All in a tangle – Dr Caroline Leaf tries to explain Alzheimer disease

In her latest blog post, Dr Caroline Leaf attempted to tackle the complex topic of Alzheimer disease.

Alzheimer disease is an important topic.  It’s the most common progressive neurodegenerative disease worldwide and accounts for 60 to 80% of dementia cases. It causes a spectrum of memory impairment from forgetting where the car keys are through to forgetting to eat or drink.  According to the 2018 report by the Alzheimer’s Association, an estimated 5.7 million Americans are diagnosed with Alzheimer dementia, costing their economy $277 billion in 2018 [1]. That’s a staggering economic cost, but the human cost is higher.  Alzheimer’s exacts a great emotional toll on someone’s family and friends, both in terms of carer stress, and in seeing the person they love gradually slip away as the disease slowly erodes their personality until there’s nothing left.

There are two main forms of Alzheimer disease, an early onset type which accounts for about 5% cases, and a late onset type which accounts for the rest.  Early onset Alzheimer disease occurs before the age of 65. It’s also called Familial Alzheimer disease because it’s caused by one of three autosomal dominant genes (if you have a copy of the gene, then you will get the disease).  Late onset Alzheimer disease, as the name suggests, occurs late, after the age of 65.  It’s more complex and is associated with a mix of both genetic, lifestyle and environmental risk factors.

The neurobiology of Alzheimer disease is complicated.  Essentially, the symptoms of Alzheimer disease result from the death of too many nerve cells in the parts of the brain that manage memory and planning, but scientists are still trying to establish exactly why the nerve cells die.  There are a number of pieces of the jigsaw already in place.

For example, scientists know that amyloid plaques and neurofibrilliary tangles are part of the disease process.  These result from genetic changes to a number of enzymes which are critical to the nerve cells maintaining their structural integrity. It was first thought that these particular cell changes were critical factors to the nerve cells dying, but there are a number of other contributing factors that are also involved, such as changes to the metabolism of the nerve cells [2], inflammation of the brain, changes in the brain’s immune function, and changes to nerve cell responses to insult or injury (technically, endocytosis and apotosis, just in case you were wondering)[3].

In fact, it may be that the plaques and tangles are not the cause of the damage but are simply present while the other causes such as neuro-inflammation are doing all of the damage in the background.  This is possible as there are a small group of people that have cellular changes of plaques and tangles, but who do not have the clinical signs of dementia.  This was one of the discoveries in the Nun Study.  We’ll talk more about the Nun Study later in the post.

Whether it’s the plaques and tangles doing the damage or not, most of these changes are happening well and truly before a person ever shows any symptoms. In fact, by the time a person has some mild cognitive impairment, the plaques have reached their maximum level and the tangles are close behind.  This makes Alzheimer disease clinically challenging.  It would be ideal if we could start treatment early in the course of the disease before the damage has been established, but right now, the fact is that by the time a person is showing signs of memory loss, the damage to the cells is already done.

This begs the question, can we reduce our risk of Alzheimer disease?  There’s no good treatment for it, and even if there was, prevention is always better that cure.  So what causes Alzheimer disease in the first place?

There are a number of factors which contribute to the development of Alzheimer disease, some of which we can change, but some of which we can’t.

Unmodifiable Risk Factors

  1. Aging

Aging is the greatest risk factor for late onset Alzheimer disease.  The older you get, the more likely you are to get the disease.  Statistically, late onset Alzheimer disease will affect 3% of people between the ages 65–74, 17% of people aged 75–84 and 32% of people that are aged 85 years or older [1].

That’s not to say that Alzheimer disease and normal aging are the same. Everything shrinks and shrivels as you get older and the brain is no exception.  And it’s true that Alzheimer disease and normal aging share some similarities in the parts of the brain most affected.  However, these occur much more rapidly in Alzheimer disease compared to normal aging [4].

