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Hallmarks of Aging

Hallmarks of Aging

The number of people above the age of 60 years is growing worldwide and that number is projected to triple by the year 2050 [1]. Aging is the predominant risk factor for the majority of diseases and conditions that limit lifespan. And is broadly defined as the time-dependent functional decline of living organisms.


Aging is characterized by progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. Numerous premature aging diseases are the consequence of DNA damage accumulation, epigenetic alteration, loss of proteostasis, and telomere attrition. 


A major health challenge for the elderly population is maintaining their independence into their later years of life. Functional independence is directly dependent on the physical fitness of an individual, and physical fitness is determined by several measurable health-related characteristics, such as cardiorespiratory health and muscle function [2].


There are nine tentative hallmarks of aging that represent the common denominators of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication (figure 1) [3]. Exposing the interconnectedness of these hallmarks and their contribution to aging can lead to improving human health while aging with minimum side effects.

Primary Hallmarks

The nine hallmarks of aging are grouped into three categories (figure two). The primary causes of aging are the agents of bodily deterioration. The common characteristic of the primary hallmarks is the fact that they are all emphatically negative. This is the case of DNA damage, mitochondrial DNA mutations and telomere loss, epigenetic alteration, and defective proteostasis [3].

Genomic Instability is a common attribute of aging, and genetic damage accumulates over the course of one’s life and is the major factor leading to various diseases such as Werner syndrome, trichothiodystrophy, and Bloom Syndrome. Epigenetic alterations are of the most notable hallmarks of aging. Your epigenome changes as you age and as a result, precise coordination of gene activity can be compromised. What is promising about this hallmark is that your epigenome can be modified by diet, exercise, additional lifestyle factors, and pharmaceuticals. 

Antagonistic Hallmarks

In contrast to the primary hallmarks, antagonistic hallmarks have opposite effects depending on their intensity. At low levels, they mediate beneficial effects, but at high levels, they become deleterious. 

This is the case for senescence, which is cell cycle arrest. Cellular senescence protects the organism from cancer, but in excess can promote aging and at chronic high levels can produce cellular damage.

These hallmarks can be viewed as designed for protecting the organism from damage or from nutrient scarcity, but when exacerbated or chronic, their purpose is destroyed and they will generate further damage to the body [4].

Integrative Hallmarks

The third category is comprised of the integrative hallmarks: stem cell exhaustion, and altered intercellular communication, which directly affect tissue homeostasis and function. 

Notwithstanding the interconnectedness between all hallmarks, we propose some degree of hierarchical relation between them (Figure 2). 

The primary hallmarks are the initiating triggers for damaging events that progressively accumulate over time. The antagonistic hallmarks, which are beneficial in principle, become progressively negative in a process that is partly promoted or accelerated by the primary hallmarks [3].

Finally, the integrative hallmarks occur when the accumulated damage caused by the primary and antagonistic hallmarks cannot be counterbalanced by tissue homeostatic mechanisms. Because the hallmarks co-occur during aging and are interconnected, understanding their exact causal network is an exciting challenge for future work to come [3].

Figure 1: Functional Interconnections between the Hallmarks of Aging

References

  1. Exercise Attenuates the Major Hallmarks of Aging 
  2. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Medicine and science in sports and exercise
  3. The hallmarks of aging
  4. Aging Hallmarks: The Benefits of Physical Exercise. Frontiers in Endocrinology

New Natural Anti-Aging Peptide Discovered by AI

New Natural Anti-Aging Peptide Discovered by AI

A new study explores the role of HDAC4 in cellular senescence and aging. Read on to learn more.

 

In this article:

  1. What Are Peptides?
  2. What Role Do Peptides Play in Skin Aging?
  3. What Is Peptide RTE62G?
  4. How Did They Discover It?
  5. How Did They Verify Its Anti-Aging Effects?
  6. What Are Its Applications in Anti-Aging?
  7. How Else Can You Prevent Skin Aging?

Everything You Need to Know About the New Anti-Aging Peptide

 

What Are Peptides?

A peptide is a compound that has two or more amino acids. They play a vital role in how the body functions. 

They can serve as biological messengers that carry information from one tissue to another through the bloodstream. On top of that, a combination of peptides also forms different types of proteins, hormones, and enzymes in your body. 

Peptides perform various functions, so they have great potential for topical therapeutics. In fact, it can already be found in a variety of skincare products.

 

What Role Do Peptides Play in Skin Aging?

Antibodies or immunoglobulins in 3D rendering | What Role Do Peptides Play in Skin Aging? | New Natural Anti-Aging Peptide Discvoered by Ai

As building blocks of proteins, peptides are also the building blocks of collagen and elastin. Collagen helps keep skin firm, while elastin maintains the skin’s elasticity. 

