The Aging Gap Between Species E-Book

Anca Ioviţă

• Herausgeber: Anca Iovita
• Kategorie: Wissenschaft und neue Technologien
• Sprache: Englisch

Veröffentlichungsjahr: 2016

Beschreibung

Aging is a puzzle to solve.
This process is traditionally studied in a couple of biological models like fruit flies, worms and mice. What all these species have in common is their fast aging. This is excellent for lab budgets. It is a great short-term strategy. Who has time to study species that live for decades?

But lifespan differences among species are magnitudes of order larger than any lifespan variation achieved in the lab. This is the reason for which I studied countless information resources in an attempt to gather highly specialized research into one easy-to-follow book. I wanted to see the forest among the trees. I wanted to expose the aging gap between species in an easy-to-follow and logical sequence. This book is my attempt at doing just that.

What are the mechanisms underlying the aging gap between species? I intentionally chose to write the answer to this question in plain English. Aging research is too important to hide it behind the closed doors of formal scientific jargon. This book could not have existed if green tea, libraries and the Internet were not invented. The amount of data I had to browse in order to keep the essential patterns is huge. Yet this book is not exhaustive. This is not a dry academic textbook. I tried to instill life in a topic that is hugely important for the extension of human lifespan. Only you can decide if I achieved this.

********* TABLE OF CONTENTS ***********

• Finding the Forest Among the Trees
• Being Reliable Counts
• The Mathematics of Aging
• The Speed of Senescence
• Case Study: Aging in Fish
• How to Estimate Chronological Age
• Taking Life Slowly
• On Temperature and Aging
• Dormancy
• The Housekeeping Problem
• Case Study: Aging in Turtles
• Intracellular Junk
• Case Study: Aging in Crustaceans
• Extracellular Junk
• Case Study: Protein Quality Control
• The Sweet Poison
• Are Cell Membranes the Pacemakers of Metabolism?
• Could Reproduction Set up the Pacemaker of Senescence?
• The Segregation of Somatic and Germ Cells
• Clonal Senescence Versus Mechanical Senescence
• Same Species, Different Lifespans
• Case Study: Eusocial Species
• Case Study: Parasite/Free-Living Populations
• Case Study: Island Versus Inland Populations
• Hormones as Pacemakers of Senescence
• Case Study: Low Hormone Levels in Long-lived Rodents
• Is Aging a Form of Dehydration?
• The Immune Pacemaker of Senescence
• Innate Versus Adaptive Immunity
• Senescent Cells
• Case Study: Thymic Involution in Negligible Senescence Species
• Reverse Engineering the Body
• Case Study: Why Are Sponges Potentially Immortal?
• Modular Growth and Aging
• Case Study: Youth Is Forever Gone. Unless You Are a Hydra. Or an Immortal Jellyfish
• Down The Neoteny Lane
• Case Study: Neoteny in Amphibians
• Case Study: Neoteny in Mammals
• It's All About Neoteny
• Does Aging Start When Growth Stops?
• Case Study: Indeterminate Growth in Crustaceans
• The Rate of Growth
• Case Study: Aging in Bivalves
• Is Telomerase The New Fountain of Youth?
• Case Study: Same Species, Different Telomerase Expression
• Telomerase Gene Therapy
• Case Study: Sea Urchins
• Perennial Plants and Their Regenerating Roots
• Case Study: The Bristlecone Pine
• Unitary Versus Colonial Organisms
• Cancer
• The Paradox of Peto
• Case Study: Cancer in Long-Lived Species
• The End
• Acknowledgments
• Bibliography

Leseprobe

THE AGING GAP BETWEEN SPECIES

ANCA IOVIŢĂ

The Aging Gap Between Species

Copyright © 2015 by Anca Ioviţă. All rights reserved under international copyright conventions. 

No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system without the written permission of the author, except where permitted by law.

Disclaimer

This book is designed to provide information on gerontology only. This information is provided and sold with the knowledge that the author and publisher do not offer any professional advice. In the case of a need for any such expertise consult with the appropriate professional. This book does not contain all information available on the subject. This book has not been created to be specific to any individual’s or organizations’ situation or needs. Every effort has been made to make this book as accurate as possible. However, there may be typographical and or content errors. Therefore, this book should serve only as a general guide and not as the ultimate source of subject information. This book contains information that might be dated and is intended only to educate and entertain. The author and publisher shall have no liability or responsibility to any person or entity regarding any loss or damage incurred, or alleged to have incurred, directly or indirectly, by the information contained in this book. You hereby agree to be bound by this disclaimer or you may return this book within the guarantee time period for a full refund. 

References are provided for informational purposes only and do not constitute endorsement of any websites or other sources. Readers should be aware that the websites listed in this book may change. 

