Chronic diseases, impaired mobility and diminished quality of life with aging seem inevitable to most. Although healthy lifestyle habits protect us, researchers say they may have found another way to reverse the aging process.
Aging cells stop working well for several reasons. Researchers have turned the spotlight to ‘senescent cells’ – cells that stop dividing. This process is thought to have several benefits like suppressing tumours, wound healing and more.
But in aging, these cells accumulate and may impact the function of surrounding cells. And animal research suggests that removing these deteriorating cells could thwart or delay age-related physical decline.
Researchers propose that DNA damage, inflammation and erosion of telomeres – protective tips at the end of chromosomes – could all explain why cells become senescent with age.
It now appears that gene regulation might also factor in.
Every cell in the body contains all the information that the body needs to function. But different genes are turned on or off according to that cell’s role – explaining for instance why the heart and brain work differently despite containing the same genes.
Genes are activated by environmental messages, facilitated by around 300 proteins called ‘splicing factors’. With aging, the number of splicing factors drops, so that aging cells are less able to respond to changes in the environment.
Researchers from the University of Exeter, UK, have been able to turn these splicing factors back on and revive old cells – in vitro at least – by treating cells with a chemical that produces small amounts of hydrogen sulphide.
Hydrogen sulphide – the gas that smells like rotten eggs – is found naturally in our bodies. But in high doses it can be toxic. The researchers found a way to send the molecule in small doses to the mitochondria – the cell’s energy powerhouse – where they think it acts.
They hope this procedure could eventually be used in living people and treat age-related diseases.
Can death itself be cured so that people can live forever?
Aubrey de Grey thinks so. He founded the organisation, Strategies for Engineered Negligible Senescence (SENS), focussed on finding ways to remove senescent cells and theoretically keep bodies alive forever.
Do people want immortality? A 2013 national survey of Americans found that 56% would not use technologies that would help them live to 120 or longer. Two-thirds of respondents were concerned about the strain on natural resources.
Jake Dunagan, director of the consulting firm Very Nice and researcher in cognitive bias, says the SENS longevity research is selfish. “’I want mine. I always want mine.’ Well what if everyone had this? What would be the long-term implications of that?”
There is a notable distinction between increasing our “health span” – the primary focus of most aging research – and increasing our life span, say other researchers like biochemist and professor of biogerontology, Judy Campisi.
Most people fear death and discussing it is taboo in many cultures. De Grey calls it “the terrible thing that awaits [us],” disparaging people who simply accept their fate.
But ‘The Art of Dying Well’ suggests that coming to terms with death can help us live more fully. “In fact,” they suggest, “consciousness of our mortality can enable us to cherish every moment of the life we have.”
People have long thought that dementia is unavoidable if you carry risky genes. Now research is slowly but surely debunking this fateful thinking as mounting evidence suggests lifestyle changes could help people retain control over their mental faculties.
In fact, a recent study collated the latest research and found that controllable factors could account for around 35% of the dementia burden – larger than that attributed to the genes typically linked with Alzheimer’s disease, the most common form of dementia.
Signposts have long pointed the way – physical conditions like hypertension, inflammation and heart disease confer greater risk of dementia. So it’s really a no-brainer that the benefits of looking after our physical wellbeing extend to better mental health.
In 2013, Spanish researchers allocated 522 people aged 55-80 at high risk for heart disease to a Mediterranean diet or low-fat diet. More than six years later, those in the Mediterranean diet group had less heart disease and scored higher on cognitive tests used for dementia.
Indeed, research has found that people who follow a Mediterranean diet have less brain atrophy and amyloid-ß that is typical of Alzheimer’s. “If you follow a Western diet, your brain ages faster. A Mediterranean diet is protective,” says neuroscientist Lisa Mosconi.
The traditional Mediterranean diet is high in plant foods: vegetables, fruit, legumes, nuts, seeds and wholegrains, and extra virgin olive oil for cooking and salads. It also features moderate consumption of fish, fermented dairy (cheese, yoghurt) and red wine with meals, and very little processed food or meat.
Physical activity has numerous health benefits, from reducing risk of heart disease and diabetes to some cancers. A grouped analysis of 15 studies in 2010 found that across the board, exercise can also protect against cognitive decline.
Other studies have shown that physical activity can enhance blood flow to the brain and increase levels of brain-derived neurotropic factor – a protective protein.
Even if you don’t fancy donning gym gear and sweating it out with aerobics classes and barbells, just taking opportunities each day to walk, move and be active will reap physical and mental rewards.
Keeping the brain active also confers striking protection against Alzheimer’s disease. Staying educated encourages new neural connections that might compensate for cognitive decline with aging. “It future-proofs your brain,” according to researcher Leon Flicker.
Even people who don’t pursue ongoing education can boost their cognitive reserves in other ways, like reading, doing puzzles or attending quiz nights. Quiz nights may have additional benefits – having a strong social network can also keep the brain healthy. Even being married reduces dementia risk dramatically.
In 2017, researchers pooled data from 27 studies on sleep. They found that sleep problems increase risk of cognitive impairment by 65% and could account for up to 15% of Alzheimer’s diagnoses.
Other protective factors include not smoking and maintaining a healthy weight and blood pressure.
Even if you have a genetic predisposition for Alzheimer’s disease, “there are still things you can do,” says Finnish geriatric epidemiologist Tiia Ngandu.
Richard Isaacson has set up a clinic for preventing Alzheimer’s in the US. The clinic offers individualised prevention strategies for people at risk for dementia.
Based on data they have collected, he estimates that 60% of lifestyle recommendations will apply to most people. Beyond that, strategies may vary from person to person, including, for instance, specific treatments for heart conditions or sleep problems.