When collagen and elastin stores are low, visible signs of skin aging begin to appear. The signs of skin aging include:

  • Wrinkles
  • Skin sagging 
  • Dry skin

As you age, collagen stores begin to decrease. Studies show that there are also age-related degradations of elastin

Researchers hope to be able to unlock the potential anti-aging mechanisms of peptides. Studies show that topical application of peptides can stimulate collagen synthesis and promote the skin’s metabolism.Unfortunately, when it comes to skincare, not all peptides are equal. There are hundreds of different peptides, so it’s important to determine which ones offer the most anti-aging benefits.

 

What Is Peptide RTE62G?

A new study published in the International Journal of Cosmetic Science identifies a new naturally occurring peptide with anti-aging effects. With the help of artificial intelligence (AI), researchers discovered peptide RTE62G. 

Peptide RTE626 is an unmodified peptide with extracellular matrix properties. This naturally occurring peptide comes from a plant source (Pisum sativum). 

 

How Did They Discover It?

In the in vitro experiments, they evaluated the effects of peptide RTE626 on human dermal fibroblasts and keratinocytes. They ran several tests to examine how it affects the following cellular functions:

  • Cell proliferation
  • Extracellular matrix protein production properties
  • Cell migration
  • Extracellular matrix protein synthesis and gene expression 

Ex vivo tests with human skin explants help clarify its effects on producing extracellular matrix proteins. To establish proof of concept, the researchers also ran a 28-day pilot test assessing the peptide’s clinical outcomes.

 

How Did They Verify Its Anti-Aging Effects?

In the in vitro experiments, they evaluated the effects of peptide RTE626 on human dermal fibroblasts and keratinocytes. They ran several tests to examine how it affects the following cellular functions:

  • Cell proliferation
  • Extracellular matrix protein production properties
  • Cell migration
  • Extracellular matrix protein synthesis and gene expression 

Ex vivo tests with human skin explants help clarify its effects on producing extracellular matrix proteins. To establish proof of concept, the researchers also ran a 28-day pilot test assessing the peptide’s clinical outcomes.

 

What Are Its Applications in Anti-Aging?

The tests show that peptide RTE626 significantly increases cellular migration and cellular proliferation. It also promotes the creation of extracellular matrix proteins for elastin and collagen. 

The 28-day clinical tests also show that peptide RTE626 has anti-wrinkling and collagen-stimulating effects. All of the tests confirm that peptide RTE626 has multi-functional anti-aging properties. So it has excellent potential as an anti-aging ingredient.

 

How Else Can You Prevent Skin Aging?

Using the right skincare products may be helpful, but there are other ways you can help reduce skin aging:

Understanding your epigenetics can help you know your skin’s state. Epigenetics doesn’t focus on just your genes, but it also looks into the different lifestyle and environmental factors that may regulate gene expression. 

By diving into your epigenome, it’ll give you a clearer picture of what your body needs. If you’re interested in learning more about epigenetics, visit the TruDiagonstic website today.

 

What are your anti-aging concerns? Please share them with us in the comments section below. 
Sources:

Obesogenic Diet Drives Epigenetic Predisposition To Metabolic Disorders

Obesogenic Diet Drives Epigenetic Predisposition To Metabolic Disorders

An obesogenic diet may cause inheritable epigenetic changes. Learn more about the possible impact of an obesogenic diet on future generations.

 

In this article:

  1. Can a Father’s Obesogenic Diet Predispose Offspring to Metabolic Disorders?
  2. Obesogenic Diet Propels an Epigenetic Predisposition to Metabolic Disorders
  3. Transgenerational and Intergenerational Nongenetic Inheritance
  4. Epigenetics and Environmental Influences
  5. Consequences for Multiple Generations Exposed to an Obesogenic Diet

Obesogenic Diet | Rethinking Epigenetic Inheritance

 

Can a Father’s Obesogenic Diet Predispose Offspring to Metabolic Disorders? 

The possibility to pass down individual epigenetic changes to future generations has made us rethink what inheritance is. Nongenetic inheritance is becoming common in current epigenetic research. 

Recent studies have begun to recognize the mechanisms underlying the acquisition of phenotypic traits induced by specific environmental cues in the parents of individuals. 

Paternal contribution to birth weight induced by an unhealthy diet can affect the metabolism of the offspring. A new study found significant evidence that paternal obesity affects the metabolic health of their progeny [5]. 

Nongenetic inheritance of received phenotypes is where changes caused by environmental cues induced within the parents, grandparents, and so on, can be transmitted to their offspring [3]. 

Epigenetic factors in gametes play an important role in the intergenerational transmission of obesity and type 2 diabetes. This has sparked interest in whether transgenerational inheritance also occurs via gametes [2, 4].