Dedicated to each inquiring mind who added a small step to our understanding of aging

Contents

Finding the Forest Among the Trees 1 

Being Reliable Counts 2 

The Mathematics of Aging 3 

The Speed of Senescence 4 

Case Study: Aging in Fish 7 

How to Estimate Chronological Age 8 

Taking Life Slowly 11 

On Temperature and Aging 12 

Dormancy 18 

The Housekeeping Problem 25 

Case Study: Aging in Turtles 27 

Intracellular Junk 28 

Case Study: Aging in Crustaceans 30 

Extracellular Junk 32 

Case Study: Protein Quality Control 33 

The Sweet Poison 35 

Are Cell Membranes the Pacemakers of Metabolism? 38 

Could Reproduction Set up the Pacemaker of Senescence? 41 

The Segregation of Somatic and Germ Cells 44 

Clonal Senescence Versus Mechanical Senescence 46 

Same Species, Different Lifespans 47 

Case Study: Eusocial Species 48 

Case Study: Parasite/Free-Living Populations 51 

Case Study: Island Versus Inland Populations 52 

Hormones as Pacemakers of Senescence 55 

Case Study: Low Hormone Levels in Long-lived Rodents 67 

Is Aging a Form of Dehydration? 72 

The Immune Pacemaker of Senescence 73 

Innate Versus Adaptive Immunity 73 

Senescent Cells 76 

Case Study: Thymic Involution in Negligible Senescence Species 78 

Reverse Engineering the Body 81 

Case Study: Why Are Sponges Potentially Immortal? 89 

Modular Growth and Aging 92 

Case Study: Youth Is Forever Gone. Unless You Are a Hydra. Or an Immortal Jellyfish. 93 

Down The Neoteny Lane 95 

Case Study: Neoteny in Amphibians 96 

Case Study: Neoteny in Mammals 100 

It's All About Neoteny 102 

Does Aging Start When Growth Stops? 105 

Case Study: Indeterminate Growth in Crustaceans 108 

The Rate of Growth 111 

Case Study: Aging in Bivalves 112 

Is Telomerase the New Fountain of Youth? 116 

Case Study: Same Species, Different Telomerase Expression 119 

Telomerase Gene Therapy 120 

Case Study: Sea Urchins 121 

Perennial Plants and Their Regenerating Roots 124 

Case Study: The Bristlecone Pine 126 

Unitary Versus Colonial Organisms 128 

Cancer 133 

The Paradox of Peto 134 

Case Study: Cancer in Long-Lived Species 136 

The End 141 

Acknowledgments 143 

Bibliography 145 

Finding the Forest Among the Trees

Aging is a puzzle to solve.

This process is traditionally studied in a couple of biological models like fruit flies, worms and mice. What all these species have in common is their fast aging. This is excellent for lab budgets. It is a great short-term strategy. Who has time to study species that live for decades? 

But lifespan differences among species are orders of magnitude larger than any lifespan variation achieved in the lab. This is the reason for which I studied countless information resources in an attempt to gather highly specialized research into one easy-to-follow book. I wanted to see the forest among the trees. I wanted to expose the aging gap between species in an easy-to-follow and logical sequence. This book is my attempt at doing just that.  

Aging is inevitable, or so I've been told. I was never one to accept things at face value just because some authority said it. So I began to question whether aging is the same in all species. While looking for answers, I was surprised to find out there is a lack of biological model diversity in gerontology. I was undeterred and I searched for the most obscure scientific papers on how other species age and what could set them apart. That's how I started typing the words you're now reading.

If you ever had a pet, you already noticed that lifespans differ widely. You may have looked the same for a decade, while your dog or cat already suffered from age-related diseases. There is huge lifespan variability, both in terms of individuals belonging to the same species and among species themselves. What are the mechanisms underlying the aging gap between species?

I intentionally chose to write the answer to this question in plain English. Aging research is too important to hide it behind the closed doors of formal scientific jargon. This book could not have existed if green tea, libraries and the Internet were not invented. The amount of data I had to browse in order to keep the essential patterns is huge. Yet this book is not exhaustive. This is not a dry academic textbook. I tried to instill life in a topic that is hugely important for the extension of human lifespan. Only you can decide if I achieved this.  

Being Reliable Counts

Depending on the number of vital parts and the resilience of each of them, systems can range from the simplest to the most complex. Aging is first of all a consequence of being complex [42]. Here is why.

A system at its simplest has one vital part only. You could say bacteria are simple because they are organisms made of one cell only. If any external or internal factor kills that one cell, the whole system is disrupted and the organism is plain dead. As you'll read later, some bacteria display a form of aging, similar to clonal senescence in complex multicellular organisms, but I included them here because they are simple biological systems everyone is aware of.

