On her 86th birthday in December, Jane Fonda declared herself the happiest she’d ever been. The actor reportedly put her younger cast mates to shame on the set of her recent movie, Book Club: The Next Chapter; rising at dawn and clocking up thousands of steps around the streets of Rome before her day began.
Fonda and many of her fellow seniors – including the baby boomer bubble now in their mid-70s – are living longer and healthier lives than any generation before them. That longevity seems set to continue for the following generations; people in their 50s and 60s can now reasonably expect to see their 90s. Older people are more active and generally healthier than ever before.
But while we’re out there biking the trails and walking the tracks, there can be changes going on inside the body that might put paid to that extended health span. Diseases of the bones and brain can stealthily start decades ahead of when they finally show up externally. Scientists are learning more, not only about new ways to treat these issues, but also about what individuals can do to lower their risk and potentially prevent them.
The fact that we’re living longer is one reason bone health is becoming more of a focus for innovative research. Unless we’ve broken bones, it’s likely we’ve devoted little time to thinking about their health. Yet bone density is linked to longevity – and having poor bone density is linked to early death.
Early in Ian Reid’s career as an endocrinologist, he started to realise that bones needed more attention.
“The epidemic of heart disease was beginning to get under control,” says Reid, a distinguished professor at the University of Auckland. “One of the problems cardiologists caused for us by not letting us die of a heart attack at three score years and 10 was that we lived to four score years and more, which was long enough for our skeletons to fall apart and start letting us down.”
The progressive increase in life expectancy over the years has seen osteoporosis go from what Reid describes as “a sort of a niche thing” to being recognised as “a very major public health problem”.
He says more than half of older Pākehā women will have a fracture at some point between menopause and when they die. Fracture rates are about half this in Māori and Pacific women who tend to have higher bone density, by about 10%. For men, one in five will have an osteoporotic fracture in their lifetime.
Hip fractures – more common in those over 70 – are particularly worrying; global estimates show that up to a third of older adults who have suffered hip fractures will die within a year. The rates go up for those with dementia or who live in a nursing home.
Long before we get to the point of fracture, there are things going on in our bodies that might lead to that moment. There’s hormonal change, for a start. Osteoporosis and its precursor, osteopenia, affect women more severely than men, and more rapidly; women lose bone at 2-3% per year over five to 10 years during perimenopause and postmenopause. After that, the bone loss in both sexes is about 0.5-1% a year.
“At the time of menopause, the production of oestrogen in the system drops dramatically,” says Reid. “And oestrogen has an important effect in maintaining bone density.”
There’s a good body of evidence to show the protective effect of oestrogen, in the form of hormone replacement therapy (HRT), on bones. Using this or another bone-protecting therapy is particularly important for younger women who’ve gone through early or surgical menopause or who’ve had their ovaries removed before the average menopause age (around 51).
Alongside hormones, there are other things we can’t control. Our genes come into play ‒ we all reach peak bone density in our early 20s and it’s substantially genetically determined.
“Pick your parents with care – get parents with strong bones, and you’ll probably have comparatively strong bones as well,” Reid quips.
Certain medical conditions can also contribute to reduced bone density. They include osteo- and rheumatoid arthritis, coeliac disease, hyperthyroidism, type 1 diabetes, lupus and others. Being too thin at any age is bad for the bones and people who have had anorexia as teens are a particular concern if they continue to have very low body weight, he says.
“We see those people coming back in their 40s and 50s with osteoporotic-type fractures, whereas those who can re-establish normal body weights in their 20s recover their bone density and don’t seem to have that problem later in life.”
Bone boosting
If our bones are slowly losing density as we get older, what can we do to mitigate it? Reid says the most important thing is maintaining a healthy body weight. “Most doctors spend their time bullying their patients for being overweight, but in the context of bone, the problem is people who are underweight.”
But at the other end of the scale, Reid says people with obesity probably have an increase in some fracture types. So keeping weight in the normal range by eating a varied, healthy diet is sensible. “That would include some dairy products or something similar if you choose to be dairy free. You need to get the protein and you need to get the calories and the other standard dietary components, including calcium.”
There’s no need to binge on calcium, despite current official recommended intakes for calcium of up to 1300mg a day for older people (a litre of milk), he says. Studies have repeatedly shown little difference in bone loss between people getting 400mg a day of calcium and those having five or six times that amount. “The vast majority of older people in New Zealand probably have an adequate calcium intake,” he says.
Calcium supplements are not recommended – the evidence doesn’t support their use for prevention of bone loss and some research suggests they can cause harm. “As with most things in the diet that matter, the body carefully regulates how much calcium it lets you absorb.”
