as an Indicator of Biological Age

▶︎ Weak grip strength (GS)—an indicator of upper-body and overall muscle strength decline [1], has been recognized as a powerful predictor of multi-morbidity [2], disability [3] and mortality [4], and is a key component of frailty [5] and sarcopenia [1, 6] in old (aged ≥65) and very old adults (paged ≥85).

Grip strength is a long-term predictor of mortality from all causes in men and impending mortality in older, disabled women.◀︎[]

Point in time grip strength measurements are used to provide clinicians with an indication of overall health, but accurate interpretation requires valid reference values so that these single data point measurements can be compared to age- and sex-specific norms derived from a large historical population.

Our requirements are significally simpler. We need to collect a baseline datapoint and then compare our progress on a fixed interval schedule.

Click on the down facing chevron (V)to open or collapse each section.

▶︎ The insulin/insulin-like growth factor 1 (IGF-1) signaling (IIS) pathway, which participates in glucose sensing, is the earliest discovered and the most well-known pathway to antagonize longevity. Paradoxically, IGF-1 declines in wild-type mice or mouse models of premature aging whereas attenuating IIS activity extends life span43. Such observations led to the potential inclusion of IIS pathway members, such as growth hormone and IGF-1, as biomarkers of aging 44,45 ◀︎ [1]
[1] [2017] Molecular and phenotypic biomarkers of aging
▶︎ Epigenetic modifications. Age-related changes in DNA methylation patterns, notably as measured by the epigenetic clock, are among the best-studied aging biomarkers18–20. Analysis of methylation profiles in the blood found that only three CpG sites could predict age with a mean absolute deviation from chronological age of less than 5 years21. The association between age and DNA methylation can be extended to age-associated diseases, such as diabetes22. For a full review of the epigenetic regulation of aging, see Sen et al.23. ◀︎ [1]
▶︎ Epigenetics is the study of DNA modifications that do not alter the DNA sequence [62•]. The most well described as a biomarker of biological age is DNA methylation. Chronological age has significant effects on DNA methylation levels in the human genome [62•]. Corresponding with advances in DNA methylation measurements and biostatistical methods, two models showed strong correlation between methylation profiles and chronological age and were named “epigenetic clocks” [63, 64].
The mechanism by which epigenetic clocks estimate chronological age can be obscure; this is not wholly unexpected, given their derivation from computer learning algorithms sorting through patterns of hundreds of methylation targets [62•]. Theories include alterations in development and age-related epigenetic maintenance systems and DNA methylation as a response to oxidative or other age-related damage to DNA [62•, 65]. Excitingly, recent work suggests that epigenetic markers represent not just a biomarker but targets for reprogramming as a means of treating aging [66••]. Even so, the claim that the epigenetic clock is presently the most predictive and well-validated biomarker of biological age is disputed [67•].
DNA methylation is both genetically and environmentally driven. Offspring of supercentenarians (105–109 years old) demonstrate patterns of DNA methylation consistent with lower epigenetic age than do age-matched controls [68]. Similarly, twin studies have estimated that epigenetic age acceleration produce heritability estimates of around 40%; interestingly, the overlap of methylation patterns diminishes both with age and between twins who either spend less of their lifetime together or whose health trajectories diverge [69]. Likewise, social and behavioral factors associated with longevity (e.g., high fish intake, moderate alcohol consumption, high education) directly correlate with epigenetic age [70•, 71•].
Although the first epigenetic clock could reliably estimate chronological age and chronological-age independent mortality risk, it was not associated with common disease risk factors [72]. A later (2018) 2-step model was used to create a novel DNA methylation informed biomarker. It was grounded in a composite of clinical markers of biological age and yielded enhanced predictions of mortality and age-related disease; even so, it was less predictive than the clinical markers used to create the model [73]. Subsequently, by differentiating the effects of chronological and phenotypic age using clinical chemistry biomarkers, this same group was able to approximate phenotypic age acceleration and found this “phenotypic age” to exceed chronological age in association with all-cause and cause-specific mortality [74]. A major advantage of this method is the ability to identify individuals at risk who are apparently healthy, and at younger ages, before the onset of clinically measurable age-related deficits [74]. This marker will require further validation in longitudinal studies [74]. The relationship between epigenetic clocks and the frailty index is unfolding, but many studies show greater discriminative ability in relation to mortality of the latter [67, 75,76,77]. ◀︎ [2]
[1] [2017] Molecular and phenotypic biomarkers of aging
[2] [2021] Determination of Biological Age: Geriatric Assessment vs Biological Biomarkers
▶︎ Telomeres are ribonucleoprotein complexes at the end of chromosomes and become shorter after each replication, as telomerase, the enzyme responsible for its replication, is not regularly expressed in somatic cells4. The length of telomeres in leukocytes has been associated with aging and life span5as well as age-related diseases, such as cardiovascular diseases6,7, cancer8, and neurological disorders9.◀︎ [1]
Telomere shortening is a well-known hallmark of both cellular senescence and organismal aging. An accelerated rate of telomere attrition is also a common feature of age-related diseases. Therefore, telomere length (TL) has been recognized for a long time as one of the best biomarkers of aging. Recent research findings, however, indicate that TL per se can only allow a rough estimate of aging rate and can hardly be regarded as a clinically important risk marker for age-related pathologies and mortality. Evidence is obtained that other indicators such as certain immune parameters, indices of epigenetic age, etc., could be stronger predictors of the health status and the risk of chronic disease. However, despite these issues and limitations, TL remains to be very informative marker in accessing the biological age when used along with other markers such as indices of homeostatic dysregulation, frailty index, epigenetic clock, etc. This review article is aimed at describing the current state of the art in the field and at discussing recent research findings and divergent viewpoints regarding the usefulness of leukocyte TL for estimating the human biological age.[2]
[1] [2017] Molecular and phenotypic biomarkers of aging
[2] [2021] Telomere Length as a Marker of Biological Age: State-of-the-Art, Open Issues, and Future Perspectives
▶︎ Telomeres are the protective caps found at the ends of genomic DNA. They comprise repeated DNA sequences and unique proteins that together create the telomere-binding complex. In this way, highly regulated telomerase activity can selectively maintain telomere length [47]. Telomere biology propels interest in aging biomarkers for several reasons. First, inherited defects in telomerase function are associated with age-associated human disease, most notably idiopathic pulmonary fibrosis, many cancers, diabetes, cardiovascular disease, and dementia [48]. Second, telomere length shortens with chronological age and predicts the onset of cellular senescence [47]. This age-related state of cell growth arrest remarkably is present across the life course [49, 50]. Finally, telomere length, as well as telomerase activity, is heritable in both humans and mice, suggesting that it could account for some of the genetic variation seen in the aging process [50,51,52].◀︎[1]
[1] [2021] Determination of Biological Age: Geriatric Assessment vs Biological Biomarkers
[2] [2021] Determination of Biological Age: Geriatric Assessment vs Biological Biomarkers