When complexity increases from bacteria to a human being like you - made up of billions of cells with several vital parts -, aging becomes a reality. Time passes and each of these parts can suffer damage. Such damage is minor, but it all adds up. A blurry lens in the form of cataracts does not normally kill people, unless they insist on driving cars or crossing the street unattended. Usually people with cataracts live for many years. But add heart failure to that. And minor kidney disease. No wonder a full-blown pneumonia infection can kill an elderly while leaving the young alive in most cases. Pneumonia may have been the final blow, but all minor and major damages a complex human being experiences lead to the final stage of involution: senility.

The Mathematics of Aging

Innovations often come from unexpected places. People searched for the fountain of youth since immemorial times, but it is only recently that aging itself  received an almost mathematical description.

The solution came from people selling life insurance. If you want to make a living out of it, you need to correctly estimate the probability of individual X dying this year, next year and so on. If you miss the boat, you may undercharge him/her and soon get out of business. Overcharge people and they will soon prefer to set such funds on their own. In order to establish such a balance, actuaries started creating life tables and they noticed the probability of dying doubled each 8 years, with the lowest risk right around puberty. This is known as mortality risk doubling time in gerontology, the science of aging [34].

Humans are the only species to buy life insurance, but the pattern of doubling mortality risk stays the same in most other species, mammals or not. What differs is the time interval at which the probability to die doubles.

Apart from the mortality risk doubling, the other mathematical feature of aging is a drop in fertility [34]. This drop can take place gradually or almost abruptly like in female mammals undergoing menopause.

The aging process is [55]: 

progressive 

endogenous 

irreversible 

deleterious to the individual 

Since it is in the interest of living beings to reproduce as many times as their bodies and the surrounding environment will allow, it is automatically in their interest to survive as much as possible. An organism does the best it can under the constraints of predators, insufficient resources and the desire to spread its genes in offspring that will survive too! According to the disposable soma theory, if an animal is predated upon during its midlife it makes no sense to divert unnecessary resources from reproduction towards better DNA repair genes that may never get the chance to be used [34]. But if the environment improves and animals reproduce at later stages in life, improving maintenance is a sure bet. 

The Speed of Senescence

During the course of this book I use 'aging' and 'senescence' as interchangeable for the sake of simplicity. In gerontological literature though, aging refers to the passage of time without mentioning whether the system changed for better or for worse. Senescence describes the wear-and-tear common in most systems after days, weeks, months or decades depending on its reliability and expected lifespan. But when people casually talk about 'aging' , involution is usually implied.

The first major gap in comparative gerontology was closed when three patterns of senescence were recognized [34].

These put the rest of the book into perspective:

rapid senescence

gradual senescence

slow or negligible senescence

Negligible senescence was the most difficult to accept by the gerontological community. All three are important for seeing the forest among the trees when it comes to aging itself.

Rapid senescence is spectacular. The Oncorhynchus Pacific salmon undergoes major damage to its organs right after spawning.  Its aortic wall gets thicker. It develops fungus infections on its skin. The fish will most likely be dead in a couple of days. It is very rare for Pacific salmons to reproduce twice in a lifetime [34].

You may think rapid senescence would be an exception since evolution would have favored species that reproduce repeatedly. But rapid senescence does not impede multiple bouts of reproduction. The bamboo tree blossoms repeatedly for decades, but it stops doing so a couple of months before succumbing to death [34]. The bamboo's fast growth is a common theme in species with rapid senescence, hence its ubiquitous use in eco-friendly wood products.

Sometimes rapid senescence is manifested in one gender only. Antechinus marsupial male mice experience deadly exhaustion after mating with several females [34].

The common denominator of rapid senescence is mostly hormonal determination, especially the secretion of cortisol, a stress hormone. Other mechanisms are waiting to be discovered.  

Gradual senescence is a milder form. Human beings are a good example. Aging occurs in decades which – given the average human lifespan – means that you spend about a third of your life growing, a third as a mature adult and the last third losing what you've built during the previous life stages. With few exceptions like the male marsupial mice mentioned earlier, most mammals undergo gradual senescence [34].

Slow or negligible senescence is where things become interesting. Such species display a constant mortality risk over their lifespan, while their fertility is constant or may even increase in time. In other words, they are potentially immortal.

An even more accurate classification of senescence according to mortality risk and fertility is the following [112]:

positive senescence – where individuals of a species develop wear and tear signs as time passes by, their mortality increases and their fertility decreases 

negligible senescence – where aging signs are apparently lacking and the older individuals have the same probability of dying as the younger ones, while fertility remains the same 

negative senescence – where such individuals enjoy a diminished probability of dying as they grow older, while their fertility increases. As an example here, it is very easy to die as a one-day turtle, but once you reach the ocean and you are the size of an adult, the probability of dying is seriously diminished. Similarly, older male lobsters enjoy greater fertility than younger ones. 