 Environmental cues can potentially modify molecular-heritable information carried by the sperm. They are demonstrating that environmentally induced epigenetic modifications are not erased through the process of epigenetic reprogramming. 

This causes the way the paternal epigenome is expressed and passed onto their offspring [5]. The evidence suggests that the father’s unhealthy diet negatively affected the metabolic health of their multigenerational descendants.

 

Obesogenic Diet Propels an Epigenetic Predisposition to Metabolic Disorders

ast food snacks and cola drink on wooden table | Obesogenic Diet Propels an Epigenetic Predisposition to Metabolic Disorders | Obesogenic Diet Drives Epigenetic Predisposition To Metabolic Disorders | Obesogenic Diet Drives Epigenetic Predisposition To Metabolic Disorders

Obesity is a growing public health concern that is responsible for 4 million deaths a year globally. The epigenetic inheritance of acquired metabolic disorders may contribute to the current obesity and diabetes pandemic [4]. 

The Western diet (WD) is a diet consisting of high-fat and high-sugar junk foods. Most studies only looked at the single generational effects of the WD on the father and his offspring’s phenotype. This new study’s findings revealed that maintaining a WD for several generations promotes the accumulation of epigenetic alterations in somatic and germline cells [5].

This study is all about the paternal maintenance of the WD’s part in multiple generations’ metabolic phenotype. Examining the function of nongenetic inheritance and the environment’s role in obese individuals has uncovered that paternal contribution to birth weight is induced by an unbalanced diet. 

This paternal contribution can affect the metabolism and metabolic pathologies of the offspring. One obese-associated pathology, hepatic steatosis, was identified and that it increased in severity with the ensuing generations that consumed the WD. 

The appearance of the obese-phenotype after multigenerational WD feeding indicates that obesogenic sensitivity is elevated by multiple generations of exposure [5].

 

Transgenerational and Intergenerational Nongenetic Inheritance

In the study, they maintained a paternal WD feeding in five consecutive generations of mice, which induced a gradual enhancement of fat mass and metabolic diseases over the course of the multiple generations being observed [5]. 

The researchers compared the metabolic parameters across the multiple generations of WD males.

The progenies of fathers with several WD-fed ancestors were consistently overweight for the following 4 generations, even if their father did not get fed the WD. Meaning the epigenetic inheritance of an obese phenotype is transgenerational (figure 1). Notably, males who were third and fourth generation-descendants of obese WD-fed males ended up not becoming overweight themselves.

So the obese phenotype triggered by environmental exposure of the WD in preceding paternal generations was not the only influencing factor on the mice’s phenotypes. Excluding the individual’s own diet is not painting the entire picture; this data supports that it is both the ancestral and individual diet that causes a severe metabolic effect [5].

 

Transgenerational and Intergenerational Nongenetic Inheritance

Epigenetic alterations associated with aging have been found to accelerate as a result of a high-fat diet, indicating that environmental factors play a significant part in the aging of an individual. 

Unlike genetic inheritance, environmentally-triggered epigenetic alterations are reversible, but environmental changes to the epigenome can persist over several generations [5]. This helps explain why some people seem to have a predisposition to obesity. 

Epigenetic information can be inherited through the germline, and sperm represents a plausible transgenerational carrier of environmental information [1]. Sperm RNA is the vector for paternal-intergenerational epigenetic inheritance of environmentally induced metabolic pathologies [3]. 

Environmentally induced epigenetic modifications in germlines contribute to the environmental adaptation of that species. This shows the importance of assessing each epigenetic vector for inheritance and how they will interact together to regulate the epigenome of the embryo during development. 

 

Consequences for Multiple Generations Exposed to an Obesogenic Diet

This study indicated that multigenerational exposure forced stress-induced phenotypes, which affected the metabolic state of the subsequent generations that were never directly exposed to a WD. The study showed that sperm RNAs are vectors of intergenerational inheritance but aren’t really good for the transgenerational inheritance of diet-induced metabolic alterations [5].

RNAs as vectors for epigenetic inheritance only works within the span of one generation from father to its progeny and isn’t capable of transcending multiple generations unless multiple generations have consecutively been exposed to the WD. But, as mentioned, the generations that were exposed back-to-back to the WD had the most severe overweight phenotype and metabolic disorders [5].

Ancestral exposure to the WD influenced the magnitude of the progeny’s weight, but it is not the only thing to think about when addressing severe obesity. 

Knowing that environmentally induced epigenetic modifications in germlines contribute to the offspring’s phenotypic traits is an essential factor when considering the health consequences of obesity and its comorbidities. 

Hopefully, by uncovering the mechanisms that drive epigenetic inheritance of phenotypes can help find therapies and preventative treatments for individuals with a predisposition to metabolic disorders.

 

Surprised by these findings? Share your thoughts in the comment section below!
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