Category Archives: Human Longevity

Welcome to the LongevityMap, a database of human genetic variants associated with longevity. Negative results are also included in the LongevityMap to provide visitors with as much information as possible regarding each gene and variant previously studied in context of longevity. As such, the LongevityMap serves as a repository of genetic association studies of longevity and reflects our current knowledge of the genetics of human longevity.

Searching the LongevityMap can be done by gene or genetic variant (e.g., refSNP number). You can enter one or more words from the gene's name or use the gene's HGNC symbol. Note that the search is case insensitive. It is also possible to search for a specific cytogenetic location but for this you need to tick the box below.

To search for a specific study in the LongevityMap, you may browse or search its literature:

You may download a zipped tab-delimited ASCII dataset with the raw data, derived from the latest stable build of the LongevityMap.

If you find an error or wish to propose a study or variant to be included in the database, please contact us. To receive the latest news and announcements, please join the HAGR-news mailing list.

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human longevity - Senescence

San Jos State University applet-magic.com Thayer Watkins Silicon Valley & Tornado Alley USA Animal Longevity and Scale

A useful line of analysis is to consider the effect of scale changes for creatures which are similar in shape and only differ in scale. As the scale of an animal increases the body weight and volume increase with the cube of scale. The volume of blood flow required to feed that bulk also increases with the cube of scale. The cross sectional area of the arteries and the veins required to carry that blood flow only increases with the square of scale. There are other area-volume relationships which impose limitations on creatures. Some of those area-volume constraints, including the above one, are:

Thus to compensate for the body needs which increase with the cube of scale but the areas increase with only the square of scale the average blood flow velocity must increase linearly with scale. Blood flow velocity is driven by pressure differences. The pressure difference must be great enough to carrying the blood flow to the top of the creature and great enough to overcome the resistance in the arteries and veins to the flow. The pressure required to pump blood from the heart to the top of the creature is proportional to scale. The pressure difference required to overcome the resistance to flow through the arteries into the capillaries and back again through the veins is more difficult to characterize in terms of scale. The greater cross sectional area reduces the resistance but the long length increases resistance. The net result of these two scale influences seems to be that the pressure difference required to drive the blood through the bulk of the creature is inversely proportional to scale. The pressure difference imposed would be the maximum of the two required pressure differences.

Shown below are the typical blood pressures for creatures of different scales.

The linear regression of the logarithm of pressure on the logarithm of height yields the following result:

The linear regression of the logarithm of pressure on the logarithm of weight yields:

If blood pressure were proportional to scale then the coefficient for *log(Height) would be 1.0 and for *log(Weight) would be 0.333 since weight to proportional to the cube of scale. The regression coefficients are not close to the theoretical values but they are of the proper order of magnitude for accepting blood pressure as being proportional to scale.

The volume of the heart of a creature is proportional to the cube of scale. The volume of the blood to be moved is also proportional to the cube of scale. From the previous analysis the flow velocity is proportional to scale. Therefore the time required to evacuate the heart's volume is proportional to scale. This means that the heartbeat rate is inversely proportional to scale. The following table gives the heart rates for a number of creatures.

A regression of the logarithm of heart rate on the logarithm of weight yields the following equation:

If heart rate were exactly inversely proportion to scale the coefficient for *log(weight) would be -0.333. This is because scale is proportional to the cube root of weight. The coefficient of -0.2 indicates that the heart rate is given an equation of the form

One salient hypothesis is that the animal heart is good for a fixed number of beats. This hypothesis can be tested by comparing the product of average heart rate and longevity for different animals. Because the heart rate is in beats per minute and longevity is in years the number of heart beats per lifetime is about 526 thousand times the value of the product. The data for a selection of animals are:

Although the lack of dependence is clear visually the confirmation in terms of regression analysis is:

The t-ratio for the slope coefficient is an insignificant 0.15, confirming that there is no dependence of lifetime heartbeats on the scale of animal size.

If a heart is good for just a fixed number of beats, say one billion, then heart longevity is this fixed quota of beats divided by the heart rate. From the above equation for heart rate, lifespan (limited by heart function) would be proportional to scale raised to the 0.6 power.

