A healthy lifestyle and a nutritious diet, aided by a temperate climate, could make for longer life, scientists believe after a study of the bones of a 114-year-old Spaniard who died recently. Apparently there were no genetic modifications which could have contributed to his longevity.
The research team, directed by Universitat Autònoma de Barcelona professor Adolfo Díez Pérez, felt the man enjoyed an excellent health right through perhaps because of his healthy lifestyle and the Mediterranean diet. He had been cycling daily until the age of 102 years. Besides a temperate climate could also have helped, the team said.
AdvertisementThe Mediterranean diet is a modern nutritional model originally inspired by the traditional dietary patterns of some of the countries of the Mediterranean Basin, including Greece and southern Italy.
This diet, in addition to "regular physical activity" (e.g. farm labor), emphasizes "abundant plant foods, fresh fruit as the typical daily dessert, olive oil as the principal source of fat, dairy products (principally cheese and yogurt), and fish and poultry consumed in low to moderate amounts, zero to four eggs consumed weekly, red meat consumed in low amounts, and wine consumed in low to moderate amounts.
The research team studied the bone mass and analysed the genetics of a man with enviable health who at the time of the study was 113 years old. The research was carried out with four other members of his family: a 101-year-old brother, two daughters aged 81 and 77, and a nephew aged 85, all of them born and still living in a small town of the island of Menorca. The research findings were recently published in the Journal of Gerontology and reported that the man's bones were in excellent conditions: his bone mass was normal, there were no anomalous curvatures and he had never sustained a fracture.
They did not find any mutations in the KLOTHO gene, which is generally related to a good level of mineral density and therefore healthy bones. Neither did they find any mutations in the LRP5 gene, which is associated with longevity. None of the members of the family who participated in the study presented any mutations in this gene.
The results of the research do not rule out the possibility that other genetic mutations could positively influence longevity. However, researchers do point out the fact that the excellent health of this family, and of the 113-year-old man in particular, is probably due to a Mediterranean diet, the temperate climate of the island, a lack of stress and regular physical activity. The article underlines the fact that until the age of 102, the man cycled every day and looked after the family orchard.
The human life-span and the nature vs nurture question raises the question of why do animals age so differently? Why is it that a tortoise, for example, can live well over a hundred years, while another similarly sized animal would be lucky to live just 10? What's the big difference?
Scientists say that the secret lies in genetic expression. A new genetic database could help reveal how and why animals age so differently. The process of mapping out this molecular maze will likely unlock some of the hidden secrets of increased longevity in humans along the way.
In some instances, even very closely related animals have drastically different life spans, a fact that has puzzled scientists for years. Mice for example live for about two years while their rodent cousins, the Southern flying squirrel, can live for two decades or so. Chimps and humans are 99 percent genetically identical, so why do humans live twice as long? New databases are helping to identify the genetic expressions that accounts for these vastly varying life spans, say Casey Kazan with Rebecca Sato in the Daily Galaxy website.
In a study of mice, researchers at Stanford University and the National Institute on Aging (NIA), have now generated a database that catalogues how gene expression, the measure for how active a gene is, changes in various parts of the body as the animal ages. Their findings indicate that different tissues age quite differently over time.
Previous studies have examined how gene expression changes with age in specific parts of the body, such as the brain or the hearts of both mice and humans. But the new study, commissioned by the NIA, simultaneously analyzed the activity of thousands of genes in 16 different tissues at different points during the animals' lives. This has allowed researchers to compare age-related patterns of gene expression between different organs.
The results, published earlier this week in the journal PLoS Genetics, established that the two main culprits previously believed to be primary contributors to the aging process—increased inflammation and slowed metabolism—are indeed guilty parties. But the researchers did find large disparities depending on the different tissues of the body. For example, expression profiles in the liver, brain, and muscle changed little with age, whereas the lungs, eyes, and thymus (an immune organ) experienced more radical transformations.
The researchers compared their results with other previous studies analyzing gene-expression. They analyzed the aging brain, muscle, and kidney tissue in humans, flies, and worms. The researchers found one central theme to gene expression and aging in all four species. They all developed a slowing of the cells' energy factories. In each species, expression of genes related to energy production dropped twofold by the time the species reached the end of its life span—2 years for mice and around 80 for humans.
"This is the only common property of growing old between the four different animals," says Stanford biologist, Stuart Kim. "Maybe that should alert us to say there is something unavoidable to getting old."
However, the researchers said there were not a lot of universal similarities, which raises the question of how well lab animals can really serve as models for humans as we attempt to unravel the longevity mystery. For example, studies have found that in humans, and some other animals, that the length of repetitive strips of DNA at the end of each chromosome, also known as telomeres, is linked to aging. However, the researchers didn't find changes in the expression of telomere-related genes in aging mice.
"I wouldn't say that this means that model organisms can't be used to study aging in humans," says Promislow. "It does suggest there is a lot more going on."
This analysis will likely be the first of many to come that will take advantage of this new database, know as AGEMAP. Scientists are still working on figuring out the precise functions of the intertwining genetic networks implicated in aging. AGEMAP serves as a way to decipher differences in genetic expression and better map out the ageing process, especially as it relates to humans.
"The scale of this study is phenomenal," says Promislow. "In some ways, this shows us where things are likely to be headed in coming years in terms of the kinds of experiments people will do to understand the genetic basis of complex traits."