People With Low Normal Thyroid Function Live Longer Than Those With High Normal

MedicalResearch.com Interview with:

Arjola Bano, MD, MSc, DSc Researcher in the Departments of Internal Medicine and Epidemiology, Erasmus Medical Center, Rotterdam the Netherlands

Dr. Bano

Arjola Bano, MD, MSc, DSc
Researcher in the Departments of Internal Medicine and Epidemiology,
Erasmus Medical Center, Rotterdam
the Netherlands

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Thyroid function is clinically defined by the measurements of serum thyroid stimulating hormone (TSH) and free thyroxine (FT4) levels. So far, abnormal TSH and FT4 levels as well as variations within the normal range have been linked to an increased risk of cardiovascular disease and death. However, it remains unclear whether there are differences in life span and years of life lived with and without cardiovascular disease, within the reference range of thyroid function. To investigate this, we performed a prospective study among 7785 middle-aged and elderly people with normal thyroid function. Participants were part of the Rotterdam Study, 65 years on average and 52% females. In our statistical analyses, we accounted for sociodemographic and cardiovascular risk factors. Over a median follow-up of 8.1 years, 789 incident cardiovascular deaths and 1357 deaths occurred. Analyses were performed separately among men and women.

Our study found differences in life expectancy within the reference range of thyroid function. At the age of 50 years, people with low-normal thyroid function lived up to 3.5 years longer than those with high-normal thyroid function. Also, people with low-normal thyroid function lived a longer life without cardiovascular disease than those with high-normal thyroid function.

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16 New Genetic Links To Longevity Discovered

MedicalResearch.com Interview with:

Dr. Zoltán Kutalik, PhD Group Leader Swiss Institute of Bioinformatics

Dr. Kutalik

Dr. Zoltán Kutalik, PhD
Group Leader
Swiss Institute of Bioinformatics
Assistant professor at the Institute of Social and Preventive Medicine

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: Why do some of us live longer than others? While the environment in which we live – including our socio-economic status or the food we eat – plays the biggest part, about 20 to 30% of the variation in human lifespan comes down to our genome. Changes in particular locations in our DNA sequence, such as single-nucleotide polymorphisms (SNPs), could therefore hold some of the keys to our longevity. Until now, the most comprehensive studies had found only two hits in the genome.

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Is Human Lifespan Really Limited to 100 Years?

MedicalResearch.com Interview with:

Pr. Siegfried Hekimi PhD McGill University

Prof. Hekimi

Pr. Siegfried Hekimi PhD
McGill University

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: We analyzed data about the longest living individuals over the period of time during which the record can be trusted.

We found that there was no detectable plateauing of the maximum possible lifespan. This is consistent with not clearly observed plateau in the currently increasing average lifespan as well.

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Caring for Others Linked to Increased Longevity

MedicalResearch.com Interview with:
Sonja Hilbrand MSc
Department of Psychology
University of Basel
Basel, Switzerland.

MedicalResearch.com: What is the background for this study?

Response: Grandparenting is a topic of both great practical and theoretical interest. For instance, grandparents in industrialized societies invest substantial amounts of time and money in their grandchildren and there are many studies examining the potential benefits for these grandchildren. Other studies have focused on potentially negative effects on grandparental mortality associated with providing custudial care for grandchildren.
In addition to previous research we wanted to ask whether there are tangible benefits to the donors (grandparents) of the resources. In other words, is caring a one-way street or not.

In our study we examined whether moderate amounts of caregiving were associated with the longevity of older adults. For our analysis we used longitudinal data of over 500 German individuals aged between 70 and 103 years.

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Long-Lived Parents Linked To Longer Life For Middle Aged Adults

MedicalResearch.com Interview with:

Dr Janice Atkins Research Fellow Epidemiology and Public Health University of Exeter Medical School RD&E Hospital Wonford Barrack Road, Exeter

Dr. Janice Atkins

Dr Janice Atkins
Research Fellow
Epidemiology and Public Health
University of Exeter Medical School
RD&E Hospital Wonford
Barrack Road, Exeter

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: We have previously shown that having longer-lived parents increases your likelihood of living longer, and family history of heart attacks is already used by physicians to identify patients at increased risk of disease. However, it has been unclear how the health advantages of having longer lived parents is transferred to their middle-aged offspring.

Our study of nearly 200,000 UK volunteers aged 55-73 at baseline, and followed for 8 years using health records data, found that having longer-lived parents reduced the risk of morbidity and mortality in the participants. We found that for each parent that lived beyond 70 years of age the participants had 20% less chance of dying from heart disease. To illustrate this, in a group of 1,000 people whose father’s died at 70 and followed for 10 years, on average 50 would die from heart disease. When compared to a group whose father’s died at 80, on average only 40 would die from heart disease over the same 10-year period. Similar trends were seen in the mother’s.