The data for testing this deduction are:

For the data in the above table, admittedly very rough and sparse, the regression of the logarithm of the lifespan on the logarithm of weight gives

Thus the net effect of scale on animal longevity is positive. Taking into account that weight is proportional to the cube of the linear scale of an animal the above equation in terms of scale would be

This says that if an animal is built on a 10 percent larger scale it will have a 6 percent longer lifespan.

Originally posted here:
Animal Longevity and Scale

Scientists may be able to make substantial gains in extending not only the length of human life, but the quality of life as we age, according to many researchers. That won't be limited to breakthroughs in the laboratory. To a significant extent, it will depend on how we live our lives.

As for the scientists, first they have to answer a very basic question. Why do humans live longer than any other mammals?

For starters, we are big. Long ago scientists recognized a relationship between body size and longevity. Humans just narrowly edge out the elephant (so size isn't the whole story) to win the Olympic gold for living longer, but recent research reveals that's just part of the story.

We also have huge brains compared to the size of our bodies. We are mobile, have few predators except for other humans, and there's a drugstore on every corner.

It wasn't always that way. During most of recorded history any human who reached the mid thirties had beaten the system. Over the past century we gained a global average of 30 years, about 25 of which are attributed to improvements in public health, according to federal statistics.

Today, the global life expectancy is 67.2 years. It's around 78 years in the United States, and a few years more in Japan, the world leader for sticking around.

Genetics, of course, play a key role in longevity. In recent years, when we entered the golden age of genetics, many hoped to discover the "longevity gene" that allowed an increasing number of humans to live more than a century. For awhile, they thought they had found it.

One gene produces sirtuins, a protein thought to increase lifespan in several organisms, and that protein quickly became the darling of producers of anti-aging creams. But last year an international team of researchers found that sirtuins have no effect on animal longevity.

That came as no surprise to scientists at the University of California, San Francisco, who had determined that there is no longevity gene. As has often been the case in genetics in recent years, it's much more complicated than that.

It turns out that there are many genes that affect lifespan, but each of those genes has a very limited role. The San Francisco researchers found that some genes make proteins that fight bacterial infections, while others ward off oxidative stress and protein damage, commonly associated with aging. But all these genes don't just do their own thing. They are apparently controlled by at least two other genes that act as drill sergeants. Research by these scientists found that when all these genes work right, the lifespan of the roundworm, C. elegans, doubled. That worm is used in much research because it is a simple organism that shares many genes with humans.

But will the same thing work for humans? Maybe.

In a related study, scientists at the University of Liverpool reported earlier this year that some proteins change over time in long living species, including humans. Joao Pedro Magalhaes and his colleagues studied 30 mammals and found that these proteins evolve during the course of the lifetime "to cope with biological processes impacted by aging, such as DNA damage." In other words, animals that live longer are better equipped to make repairs in tissues and organs that help them fight the aging process.

There is a huge body of evidence showing that size really does matter, both in terms of body mass and cerebral tissue. Researchers in Barcelona studied 493 mammal species and found that a larger brain leads to a longer life.

A smarter animal is better equipped to deal with environmental challenges and less likely to take silly chances, like picking a fight with a much bigger animal. That may seem obvious, but it's less clear why body size should contribute to longer lifespan. Among mammals, the top four are humans, followed by elephants, horses and hippopotamuses, but most likely the hippo wouldn't score all that high on an IQ test.

The turkey buzzard tops the list for birds at 118 years, maybe because it's smart enough to wait for road kill instead of attacking a live animal.

But the giant tortoise is the real champ. The world mourned the passing of Lonesome George in the Galapagos Islands earlier this year. The actual age of old George is unknown, although it's clear he made it well past the century mark. Among the superachievers was Tu'I Malila, who was presented to the royal family of Tonga by Capt. James Cook in 1777. He was thought to be 188 when he died in 1965. That still leaves the question of why size matters. Adrian Bejan, a mechanical engineering professor at Duke University, has spent years studying the relationship between size and lifespan, and he is out with a new idea.

Bejan argues in a paper published this week in Nature Scientific Reports that big animals live longer because they travel farther, thus giving them access to more resources. Mobility is the key. Get off the couch.

