Dementia is a cluster of brain conditions that negatively impact memory, cognitive functioning, behaviour and the ability to perform everyday activities. In 2008 the World Health Organization declared dementia to be a ‘priority condition’. This is largely because across the globe, a new case presents every 4 seconds, with the incidence of dementia doubling every 20 years. Because there is no treatment and no cure available, and because of its increasing prevalence, it truly is ‘an elephant in the room’ for all concerned when it comes to lifestyle-related chronic disease. Alzheimer’s is the most common form of dementia, accounting for between 60 and 70% of all dementia.
Why would I suggest that we should consider Alzheimer’s to be a disease predominately (but obviously not exclusively) affecting young women? Well, to start with Alzheimer’s is almost never diagnosed in young women and rarely in middle-aged women. Most of us know that Alzheimer’s is mostly diagnosed in the elderly. The keyword in this statement is ‘diagnosed’. Diagnosis is only one stage in the trajectory of Alzheimer’s. But do we ever stop to think about when the disease process actually begins?
This question struck home as recently I spent some time thinking about Alzheimer’s. What went through my mind was that while the disease may often be diagnosed in later life, its pathogenesis – or development – coupled with the chronic progressive nature of the disease indicates that it starts its devastating journey much earlier on in life. Furthermore, Alzheimer’s incidence data reveals that almost 2 out of 3 cases of Alzheimer’s occurs in women. Therefore, it may justifiably be labelled a chronic disease mainly of young women. The combination of female gender; the development and progressive nature of Alzheimer’s, has significant implications for the way in which we think about preventing and treating this devastating chronic disease.
Currently, there are no effective treatments, let alone cures, for Alzheimer’s. Nothing – the medicine chest is empty! Fortunately, we have prevention to turn to. Think about this statement: The best way of treating any chronic disease is to (where possible) prevent it from occurring in the first place. Now, this may not be entirely possible with Alzheimer’s because of a range of contributing risk factors. For example, there are the demographic factors of age and race. And then there are our genes to consider: the presence of one copy of the e4 allele of the gene APOE increases the risk of developing Alzheimer’s and those of us who have inherited two copies are at even greater risk. Nevertheless, it is important to note that being genetically at increased risk does not necessarily mean that the disease will develop. We are able to prevent the over-expression of such genes.
Then there are the lifestyle-related and environmental factors to consider. Obesity, diabetes and high blood pressure, as well as poor lifestyle choices such as smoking and excessive alcohol consumption, all of which appear to be negatively associated with Alzheimer’s. A long-running Norwegian study revealed that while both abstinence, as well as excessive alcohol consumption, are associated with an increased incidence of Alzheimer’s, moderate consumption was not. In fact, the well-reviewed Rotterdam study revealed that light to moderate alcohol consumption, which is defined as one to three drinks per day, was significantly associated with a lower risk of any form of dementia – really good news for those who enjoy having a glass or two of their favourite tipple.
I have written elsewhere about the roles that dietary lifestyle measures, for example eliminating or significantly reducing refined carbohydrates in our diets and increasing healthy fat consumption, play in preventing Type 2 diabetes, obesity and other chronic diseases. The importance of having a healthy gut microbiome – optimising the so-called gut-brain axis is also really important. Exercise it turns out can play an important role in brain health and not just Alzheimer’s. Research reveals that a toxin called lipopolysaccharide or LPS, which causes inflammation is produced by certain gram-negative bacteria in the gut, especially where a condition known as ‘leaky gut’ exists. LPS has been shown to play a role in preventing neurogenesis, which is the development of new brain cells in the hippocampus – the area of the brain most affected by Alzheimer’s.
Research published in the Journal of Neuroinflammation shows that ‘elderly’ mice with high levels of LPS are able to produce new hippocampal neurons or brain cells after running on an exercise wheel, in other words – after exercising aerobically. This effect did not hold true for the ‘elderly’ mice who were purposely not given access to a running wheel, i.e. they did not exercise. The non-exercising mice’s ability to produce new hippocampal neurons was significantly reduced.
Now, if this research data were to hold true for humans as it does for lab-raised mice, then exercise, and especially aerobic exercise, may turn out to be another important arrow in the quivers of not only young women, but also of their mothers, aunts and older sisters too. The mouse study I mentioned was not gender specific and so if what’s good for the goose is probably also good for the gander when it comes to exercise and Alzheimer’s.
Exercise plays other important roles in preventing Alzheimer’s, as well as in improving brain health in general. It improves the production of BDNF, a brain cell ‘growth hormone’ allowing the brain to produce more key brain cells; it reduces inflammation and stress, improves mood, sleep and blood flow and oxygen supply to brain cells helping to remove toxic by-products of brain metabolism.
If you are a young, middle-aged or even older woman and you would like to know more about how you can improve your and your family’s brain health self-care and so work to prevent the development of this serious chronic disease, then please email me at firstname.lastname@example.org. I’d like to hear from you.
Till next time: stay healthy and safe