The relationship between parental age at death and survival and health in their offspring is complex, with many factors playing a role. Shared environment and lifestyle choices play a large role, including smoking habits, high alcohol consumption, low physical activity and obesity; but even accounting for these factors parents lifespan was still predictive in their offspring. The biggest genetics effects on lifespan in our studies affected the participant’s blood pressure, their cholesterol levels, their Body Mass Index, and their likelihood to be addicted to tobacco. These are all factors that affect risk of heart disease, so is consistent with the lower rates of heart disease in the offspring.

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Fewer Childhood Infections Do Not Explain Marked Increase In Human Longevity

MedicalResearch.com Interview with:

Adam Hayward PhD Impact Research Fellow University of Stirling

Dr. Adam Hayward

Adam Hayward PhD
Impact Research Fellow
University of Stirling

MedicalResearch.com: What is the background for this study?

Response: Adult life expectancies in industrialized countries have increased dramatically in the last 150 years, even once we’ve accounted for the fact that previously common deaths in childhood and now very rare. One hypothesis seeking to explain this increase is that childhood infections cause chronic inflammation, which are then linked with heart disease and stroke in later life, reducing lifespan.

Since such childhood infections were previously common but are now, thanks to vaccine and sanitation, much rarer, chronic inflammation should be lower and people should live longer and be less likely to die from early-onset heart disease. If this hypothesis is correct, we should see that higher exposure to infections in early life leads to increased adult mortality and deaths from heart disease and stroke.

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Genetic and Environmental Factors Linked To Delay of Aging-Related Diseases

MedicalResearch.com Interview with:
Arlene Ash Ph.D., Professor
David Hoaglin Ph.D., Professor
and
Aimee R. Kroll-Desrosiers, MS
Department of Quantitative Health Sciences
University of Massachusetts Medical School
Worcester, MA

Medical Research: What is the background for this study? What are the main findings?

Response: The Long Life Family Study (LLFS) is an international collaborative investigation of the genetics and familial components of exceptional survival, longevity, and healthy aging. It has enrolled members of long-lived sibships, their offspring, and spouses of either group.  Medicare claims data is a unique, nationally representative source of data on all treated diseases for most Americans over the age of 65.

Our main question was: Does membership in a long-lived family protect against disease?

For each American LLFS participant who was at least age 65 in 2008 and alive in 2009, we selected four persons from the general Medicare population who matched the participant on age, sex, and ZIP code of residence. We then used 2008–2010 Beneficiary Annual Summary Files from the Centers for Medicare & Medicaid Services (CMS) to compare the prevalence of 17 conditions among 781 LLFS participants in Medicare with those of 3,227 non-LLFS matches.* Analyses accounted for nesting within LLFS families and adjusted for age, sex, race, and year.

Among LLFS participants identified as members of a long-lived sibship, 7 of the 17 conditions were significantly less common than for similarly aged controls (Alzheimer’s, hip fracture, diabetes, depression, prostate cancer, heart failure and chronic kidney disease); in contrast, 4 (arthritis, cataract, osteoporosis and glaucoma) were significantly more common. Spouses, offspring and offspring spouses of these long-lived siblings share in significantly lower risk for Alzheimer’s, diabetes and heart failure.

Several additional analyses found suggestive (although not statistically significant) evidence of lower disease prevalence in both genetically and maritally-related LLFS cohort members.

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Living Past 100 May Be In Your Genes

MedicalResearch.com Interview with: Thomas Perls, MD, MPH Professor Boston University School of MedicineMedicalResearch.com Interview with:
Thomas Perls, MD, MPH Professor
Boston University School of Medicine

Medical Research: What is the background for this study?

Dr. Perls:   For years now, Gerontology scholars continue to state that 25% of what they interchangeably call aging, longevity, life expectancy and life span is genetic and 75% is due to the environment and health-related behaviors. This assertion is based on Scandinavian twins reared apart, but the oldest participants in those studies lived to their 70s and 80s. Part of the problem here is the lack of consistency in what people mean by the terms Aging, Life Span and Longevity.