If he's right, then that leaves longevity largely in our own hands. Do the right thing and you'll live longer. Physicians tell us that all the time. Don't smoke. Get plenty of exercise. Eat right. Researchers at Newcastle University in England think they have figured out why something like eating a low calorie diet can increase lifespan. Aging is strongly influenced by senescence, the end of a cell's ability to replicate itself. They fed mice a low calorie diet and the accumulation of senescent cells plummeted, thus defeating much of the aging process.

It worked even for older mice, suggesting that eating less or at least fewer calories may be our best defense against aging and an early death.

No more ice cream? I'm waiting for a magic pill.

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Can Humans Live Forever? Longevity Research Suggests ...

Genetics of Human Longevity: New Ideas & Findings

Natalia Gavrilova

Center on Aging, NORC at the University of Chicago

(Abstract of presentation at the International Conference on Longevity, Sydney, Australia, March 5-7, 2004)

In contrast to the remarkable progress in the genetics of yeast and nematode aging, little is known about genes that control human longevity. What is behind the records of extreme human longevity: just lucky chance, favorable environment, or 'good' genes? How to resolve the apparent controversy between strong familial clustering of human longevity, and poor resemblance in lifespan among blood relatives?

We applied methods of genetic epidemiology and survival analysis to family-linked data on human lifespan. Special efforts were undertaken to collect detailed and reliable human genealogies an important data source for genetic studies of human longevity. We found that the dependence of offspring lifespan on parental lifespan is essentially non-linear, with very weak resemblance before parental lifespan of 80 years and very steep offspring-parent dependence (high narrow-sense heritability) for longer lived parents. There is no correlation between lifespan of spouses, who share familial environment. These observations suggest that chances to survive beyond age 80 are significantly influenced by genetic factors rather than shared familial environment. These findings explain the existing longevity paradox: although the heritability estimates for lifespan are rather low, the exceptional longevity has a strong familial association.

We also tested the prediction of mutation theory of aging that accumulation of mutations in parental germ cells may affect progeny lifespan when progeny was conceived to older parents. We found that daughters conceived to older fathers live shorter lives, while sons are not affected. Maternal age effects on lifespan of adult progeny are negligible compared to effects of paternal age, which is consistent with the notion of higher rates of DNA copy-errors in paternal germ cells caused by more intensive cell divisions during spermatogenesis.

Genealogical data also are useful for testing the prediction of the disposable soma theory that human longevity comes with the cost of impaired reproductive success. We found that in contrast to previous reports by other authors, woman's exceptional longevity is not associated with infertility. Thus, the concept of heavy infertility cost for human longevity is not supported by data, when these data are carefully cross-checked, cleaned and reanalyzed. These results demonstrate the importance of high quality genealogical data for genetic studies of human longevity.

Relevant Publications:

Gavrilov, L.A., Gavrilova, N.S. Early-life factors modulating lifespan. In: Rattan, S.I.S. (Ed.).Modulating Aging and Longevity. Kluwer Academic Publishers, Dordrecht, The Netherlands, 2003, 27-50.

Gavrilova, N.S., Gavrilov, L.A. Evolution of Aging. In: David J. Ekerdt (eds.) Encyclopedia of Aging, New York, Macmillan Reference USA, 2002, vol. 2, 458-467.

Gavrilov, L.A., Gavrilova, N.S. Human longevity and parental age at conception. In: J.-M.Robine et al. (eds.) Sex and Longevity: Sexuality, Gender, Reproduction, Parenthood, Berlin, Heidelberg: Springer-Verlag, 2000, 7-31.

Gavrilova N.S., Gavrilov L.A., Evdokushkina, G.N., Semyonova, V.G. Early-life predictors of human longevity: Analysis of the 19th Century birth cohorts. Annales de Demographie Historique, 2003, 2: 177-198.

Gavrilova NS, Gavrilov LA, Semyonova VG, Evdokushkina GN. Does Exceptional Human Longevity Come With High Cost of Infertility? Testing the Evolutionary Theories of Aging. Biogerontology. 4(Suppl.1): 35-35, 19 Sep 2003

Gavrilov, L.A., Gavrilova, N.S. Evolutionary theories of aging and longevity. TheScientificWorldJOURNAL, 2002, 2: 339-356. Available: http://www.thescientificworld.com/

Gavrilova, N.S., Gavrilov, L.A. When does human longevity start?: Demarcation of the boundaries for human longevity. Journal of Anti-Aging Medicine, 2001, 4(2): 115-124.