So, while aging is a necessary and significant risk factor for late onset Alzheimer disease, aging alone is not sufficient to cause Alzheimer disease.

Also, normal aging of the brain is not dementia.  And forgetting things is not dementia.  Everyone forgets things.  My teenage children forget lots of things I tell them.  They don’t have dementia.  Getting old doesn’t mean getting senile.  Some elderly people remain as sharp as a tack until the rest of their body gives up on them.

  1. Genetics

There are a number of genes which have been associated with Alzheimer disease.

As I alluded to earlier, early onset Alzheimer disease is strongly hereditary, with three different autosomal dominant genes that lead to its development.  They are known as APP, PSEN1and PSEN2genes[5].  The APPgene encodes for a protein is sequentially cleaved into peptides which then aggregate and form amyloid plaques.  PSEN1and PSEN2encode subunits of one of the enzymes which breaks up the amyloid protein.  Then there is a problem with one of the genes, the breakdown of the amyloid proteins is limited and the amyloid plaques start to accumulate at a much earlier age.

For late onset Alzheimer disease, there are 21 associated gene variants which are either splice variants, or single nucleotide polymorphisms (SNPs), and while they don’t cause Alzheimer disease, they increase the risk when they interact with other risk factors.  Each of the genes is important to one of the five main biological processes that influence the cellular structure and function of nerve cells.

(taken from Eid A, Mhatre I, Richardson JR. Gene-environment interactions in Alzheimer’s disease: A potential path to precision medicine. Pharmacol Ther. 2019;199:173-87)

The risk that any of these genes confers for developing Alzheimer disease is ultimately dependent on other risk factors, but one of the most well-known of the genes related to Alzheimer disease is the gene APOE4.  Apolipoprotein (APO) is a lipid carrier and is significantly involved in cholesterol metabolism.  In humans, it’s expressed as either E2, E3 or E4 variants.  The E4 variant has a much lower affinity for lipoproteins than its siblings, and if you have the APOE4, you have much poorer cholesterol metabolism – in your liver cells and in your brain cells.  Again, this fact may not seem important now but it will be more important later in the post.

If you inherit a copy of the APOE4 gene from your mother and your father, you have an 8 – 12 times greater risk of developing Alzheimer disease than another person without both copies of the gene.

  1. Family history

So if there are genes that can send your risk of Alzheimer disease through the roof, then it follows that having a family history of Alzheimer disease is a risk factor.

Individuals who have a first-degree relative, such as a parent, brother or sister who was diagnosed with Alzheimer disease are predisposed to develop the disease with a 4–10 times increased risk, compared to individuals who do not [6].

Of course, family history is not all to do with genetic risk factors, but it’s usually a combination of both genetics and share home environment between parents and siblings, hence why the risk conferred is not as high as APOE4, but is still very high.

  1. Ethnicity

Early studies suggested that Alzheimer disease was more common in certain races, although the thought was that the risk was related to social and economic conditions common to those races, and not to specific genes.

Recently, better genetic studies have linked a few genes with some races.  For example, there is a link with genes such as APOE4 which is twice as likely in African-American’s than other races, or a higher rate of mutations in the CLU gene amongst Caucasians [7].

  1. Gender

There is a strong gender difference for Alzheimer disease.  Overall, women are twice as likely to develop Alzheimer disease than men are.

There are a few possible reasons why this might be so.  Inflammatory mechanisms might play a part, as does the function of the part of the cell called mitochondria.  Hormonal differences might make some differences as well, specifically in relation to the oestrogen or the cell receptors for oestrogen.

There are also some gender differences in the way other genes play out.  For example, it’s known that women with the APOE4 gene will experience a faster cognitive decline than men with the same gene [8].  Sorry ladies.

Modifiable Risk Factors

So whether we like it or not, there are some risk factors for Alzheimer disease that we can’t change.  We can’t change our genes, our race, or our gender.  We can’t get any younger either.

What about the risk factors for Alzheimer disease that we might be able to change?