In fact, the Seventh Day Adventists, who generally have a high prevalence of healthy behaviors (vegetarian, daily exercise, eat in moderation, abstain from tobacco and alcohol, and activities that help manage stress well) have an average live expectancy of approximately 88 years. Yet, 7th Day Adventists are ethnically and racially heterogeneous and thus it appears that those healthy behaviors explain the vast majority of the variation in how old these people live to be. This finding is consistent with the optimistic view of the twin studies, that much of living to one’s 80’s is in our hands. Living to only our 50s-70’s is also in our hands (e.g. 75% behaviors) if we choose to smoke, eat red meat frequently, be obese, not exercise, be exposed to gun violence, have unsafe sex, do IV drugs, etc. So it is safe to say, in my opinion, that 75% of the variation in how old we live to be, is on average due to our behavior and exposure choices. The empowering and important point is that if we all lived like the Seventh Day Adventists, average life expectancy would increase almost 8 years and health costs would markedly decline because we would be getting to these older ages because we are healthier not because we are pouring more resources into more effectively treating diseases.

The New England Centenarian Study, which I direct, and a number of other studies of nonagenarians (people in their 90s) have demonstrated via direct genetic studies as well as studies of family trees where at least some family members get to these very old ages, that with older and older ages of survival beyond age ~95 years, variations in genetic profiles explain a greater and greater proportion of the variation in how old people live to be at these ages. So much so that I believe the findings to date are consistent with the roles of genes and environment being reversed for survival to age 106+ years, that is, 75% genetics and 25% environment/behaviors. This supposition is based upon several observations:

(1) as people reach the age of 105+ years, they become more and more alike in terms of what age-related diseases they get and when they get them. Consistent with Jim Fries; “Compression of Morbidity” hypothesis, people who survive to ages 110+ (called supercentenarians) and who therefore approximate the limit of human lifespan are on average disease and disability-free up until the last 5 or so years of their lives. This increasing homogeneity, especially compared to the increasing heterogeneity in the rates of aging and incidences of age-related diseases at younger percentiles or ages of survival, suggests underlying genetic similarities (similar genetic profiles) amongst groups of these supercentenarians; and

(2) the New England Centenarian Study previously discovered genetic signatures (made up of longevity-associated variations of about 130 genes) that were associated with surviving to age 106+ years with 80% accuracy, but with only 60% accuracy for accurately picking out people living to ~100 years. This increasing accuracy with older and older ages also suggests a stronger and stronger genetic influence upon survival to these rarest percentiles of survival.

With the above background, we set out in this study and subsequent paper, to

(1) assess sibling relative risk using the largest-ever collection of validated pedigrees of centenarians,

(2) to assess the risk of a sibling achieving the same age as their very old sibling (e.g. ages 95, 100, or 105+ years) relative to average people born around the same time, and

(3) to look at how when a person was born (eg before or after 1890) made a difference in these relative risks.

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Cellular Energy Sensor Links Calorie Restriction With Healthy Aging

William Mair, Ph.D Assistant Professor Department of Genetics and Complex Diseases Harvard T. H Chan School of Public Health Boston, MA 02115MedicalResearch.com Interview with:
William Mair, Ph.D
Assistant Professor
Department of Genetics and Complex Diseases
Harvard T. H Chan School of Public Health
Boston, MA 02115

MedicalResearch: What is the background for this study? What are the main findings?

Dr. Mair: Dietary restriction, the reduction of food intake without malnutrition has been known for 80 years to prolong lifespan in organisms ranging from single celled yeast to non human primates, and early signs suggest improvement of metabolic parameters in patients undergoing clinical trials. However, negative side effects associated with low calorie intake remain, and compliance and lifestyle factors make it an unappealing therapeutic. Since calorie restriction (CR) can have remarkable protective effects against multiple age onset diseases in mouse models – ranging from cancer to neurodegeneration to metabolic disease – finding molecular mechanisms though which calorie restriction functions might provide novel therapeutic targets that promote healthy aging. Using a model system, the nematode worm C. elegans, we show that perception of energy intake in the nervous system may be as critical for the effects of low energy on aging as actual calorie intake itself. Animals expressing an active form of a protein called AMPK, which is a cellular energy sensor, were long lived despite eating normally but this longevity could be turned off or on by changes to a neurotransmitter in just a few neurons. This suggests that therapeutic targets that modulate the perception of energy status in the nervous system might provide novel ways to gain the benefit of calorie restriction and promote healthy aging.

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Education Remains Strong Predictor of Longevity

MedicalResearch.com Interview with:
Robert M. Kaplan

Office of Behavioral and Social Sciences Research
National Institutes of Health
Bethesda, MD 20892

Medical Research: What is the background for this study? What are the main findings?

Response: Years of formal education is one of the strongest correlates of life expectancy. The purpose of this study was to examine the relationship between educational attainment and life expectancy with adjustments for other social, behavioral, and biological factors. Using data from a large cohort of nearly 30,000 adults, we found that education was a very strong predictor of survival and that biological and behavioral factors only partially explained the relationship.

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