Gavrilov L.A., Gavrilova N.S. Epidemiology of human longevity: The search for appropriate methodology. Journal of Anti-Aging Medicine, 2001, 4(1): 13-30.

Gavrilov, L.A., Gavrilova, N.S. Biodemographic study of familial determinants of human longevity. Population: An English Selection, 2001, 13(1): 197-222.

Gavrilova, N.S., Gavrilov, L.A. Consanguinity and human longevity: Findings from the International Centenarian Study. Gerontologist, 2001, 41 (Sp. issue): 87-87.

Gavrilov, L.A., Gavrilova, N.S. Is there a reproductive cost for human longevity? Journal of Anti-Aging Medicine, 1999, 2(2): 121-123.

Gavrilova, N.S., Gavrilov, L.A., Evdokushkina G.N., Semyonova, V.G., Gavrilova, A.L., Evdokushkina, N.N., Kushnareva, Yu.E., Kroutko, V.N., Andreyev, A.Yu. Evolution, mutations and human longevity. Human Biology, 1998, 70(4): 799-804.

Gavrilov, L.A., Gavrilova, N.S. Parental age at conception and offspring longevity. Reviews in Clinical Gerontology, 1997, 7: 5-12.

Gavrilov L.A., Gavrilova, N.S., Kroutko, V.N., Evdokushkina, G.N., Semyonova, V.G., Gavrilova, A.L., Lapshin, E.V., Evdokushkina N.N., Kushnareva, Yu.E. Mutation load and human longevity. Mutation Research, 1997, 377(1): 61-62.

Gavrilov, L.A., Gavrilova, N.S. When Fatherhood Should Stop? Letter. Science, 1997, 277(5322): 17-18.

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Genetics of Human Longevity

LA JOLLA, Calif., June 24, 2015 /PRNewswire/ --Human Longevity, Inc. (HLI), the genomics-based, technology-driven company, announced today the HLI Research Fellows Program, designed to engage experts in the fields of genomics, informatics/bioinformatics, and machine learning to explore the latest findings and knowledge on genetics with clinically relevant outcomes. The program gives scholars a unique opportunity to participate in innovative analysis of large scale genome data and to work with groups of scientists, bioinformaticians and machine learning specialists to ensure state-of-the-art annotation and interpretation of the human genome.

HLI is working to revolutionize the practice of medicine by building the world's largest, most comprehensive database of whole genome, phenotype and clinical data. From there, HLI's team develops and applies large scale computing, machine learning, and scientific analysis to make novel discoveries. The company is enabling pharmaceutical companies, insurers and healthcare providers to impact and improve health.

"The HLI Research Fellows Program invites leaders in precision medicine and technology to engage with a world-class team on the front lines of health innovation," said Dr. J. Craig Venter, Co-Founder and CEO of Human Longevity, Inc. "We look forward to welcoming these experts and transforming healthcare together."

The 6-12 month program is open to post graduate scholars and field experts at HLI's locations in San Diego, Mountain View and Singapore.

APPLICATION DETAILS The deadline for application submissions is September 1, 2015 to researchfellows@humanlongevity.com. Please see http://www.humanlongevity.com for application and program information.

About Human Longevity, Inc.Human Longevity Inc. (HLI) is the genomics-based, technology-driven company creating the world's largest and most comprehensive database of whole genome, phenotype and clinical data. HLI is developing and applying large scale computing and machine learning to make novel discoveries to revolutionize the practice of medicine. A privately held company headquartered in San Diego, CA, HLI was founded in 2013 by pioneers in the fields of genomics and stem cell therapy. HLI will be licensing access to its database, and developing new diagnostics and therapeutics as part of their product offerings. For more information please visit, http://www.humanlongevity.com.

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SOURCE Human Longevity, Inc.

RELATED LINKS http://www.humanlongevity.com

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Human Longevity, Inc. Announces Research Fellows Program

PR Newswire

SAN DIEGO, Aug. 25, 2015

SAN DIEGO, Aug. 25, 2015 /PRNewswire/ -- Human Longevity, Inc. (HLI), the genomics-based, technology-driven company, announced today that Mark A. Winham has joined the company as Chief Operating Officer. Winham, who brings more than 25 years of life sciences, medical operations and technical experience, will report directly to HLI's CEO, J. Craig Venter, Ph.D.