It took a long time until the second and third patterns of senescence were accepted by the gerontology community. The status quo was that we were all destined to age no matter our genetic heritage. Whether one species belongs for certain to one of these three senescence phenotypes remains to be researched for most organisms.

Case Study: Aging in Fish

There is probably no other category of animals in which the speed of aging is so different. From the outside, fish look mostly the same. Their size may be different, but their anatomy is very similar. Fish are more homogeneous than birds or mammals. Yet their maximum lifespan ranges from a couple of months to more than 200 years and their rate of aging is just as different [87].

Fish which undergo rapid aging often breed only once. In other words, they are semelparous. Such species include:

the Oncorhynchus Pacific salmon

the Anguilla anguilla eel

the Mallotus villosus capelin

the Petromyzontiformes lamprey 

Fish which undergo gradual aging include many species familiar to aquarium hobbyists: 

the Poecilia reticulata guppy

the killifish group

the Danio rerio zebrafish

the Oryzias Japanese rice fish

the Xiphophorus platy fish

Negligible aging fish grow slowly throughout their lifetime and have very low metabolic rates at old age. Examples include:

the Sebastes rockfish

the Acipenser sturgeons

the Huso huso beluga

the Allocyttus verrucosus warty oreo

the Polyodontidae paddlefish

the female plaice

Fish have plenty of predators. Yet relative to other vertebrates, fish often express delayed senescence because of indeterminate growth, a case where fecundity increases with age thereby favoring the older individuals in the total gene pool [93]. Whether these differences in aging speeds are due to hormones, telomerase or any other mechanism is still an open question.

How to Estimate Chronological Age

Birth certificates are a recent human invention. Most people nowadays are able to tell you their age and have a piece of paper to prove it too. Yet gerontology is about studying aging in other species as well. Except for certain pets, most of them don't receive any additional documentation at the moment of their birth.

This little piece of information is hugely important when determining the maximum lifespan of different species. Fortunately, gerontologists developed several age estimation methods.

Several species leave a trail of their periodic growth increments in the hard structures of their body. Trees display growth rings in their trunks, giving birth to the scientific method of dendrochronology or tree-ring dating. Bivalve shells archive their age in periodic growth lines. Corals display growth rings as well. Marine mammals have cementum layers in their teeth. Baleen whales have no teeth, but they grow ear wax plugs as they age [109]. Fish retain such growth patterns in their inner ear bones called otoliths, as well as in their vertebrae and scales.

The caveat is that growth patterns depend on local temperatures, seasonal food supplies as well as hormonal patterns such as reproduction. In order to be used as a method of age estimation, the above growth ring counting has to be calibrated for each species.

Such calibration can be done two ways:

tag and later recapture individuals from the set species

measure known radioactive decay in the hard structures and compare the result with the number of growth rings.  

Only after calibration can you make sure whether a growth ring counts for one year.

Many plants and animals leave behind trails in the form of hard structures: shells, bones, teeth. But not all of them do that. So how do you determine the age of such an individual?

The tissue proportion of lipofuscin, a well known aging pigment, tells you the physiological age of that individual. Depending on the oxidative stress it encountered, this estimate may or may not coincide with the chronological age. For example, if you put under the microscope a sheet of tissue from someone suffering of lipofuscinosis, you may obtain a larger number of years compared to the one deducted from a healthy individual's identity card. Beyond humans, lipofuscin is deposited in several animal tissues.

Another estimation method could be the telomere length in somatic tissues. This method is reliable in species which don't express indeterminate growth by turning on the telomerase enzyme. As you'll see in the following pages, this method doesn't work in indeterminate growth species such as lobsters, crabs, sea urchins and some fish.

Taking Life Slowly

Entropy is commonly understood as a measure of disorder. A closed system with no external energy source has no choice but to reach maximum entropy. I often wondered whether aging is an example of entropy. Organisms need energy to at least survive, if not reproduce as well. Biological systems are open systems, hence according to the second law of thermodynamics, they can decrease their entropy if they increase entropy around them by at least that same amount. In other words, open systems can increase or maintain order if they create at least the same degree of disorder around them. I say 'at least' because energy is partly transformed in heat.  

Entropy is directly proportional to energy and inversely proportional to temperature.  

Depressing metabolism in different forms of dormancy like hibernation, estivation, diapause and many others is one way through which negligible and very slow senescence species buy themselves some time during which aging doesn’t seem to take place.