Vitamin D is also important for bones; it’s a precursor to a hormone that regulates how the body absorbs calcium from the diet. We get vitamin D mainly from sun exposure. In supplement form, it might be useful for those who are rarely outside, are always veiled or who have dark skin which absorbs vitamin D from the sun at lower levels. “But if you’ve got a 75-year-old who’s fit and active and getting outdoors and getting normal sunshine exposure, that person will not be vitamin D deficient and they would derive no benefit from taking extra vitamin D.”
Getting good amounts of protein, regular exercise (see “Move it or lose it”, below), and not smoking or drinking too much are all useful for bone health.
It’s also worth knowing your risk of fracture, so preventive treatment can be started as early as it’s needed. Reid is enthusiastic about the nuanced tools now at the disposal of doctors that can predict a patient’s likelihood of fracture in the form of algorithms. “I think that means we’re getting more sensible in terms of when we start offering medications to strengthen bones. We don’t all need to start taking medications at the age of 51.”
Based on these screenings, about a third of the population probably won’t need medication at all – “perhaps a third should start in their 60s or 70s and a third should start later on.”
Useful medications have become a lot cheaper as they’ve come off patent over the years and a lot more is known about their safety and effectiveness.
Reid stresses that bone density is only one component of fracture risk. But he also says it’s sensible for most women, once they’re in their 60s, to have a bone density scan to establish a benchmark, “or earlier if they’re having fractures or if they’ve got a strong family history of osteoporosis”.
Men can safely wait a decade before doing this.
Our fracture risk changes over time. A healthy 55-year-old has a low risk of fracture, “but 20, and certainly 30 years later, that person will have a much higher risk of fracture. So this is something that needs to be looked at, not from year to year, but from decade to decade.”
Alzheimer’s puzzle
Brain function is another thing we may rarely think about. But as with bones, the precursors to trouble can be happening, unseen, decades before symptoms show. Simon Laws, director of the Centre for Precision Health at Perth’s Edith Cowan University, has devoted the past 25 years to researching Alzheimer’s disease. He says the disease – which accounts for 60-80% of dementia cases – develops over a long time. Research has shown “that the disease trajectory can be greater than 20 years”.
The overriding hypothesis that underpins Alzheimer’s disease is what’s called the amyloid cascade ‒ the build-up of a protein in the brain called beta amyloid, which leads to a cascade of pathological events and ultimately to symptoms of dementia. That protein can start building up as early as our 40s. (So can another key biomarker of Alzheimer’s called plasma p-tau217; this is the subject of newly published research on a blood test that it is hoped can be used as a simple early screening tool).
Not everyone with protein build-up will go on to develop Alzheimer’s. So the “why” of the disease is still a jigsaw puzzle. There are known non-modifiable risk factors: being female, once again, is a disadvantage. Women are almost twice as likely as men to develop the disease; it’s thought hormones play a role here, too, with oestrogen offering protective effects on the brain that disappear after menopause.
Genetics is another important factor. The major genetic risk factor for Alzheimer’s disease is the apolipoprotein E (Apo-E) gene, which is involved in making a protein that helps carry cholesterol and other types of fat in the bloodstream.
If you carry the gene, you have a three- to five-fold increased risk of Alzheimer’s, explains Laws, “and those who carry two copies of Apo-E 4 [a particular form] – they have up to a 20-fold greater risk.” (Testing for Apo-E 4 is possible but not necessarily recommended for people as a predictor of future disease.)
Gut-heart-brain axis
Another fascinating emerging genetic link is the potential connection between what’s going on in the gut and the development of dementia.
Laws supervised a study which identified shared genetics between common gut disorders and Alzheimer’s disease. In particular, the research confirmed shared genetic pathways between Alzheimer’s and gastro oesophageal reflux disease (acid reflux) as well as irritable bowel syndrome and diverticular disease – all common gut disorders. “A lot of [these pathways] are actually linked to – would you believe – cholesterol transport,” says Laws. “So then it’s bringing in that gut-heart-brain link.”
The gut-brain axis – the bi-directional relationship and communication between the central nervous system and the enteric nervous system – is a huge area of research.
“How that actually results [in brain changes], we’re still investigating. But these studies really show that when you take away all the conflicting information from individuals’ diets and so forth, there is still a biological basis for it.”
New therapies
Other risk factors for Alzheimer’s include things that may lead to lowered cognitive reserve – that’s the ability to compensate for the loss of cognitive power that dementia might cause. Lower education levels and low socioeconomic status fall under this umbrella.
Laws stresses many Alzheimer’s risk factors are things we can address long before we hit old age. They include hypertension, hearing impairment, smoking, obesity, depression, physical inactivity, diabetes, infrequent social contact and excessive alcohol intake. What’s good for the heart and gut is good for the brain, so healthy eating comes into play, as does physical activity (see “Move it or lose it”, below).
He is excited about emerging treatments for Alzheimer’s that target the trajectory of the disease’s development. The new therapies target the clearance of beta amyloid and “they’re seeing some marked results in terms of improvement in the memory and cognitive performance in the trials for those. It could be a massive game changer.”