In this new role as COO, Winham will be responsible for managing all HLI sequencing, laboratory and product pipeline operations as well as all facility operations. HLI currently has three locations in San Diego and Mountain View, California and Singapore.

Winham comes to HLI most recently from Millennium Health, where he was COO and was primarily responsible for strategic planning, development of Laboratory Operations and R&D activities.

Prior to his role at Millennium Health, Mark spent 10 years at Life Technologies, where he held a series of significant positions including Vice President of Global Manufacturing. There he was responsible for a manufacturing organization with more than 40 sites world-wide having approximately 2,500 employees and developing products and services totalling $2.9 billion in revenue. Winham was VP of Global Manufacturing with Applied Biosystems when the company was acquired by Life Technologies.

Winham's early career was shaped at Sanofi Aventis, Johnson and Johnson and Advanced Medical Solutions.

"Mark brings substantial operational vision and technical leadership to HLI. He will play a critical role in helping to manage the growth and complexities of our business as we expand our operations globally," said Dr. J. Craig Venter, Co-Founder and CEO of Human Longevity, Inc.

Winham holds a Bachelor of Sciences degree from Napier University in Edinburgh, Scotland.

About Human Longevity, Inc. Human Longevity, Inc. (HLI) is the genomics-based, technology-driven company creating the world's largest and most comprehensive database of whole genome, phenotype and clinical data. HLI is developing and applying large scale computing and machine learning to make novel discoveries to revolutionize the practice of medicine. A privately held company headquartered in San Diego, CA, HLI was founded in 2013 by pioneers in the fields of genomics and stem cell therapy. HLI will be licensing access to its database, and developing new diagnostics and therapeutics as part of their product offerings. For more information please visit, http://www.humanlongevity.com.

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To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/human-longevity-inc-hires-life-sciences-leader-mark-winham-as-chief-operating-officer-300132976.html

SOURCE Human Longevity, Inc.

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Human Longevity, Inc. Hires Life Sciences Leader, Mark ...

Division of Human Resources

Longevity pay coming soon

Since it happens once a year, its easy to forget about the longevity increment as one of the benefits of working at WVU. But its that time again and the annual payment is on its way!

Classified and Non-classified employees with three or more years of service will be getting longevity pay on July 31, 2015. Eligible employees will receive an annual salary supplement equal to sixty dollars times the employees years of service.

Employees in a regular position appointment earn years of service experience for longevity purposes based on the total years of service with state agencies and/or state spending units. For further information, please review WVU BOG Policy 32 Rule on Annual Increment regarding Annual Increment Pay.

Faculty and FE/AP must be 1.00 FTE for at least nine months in each fiscal year to receive credit toward longevity. Any time worked less than 1.00 FTE does not count toward longevity.

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Longevity Pay | Division of Human Resources | West ...

Longevity is influenced by genetic and environmental factors. The brain's dopamine system may be particularly relevant, since it modulates traits (e.g., sensitivity to reward, incentive motivation, sustained effort) that impact behavioral responses to the environment. In particular, the dopamine D4 receptor (DRD4) has been shown to moderate the impact of environments on behavior and health. We tested the hypothesis that the DRD4 gene influences longevity and that its impact is mediated through environmental effects. Surviving participants of a 30-year-old population-based health survey (N = 310; age range, 90-109 years; the 90+ Study) were genotyped/resequenced at the DRD4 gene and compared with a European ancestry-matched younger population (N = 2902; age range, 7-45 years). We found that the oldest-old population had a 66% increase in individuals carrying the DRD4 7R allele relative to the younger sample (p = 3.5 10(-9)), and that this genotype was strongly correlated with increased levels of physical activity. Consistent with these results, DRD4 knock-out mice, when compared with wild-type and heterozygous mice, displayed a 7-9.7% decrease in lifespan, reduced spontaneous locomotor activity, and no lifespan increase when reared in an enriched environment. These results support the hypothesis that DRD4 gene variants contribute to longevity in humans and in mice, and suggest that this effect is mediated by shaping behavioral responses to the environment.

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DRD4 genotype predicts longevity in mouse and human.