  1. Education

There’s some correlation between how much education someone has had and their risk of Alzheimer disease.

A meta-analysis by Larsson and colleagues which examined studies through to mid 2014 reported a statistical association of low education attainment (less than or equivalent to primary school) and increased Alzheimer disease risk.  For those with a primary education or lower, the risk of Alzheimer disease was 41 to 60 percent higher compared to someone who had better than primary school.  In a separate study, those who completed higher education (university level or above) had a lower risk of Alzheimer disease compared to those without higher education – approximately 11 percent per year of completed university level education [9].  There is some evidence that Alzheimer disease patients with higher education have a bigger part of the brain related to memory which is thought to be protective (if you have a bigger memory part of the brain, it will take longer to shrink in Alzheimer’s).

Two points to think about here.  First, these studies are not demonstrating cause and effect.  They don’t definitely prove that learning more stuff protects you from Alzheimer disease.  The statistics could simply reflect that people with the ability to learn more information had more robust nerve cells and connections to start with.

Also, while a 60 percent increase in risk sounds high, remember that the APOE4 gene carries a 1200 percent increased risk.  Comparatively speaking, the effect of education is actually quite small compared to other risk factors.

  1. Metabolic factors

Remember how we talked before about cholesterol and the APOE4 variants?  If you have both copies of the APOE4 gene, your liver cells and your brain cells aren’t good at handling lipoproteins.

Your liver cells are important in regulating your blood cholesterol.  Your brain cells are important for handling the amyloid proteins and lipids for making new nerve cell branches.

With APOE4, the liver doesn’t handle the blood cholesterol properly and you end up with high cholesterol and cholesterol plaques in the coronary arteries. When the brain cells don’t handle cholesterol properly, there is an increase in plaques and tangles and neuro-inflammation which increases the risk of Alzheimer disease.

At one stage, researchers thought that having a higher blood cholesterol was linked to Alzheimer disease but further research has shown that the results are inconsistent – some studies show a link while others show no link at all.  So all in all, there’s probably no cause and effect relationship with cholesterol and Alzheimer disease.  In fact, there’s some suggestion that high cholesterol is not a causative factor, but rather the result of Alzheimer disease [10] or simply a correlation, related to an underlying genetic or metabolic disorder which is common to both conditions.

Blood sugar was also considered to be a key factor for Alzheimer disease.  The Rotterdam Study conducted in the 1990s linked diabetes to Alzheimer disease [11], while a more recent nationwide population-based study in Taiwan showed that there was a higher incidence of dementia in diabetic patients [12].

While it may be that high blood sugar leads to Alzheimer disease, more recent research has suggested that there is a two-way interaction between Alzheimer disease and diabetes – diabetes increases the risk of Alzheimer disease, but Alzheimer disease increases the risk of diabetes.  Other scientists have recognised that there is a metabolic disease with overlapping molecular mechanisms shared between diabetes and Alzheimer disease.  These molecular mechanisms relate to less total insulin and higher insulin resistance, a mix of the pathologies seen in type 1 and type 2 diabetes – hence why one scientist called the underlying metabolic disorder “type 3 diabetes” [13].

So while cholesterol and blood sugar are linked to Alzheimer disease, it’s not clear whether aggressively lowering them would decrease the risk of Alzheimer disease or not.

  1. Lifestyle choices (food and exercise)

If it’s not clear how much our metabolic factors have on our Alzheimer disease risk, what about the food we eat?

There’s some evidence that having a healthy lifestyle reduces the risk of Alzheimer disease, but it’s not known what factors of lifestyle are the most important.  There was a study done on residents of New York City, and those who had a strict adherence to a Mediterranean diet and who participated in physical activity decreased their Alzheimer disease risk by about 35 percent [14].  That’s promising, but while there have been lots of studies into various aspects of diet and Alzheimer disease, it’s not clear what exactly works and why [15].

