Urine test for detecting aging

Researchers find that a substance indicating oxidative damage increases in urine as people get older. Aging Neuroscience described a way to measure levels of this marker in human urine samples. The new marker potentially provides a method to measure how much human body has aged-biological rather than chronological age.

Everyone born in the same year has the same chronological age,  the bodies of different people age at different rates. This means that the risk of many diseases increases with age, the link between age in years and our health and lifespan is relatively loose. Many people enjoy long lives, relatively free of disease, while others suffer chronic illness and premature death.

The rate of cellular damage can vary from person to person, and may be dictated by genetics, lifestyle and the environment we live in. This cellular damage may be a more accurate indication of  biological age than the number of years. Measuring biological age could predict the risk of developing age-related diseases and death.

One mechanism thought to underlie biological aging involves a molecule vital to human survival- oxygen-the free radical theory of aging. Oxygen by-products produced during normal metabolism can cause oxidative damage to biomolecules in cells, such as DNA and RNA," explains Jian-Ping Cai, a researcher involved in the study. "As we age, we suffer increasing oxidative damage , and so the levels of oxidative markers increase in our body."

One such marker, with the catchy name of 8-oxo-7,8-dihydroguanosine-or 8-oxoGsn for short-results from oxidation of a crucial molecule in our cells called RNA. In previous studies in animals, Cai and colleagues found that 8-oxoGsn levels increase in urine with age. To see if this is true for humans as well, the researchers measured 8-oxoGsn in urine samples from 1,228 Chinese residents aged 2-90 years old, using a rapid analysis technique called ultra-high-performance liquid chromatography. Age-dependent increase in urinary 8-oxoGsn in participants 21 years old and older."

Therefore, urinary 8-oxoGsn is promising as a new marker of aging. Levels of 8-oxoGsn were roughly the same between men and women, except in post-menopausal women, who showed higher levels. This may have been caused by the decrease in estrogen levels that happens during menopause, as estrogen is known to have anti-oxidant effects. Urinary 8-oxoGsn may reflect the real condition of human body better than chronological age, and may help us to predict the risk of age-related diseases.
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Low protein diet for longevity

Having a low-protein diet early in life may help you live longer. A study found fruit flies which share more than two thirds of humans genes live twice as long when given minimal protein diet at tender age. A typical western diet is high in protein and fats from meat, diary, and eggs with red meat in linked to heart disease and cancer. There is an evidence that eating too much protein long-term can lead to an increased risk of osteoporosis and kidney problems.

The researchers also believe their findings could be explained because a low-protein diet produces less toxic lipids secreted by the skin. Health skin lipids form a natural barrier keeping out dirt, impurities and harmful chemicals that can accelerate ageing. Scientists used the fly drosophila melanogaster to understand how diet in early life acts to alter lifespan. These insects are used in lifespan experiments because it lives for only two to three months.

The team stressed that there was enough evidence to recommend pregnant women go on low-protein diets to boost their unborn child's health. There is evidence in humans and other mammals that a mother's diet can alter the risk of her offspring developing cardiovascular disease and diabetes later in life, but the genetic processes underlying this effect remain to be identified.
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Intermittent fasting prevents aging

Intermittent fasting can keep the body younger, extend lifespan and improve overall health, various forms of fasting are healthy; from weight loss to productivity enhancement. According to the latest research, temporary restricting diet keeps the mitochondria – an important part of the cell to health aging – in homeostasis, which improves lifespan.

Some research has shown that intermittent fasting offers no benefits over daily dietary restrictions, but animal studies have found that it was linked to longer life spans. The latest research confirmed the crucial role of the mitochondria in human cell aging, and therefore, the aging of  human bodies.

Mitochondria break down carbohydrates and fatty acids, giving energy to the cell. For this reason, they are often referred to as the powerhouses of human cells. Researchers discovered that without aged mitochondria, cells appeared younger.
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Ketogenic diet prevents inflammation

The high-fat, low-carbohydrate regimen of ketogenic diets changes the way the body uses energy. In response to the shortage of carb-derived sugars such as glucose, the body begins breaking down fat into ketones and ketoacids, which it uses as alternative fuels.

In rodents, ketogenic diets and caloric restriction reduce inflammation, improve outcomes after brain injury, and extend lifespan. These benefits have not been confirmed in human.
Ketogenic diets can modulate the inflammatory response in rodents.
Researchers used a small molecule known as 2-deoxyglucose, 2DG, to block glucose metabolism and produce a ketogenic state in rats and controlled laboratory cell lines.

The team found that 2DG could bring inflammation to control levels. Reduced glucose metabolism lowered a key barometer of energy metabolism – the NADH/NAD+ ratio which in turn activated a protein called CtBP that acts to suppress activity of inflammatory genes. Researchers designed a drug-like peptide molecule that blocks the ability of CtBP to enter its inactive state – essentially forcing the protein to constantly block inflammatory gene activity and mimicking the effect of a ketogenic state.