Chilli peppers were among the most popular spicy plants recorded in research on the diets of 500,000 people in China. Photograph: Linda Perry/PA

People who request an extra kick to their curry could also be adding years to their life, according to a large study which linked frequent consumption of spicy food to longevity.

Researchers examining the diets of almost 500,000 people in China over seven years recorded that those who ate spicy foods one or two days a week had a 10% reduced risk of death compared with those who ate such meals less than once a week. The risk was 14% lower for those who ate spicy food between three and seven days a week.

As the study, published in the BMJ on Tuesday, was observational, conclusions could not be drawn about cause and effect but the team of international authors, led by researchers at the Chinese Academy of Medical Sciences, suggested that more research could lead to dietary advice being updated. Experts warned that the study did not provide evidence to prompt a change in diet.

In an accompanying editorial to the research, Nita Forouhi, from the University of Cambridge, said that there had been suggestions already of many potential benefits from chilli and its bioactive compound capsaicin; these included anti-oxidant, anti-inflammatory and anti-cancer properties. Scientists had also noted the benefits for gut microbiota and anti-obesity effects from chilli. Future research is needed to establish whether spicy food consumption has the potential to improve health and reduce mortality directly, or if it is merely a marker of other dietary and lifestyle factors.

The study involved people aged between 35 and 79 from 10 geographically diverse areas across China. The research ran from 2004 to 2008. During a median follow-up of 7.2 years there were 20,224 deaths. Participants with a history of serious disease were excluded, and factors such as age, marital status, education, physical activity, family history and general diet, were taken into account.

The participants in the study were asked about the type of spicy foods they ate and how often they consumed them. Chilli pepper, among the most popular spicy foods eaten in China, was the most commonly used spice noted in the responses. However, the authors pointed out that the use of other types of spices generally increased with that of chilli pepper.

Further analysis showed those who consumed fresh, as opposed to dry, chilli tended to have a lower risk of death from cancer, ischaemic heart disease and diabetes.

Kevin McConway, professor of applied statistics at the Open University, warned against reading too much into the results. Maybe this is something in the way spices are used in Chinese cooking, or [it is] related to other things people eat or drink with the spicy food. Maybe it has something to do with the sort of people, in China, who tend to eat more spicy food.

The Chinese population that they studied is different from the population in Britain, in terms of cooking practices, social relations, health care systems, genetics, and a lot else. And its important to realise that the study gives very little encouragement for the stereotypical English pastime of going out for several pints of beer and a hot curry. The relationship between eating spicy food and a lower death rate was apparent really only in people who didnt drink alcohol at all.

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Frequent spicy meals linked to human longevity | World ...

University of Chicago

Syllabus

Sociology 219/319 Biodemography of Human Mortality and Longevity

Spring 2001 Wednesday, 3:00-5:50 Cobb Lecture Hall, 5811-27 S. Ellis Ave. Room 214

Dr. Leonid A. Gavrilov, Ph.D. (concepts and theories in biodemography) Dr. Natalia S. Gavrilova, Ph.D. (methods of data analysis in biodemography) Center on Aging, NORC, 1155 East 60th Street, Room 382 Telephone: 256-6359 E-mail: gavrilov@aol.com Website: http://longevity-science.org/

Course Description: This course is a broad overview of biodemographic ideas, models, methods, and findings regarding human aging, mortality, and longevity. Topics include the construction and analysis of life tables, mortality laws, gender differences in life span, the limits to human longevity, mathematical theories of human aging and mortality, genetics and evolution of human life span, similarities and differences between human and animal mortality patterns. The course is intended to provide students with general understanding of the driving forces behind mortality trends and differences.

Textbook: The course largely follows the following book:

Gavrilov L.A., Gavrilova N.S. The Biology of Life Span: A Quantitative Approach, NY: Harwood Academic Publisher, 1991, 385p. http://catalog.gbhap-us.com/fc3/catalog?/books/TITL_PBPUBREC_0001583 http://www.amazon.com/exec/obidos/ASIN/3718649837/ Selected chapters will be assigned each week. The text of updated chapters of the book will be disseminated prior to each lecture.

Additional reading on biodemography includes:

1. Biodemographic Perspectives on Human Longevity. Population, Special Issue. 2001, vol.13-1. http://www.ined.fr/englishversion/publications/population/englishselection/

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Syllabus of our course "Biodemography of Human Mortality ...