Combining these therapies with other interventions could be the way of the future. “It is very promising and has put a lot of impetus around early diagnosis, because the sooner you treat individuals with these therapies, when they become available, the better it’ll be. Early intervention is always key.”
To that end, Laws and the Edith Cowan researchers are working on ways to identify the disease earlier. He sees a future of personalised medicine, where interventions can happen at the earliest stages of Alzheimer’s and prevent symptoms from developing.
“But at present, any slowing down of the disease progress – even if it’s someone who’s got mild dementia at 60, 65 years of age – will be a major win. Alzheimer’s is one of the worst conditions you can see someone suffering from.”
Bone density link
Although it’s not known if low bone density causes dementia – or vice versa – there are some intriguing links. A study published in the journal Neurology last year found people who have low bone density may have an increased risk of developing dementia.
The conditions often affect older people simultaneously, with bone loss often increasing due to physical inactivity and poor nutrition during dementia. But the study found bone loss also happening before dementia, linking it to a higher risk.
The researchers suggested bone loss might occur in the earliest phases of dementia, years before any clinical symptoms manifest, meaning people with bone loss could be targeted for screening and improved care.
Screening for bone loss could be a tool for brain protection in other ways, too. Laws’ colleague at Edith Cowan, Josh Lewis, led recent research which found that abdominal aortic calcification, or AAC – calcification of the plaques which can build up within the abdominal aorta (the body’s main artery) and is a predictor of cardiovascular disease risk – is also a reliable marker for late-life dementia. AAC is easily detected using lateral spine scans from bone density machines.
“It’s really been a question of mine for over a decade now: why, as you age, do you get less bone in your bones and more in your blood vessels?” Lewis says.
“The reason we’ve focused on abdominal aortic calcification is because that’s one of the first sites where you see calcium within the blood vessel wall. And we know that a healthy blood vessel shouldn’t have any calcium in it. So that’s a marker of problems with cardiovascular disease and also osteoporosis.”
The study results were startling. “Roughly one in two of these older women had what we call moderate or severe AAC, which means that they have about 10% of their abdominal aorta affected by calcium in the blood vessel wall. And those women were about twice as likely to go on to have a late-life dementia hospitalisation and 3-4 times more likely to have a dementia-related death in the next 15 years.”
The scientists are now looking at populations of younger people, in their 30s and 40s, to see what can be learnt about identifying dementia risk earlier in life. And they will continue looking to tease apart the links between conditions and which directions those connections go in. This, says Laws, is the new frontier in ageing research.
Move it or lose it
A key part of protecting bones and brain is exercise. For bones, we need weight-bearing physical activity – things that work the muscles against gravity. That includes walking, running, dancing, tennis – anything where you’re on your feet. Strength-focused training – using weights or gym equipment – is also emerging as a clear longevity booster.
Loss of muscle mass (sarcopenia) is an independent risk factor for early death. Auckland endocrinologist Ian Reid says strength training is good for bones “directly, because the muscles pull on the bones and so bone density goes up by a few [percentage] points”.
Strength also contributes to one of the most important aspects of exercise for older people: improving balance. Alzheimer’s researcher Simon Laws says people with dementia have a much greater risk of falls. “A lot of evidence is suggesting resistance training is the way to go,” he says.
Penny Wilson knows the value of working on strength and balance first-hand. Ten years ago, the then-71-year-old was walking her dog Pixie when she tumbled on uneven ground. She had the dog lead in one hand, her shopping bag in the other, and her face took the full impact of the fall.
“I had this horrible, sickening feeling that I was falling. I was about to hit the ground with my face, and I couldn’t do anything about it,” she remembers.
While her cheek fracture healed after six weeks, the fall, Wilson says, “really knocked my confidence and it made me think. I knew that my balance wasn’t good enough and I had to do something about it.”
Wilson started using Nymbl – a free balance-training app developed by ACC. The app is designed to help seniors stay steady on their feet using dual tasking, combining simple body movements with easy brain games to challenge both the brain and body. ACC launched the app as part of its older people’s programme, Live Stronger for Longer, which is focused on preventing falls and fractures. Research on the app shows people using it three times a week for 10 minutes a day have reduced their chance of having a fall-related injury by 30%.
Wilson says when she first started, she couldn’t do balance exercises such as the tandem stand, the tandem walk or standing on one leg while holding the other leg up in the air.
“I can now. That is a big difference.”
The practical benefits became clear recently when she found herself on the verge of another fall in the local park. “I had that same sickening feeling – I am going to hit the ground again and I can’t stop,” she says. But this time, without any conscious thought, she righted herself. “None of the bystanders could believe it. They all assumed I was going to land flat on my face.” She attributes that to the app and the work she’s done on her balance. “I keep saying you need to work on your balance every day,” she says. “You see people my age have a horrible fall and that is the end of their independence.”