Peptides, which are small proteins, don't work well themselves as drugs because they are unstable and people make antibodies against them. But other molecules that act the same way as the peptide could provide ketogenic benefits without extreme dietary changes. Excess glucose in people with diabetes, is associated with a pro-inflammatory state that often leads to atherosclerosis; the buildup of fatty plaques that can block key arteries.
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The 16 genetic markers associated with short lifespan

How long we will live is encoded in our genome. Researchers have identified 16 genetic markers associated with a short lifespan. This reveals computational framework to uncover the genetics of our time of death and disease. It explained why some people live longer than others. 

 About 30 percent 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 be responsible for some of the reasons for our longevity.

Changes in the DNA is linked to age-related diseases. About 1 in 10 people carry some configurations of these markers that shorten their life by over a year compared with the population average. Those who inherited a lifespan-shortening version of one of these SNPs may die earlier than their mate. 

The researchers explore how the DNA changes affected lifespan in a holistic way. They discovered that most SNPs had an effect on lifespan by impacting more than a single disease or risk factor, for example through being more addicted to smoking as well as through being predisposed to schizophrenia.

The discovered SNPs and gene expression data, allowed the researchers to identify that lower brain expression of three genes neighbouring the SNPs- RBM6, SULT1A1 and CHRNA5, involved in nicotine dependence was linked to increased lifespan. These three genes could therefore act as biomarkers for surviving beyond 100 years. 

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Brain cells control aging

Scientists have discovered that stem cells in the brain's hypothalamus control how fast aging occurs in the body. This discovery could lead to new method of preventing diseases and increasing lifespan.

The hypothalamus regulates growth, development, reproduction, metabolism and aging. The number of hypothalamic neural stem cells naturally declines and this accelerates aging.
Replenishing stem cells can slow down the process of aging but the loss are not irreversible.

Researchers disrupted the hypothalamic stem cells in middle-aged mice and discovered that disruption accelerated aging. They injected hypothalamic stem cells into the brains of middle-aged mice whose stem cells had been destroyed as well as into the brains of normal old mice.

The treatment showed different measures of aging in both groups. Hypothalamic stem cells exert their anti-aging effects by releasing microRNAs (miRNAs).

The researchers extracted miRNA-containing exosomes from hypothalamic stem cells and injected them into the cerebrospinal fluid of middle-aged mice whose hypothalamic stem cells had been destroyed and normal middle-aged mice.

This treatment slowed aging in both groups of animals as measured by tissue analysis and behavioral testing that involved assessing changes in the animals' muscle endurance, coordination, social behavior and cognitive ability.
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How artificial intelligence predicts patience lifespan

A computer has ability to predict a patient's lifespan by looking at images of their organs. Scientists used artificial
intelligence to analyse the medical imaging of 48 patients' chests. This computer-based analysis was able to predict which patients would die within five years, with 69% accuracy.

Predicting the lifespan of a patient is useful because it may enable doctors to tailor treatments to the individual.
The accurate assessment of biological age and the prediction of a patient's longevity has so far been limited by doctors' inability to look inside the body and measure the health of each organ.

Instead of focusing on diagnosing diseases, the automated systems can predict medical outcomes in a way that doctors are not trained to do.

Our research opens new avenues for the application of artificial intelligence technology in medical image analysis, and could offer new hope for the early detection of serious illness, requiring specific medical interventions. The researchers hope to apply the same techniques to predict other important medical conditions, like the onset of heart attacks.

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Spermidine foods can prevent liver cancer

Cheese is one of the foods that contain spermidine, it is made from milk, it can be in different flavors. Eating cheese like Cheddar, Blue, Brie, Parmesan, Gouda and Gruyere can prevent liver disease. Spermidine in cheese prevents damaged liver cells from replicating.

Researchers used spermidine to treat mice, it increased their lifespan by 25 percent.

Apart from spermidine, researchers discovered that food like mushroom, soya, legumes and whole grains can increase lifespan.

Researchers suggested reduction of calories consumption, reducing animal protein and use of rapamycin can increase lifespan of liver patients.

Scientists from Aarhus University Hospital, Denmark, encouraged liver patients to brush their teeth property because inflamed gums can breed bacteria in the mouth that can move to the liver.

Too much protein can reduce your lifespan

Latest research states that high protein diet at 50 years could reduce your lifespan, changes in metabolism dictates changes in diet.

According to Steve Simpson, a professor of life sciences at the University of Sydney,  the standard balanced diet suggested by National Health Service is five different fruits and vegetables a day, carbohydrates and few portions of protein.

The different classes of food are useful for proper development, but we must change them as we grow.

Eating diet high in protein from age 50 reduces lifespan, the Okinawa islanders of Japan eat less of animal protein and more of plant based diet, they have more of people who lived beyond 100 years.