Researchers are now optimistic that people can prevent their risk of dementia, and current large studies are underway to strengthen the evidence base.
Some decline in cognitive faculties is inevitable in the twilight years. But several lifestyle factors can help mitigate waning acuity and increasing forgetfulness. One of those could be a pine bark extract that has antioxidant and anti-inflammatory properties.
Fading mental functions and thought processes that occur with aging impact attention, speed of processing information, memory and other aspects of intelligence. The reasons for this are not fully understood. But the accelerated oxidative stress that occurs in aging could be a factor.
A recent study, published by researchers at the Swinburne University of Technology in Melbourne, found that F2-Isoprostanes – a marker of oxidative stress – were associated with impaired ability to verbally retrieve episodic memories in healthy older adults.
Chronic inflammation could also contribute – it has been linked to several chronic conditions including heart disease, depression and dementia, and might help explain the high overlap between these diseases.
A 2017 study investigated blood markers of inflammation in 1,633 adults aged 53 on average. At a follow-up 24 years later, higher levels of inflammation were associated with poorer episodic memory and reduced volume of the hippocampus – a brain region associated with memory – and other areas of the brain associated with Alzheimer’s disease.
A body of research has investigated health benefits of Pycnogenol, the registered trademark name for a product derived from the bark of a pine tree (Pinus pinaster). The active ingredient is also contained in peanut skin, grape seed, and witch hazel bark.
Pycnogenol contains several polyphenolic compounds with antioxidant and anti-inflammatory properties. Some evidence suggests it could reduce symptoms of allergy and asthma and improve circulation and symptoms of ADHD in children.
It may alleviate problems associated with clogged arteries, deep vein thrombosis, high blood sugar, circulation problems in diabetes, blood pressure, menopause and other physical ailments, but more evidence is needed.
Some research has shown that taking Pycnogenol could improve mental function and memory in adults both young and old.
A study published last month builds on this evidence in 55 to 70-year-old healthy adults with signs of mild cognitive impairment – a risk factor for Alzheimer’s disease.
All participants continued their standard care, including healthy sleep patterns, regular exercise, and low sodium and sugar meals. Additionally, half of them were given 150mg Pycnogenol per day for two months.
The treatment group’s Mini-Mental State Examination (MMSE) scores increased significantly by 4 points on average compared to about half a point in controls. The median increase was 18% in the Pycnogenol group and 2.48% in the control group.
Several other tests of cognitive function and memory improved by 19.4% to 39.4% in the treatment group compared to 0% to 12.5% in controls. The treatment group also showed a 16 percent reduction in oxidative stress.
Advances in mapping the human genome have fostered understanding of our genomic blueprint and its influence on molecular processes, health and disease. This has extended to investigations of nutritional genomics.
Proponents hope nutritional genomics will lead to greater understanding of how specific food components influence metabolic pathways and long-term disease-risk, enabling individual tailoring of dietary advice and preventive medicine.
This field consists of two primary areas of investigation:
Nutrigenomics is concerned with how food and nutritional components influence gene expression and gene regulation, and their resulting impact on metabolism. It aims to identify individual nutritional needs.
Nutrigenetics, conversely, investigates individual genetic differences in how people respond to dietary intake, and why people have different reactions to the same nutrient.
Ultimately the aim is to achieve better health outcomes by understanding links between genes and diet. According to Ruth Debusk, “The future of dietetics is unquestionable intertwined with nutritional genomics.”
It cannot be disputed that poor diet plays a pivotal role in modern chronic lifestyle diseases like cancer, diabetes, obesity, heart disease, neurological and inflammatory disorders.
But why do some people gain weight more easily, or develop heart disease when others with similar diets don’t? Nutritional genomics hopes to answer these questions so that therapeutic intervention and nutrition guidelines can be individually tailored.
For instance, the APOE gene has a variant that is associated with high LDL cholesterol – so people with this genetic variant may be more vulnerable to the adverse effects of a high fat diet.
Another genotype has been associated with higher concentrations of the “good” HDL cholesterol, but only if saturated fat from animals is less than 30% of energy intake. People with these genes might benefit from a diet higher in vegetable fat.
Other research found that caffeinated coffee increased the risk of heart attacks in people carrying a particular gene that slows caffeine metabolism, while having no effect on those lucky fast coffee metabolisers.
Inflammation is a common feature underlying chronic diseases. Some individuals may produce more inflammatory markers than others, so anti-inflammatory nutrients like omega-3 or turmeric could reduce their susceptibility.
People also have different nutrition requirements, and these vary at different life stages. A vitamin deficiency could be caused by inadequate intake, or because of a genetic variation that impacts its metabolism. These people may need higher amounts of that nutrient, and that could be further impacted by aging.
Although nutritional genomics is generating much excitement and challenging the “one size fits all” approach to nutrition throughout the lifespan, there is much yet to understand.
Unlike single-gene diseases, diet-gene interactions likely involve multiple genes that have multiple interactions with multiple environmental factors – of which bioactive dietary nutrients are not the only contributors.
For instance, several genes are involved in lipid transport alone – just one factor that can influence heart disease risk – including lipid transport proteins, their receptors and lipid-processing enzymes.
New research on the 100 trillion microbes that live in our gut has added further complexity to the broader picture of genetics and human health. And metabolomics seeks to pinpoint metabolites at each step of metabolic pathways that might also help to fine tune dietary advice.
Finally, the unhealthy diets and sedentary behaviours that dominate modern lifestyles will not be solved by nutritional genomics. They bring epigenetics into the bigger picture – the impact that diet and environment has on our genes.