We can’t dismiss lifestyle changes, but more research is needed.

  1. Others

Smoking and alcohol are usually implicated in everything bad, and one would expect that their role in Alzheimer disease would be the same.  So it surprised everyone when one meta-analysis declared that smoking had a protective effect on Alzheimer disease.

The result sounded too good to be true and it probably is.  It’s likely that either smoking killed off all of the weaker people and only left those “healthier” smokers for the study population, or that smokers would have gotten Alzheimer disease had it not been for the fact that the smoking simply killed them off first.

Moral of the story – don’t take up smoking in the hope it will protect you from Alzheimer disease.  Even if it did, the lung cancer and emphysema will get you first.

Alcohol, on the other hand, was fairly neutral in broad population studies. That may be because the benefits of a small amount of wine drinking were being averaged out by the harmful effects of drinking too much hard liquor.  When the amount and type of alcohol drunk was separated out, there’s some evidence that a little bit of wine infrequently is somewhat preventative of Alzheimer disease [16].

Air pollution is a potential risk factor for Alzheimer disease.  It’s thought that the high exposure to chemicals and particulate matter in the air increases neuro-inflammation and death of the nerve cells leading to Alzheimer disease.  In a case-control study in Taiwan, individuals with the highest exposure to air pollution had a 2 to 4-fold increased risk in developing Alzheimer disease [17].

There are similar concerns about the risk of pesticide exposure and Alzheimer disease, although there are often a lot more confounders within the research itself, which makes the associations somewhat weaker.  Still, evidence is generally supportive of a link between pesticide exposure and the development of Alzheimer disease.

Risk factors – what can we learn?

In summary, there are a lot of different risk factors which are involved in Alzheimer disease, some of which can be influenced, and some which cannot.

Alzheimer disease is not a homogeneous disease that can be treated with one specific drug, but rather AD presents as a spectrum, with complex interactions between genetic, lifestyle and environmental factors.  So to really understand a person’s risk for Alzheimer disease, the interactions of these risk factors need to be understood which actually makes things exponentially harder.

That means that anyone telling you to eat this, or learn that, or do my program to reduce the risk of Alzheimer disease clearly doesn’t understand just how complicated Alzheimer disease is and has oversimplified things way too much.

Which brings us back to Dr Leaf and her blog.

I was surprised that Dr Leaf even tried to broach the subject of Alzheimer disease, because diseases like Alzheimers disprove her most fundamental assumption.  Dr Leaf has always taught that the mind is separate to the brain and is in control of the brain.  But if that were the case, the brain changes in Alzheimer disease would make no difference to a person’s cognition and memory.  Yet Dr Leaf admits throughout the entire post that the brain changes in Alzheimer disease do cause changes in the mind.

Dr Leaf can’t have it both ways.  Real cognitive neuroscientists don’t constantly contradict themselves, tripping themselves up on the most fundamental of all facts.  Dr Leaf needs to correct her most fundamental of all her assumptions and admit that the mind is a product of the physical brain and does not control the brain.

Dr Leaf also needs to stop exaggerating her “research and clinical experience”. She’s quick to point over every time she opens her mouth that she has decades of research and clinical experience, but such repeated and unjustified exaggeration is just another form of lying.  Her research was an outdated and irrelevant PhD in the late 1990’s, based on a theory which she tested on school children. Her limited clinical experience was as a therapist for children with acquired brain injuries.

Alzheimer disease affects the other end of the age spectrum and has nothing to do with acquired brain injury.  It is the absolute polar opposite of Dr Leaf’s already limited research and clinical experience.  Dr Leaf is like an Eskimo trying to build an igloo in the Sahara.

Dr Leaf’s credibility on the subject quickly evaporates with her introductory caution:

Before we go into too much detail, I want to remind you that our expectations can change the nature of our biology, including our brains! Indeed, recent research suggests just fearing that you will get Alzheimer’s can potentially increase your chance of getting it by up to 60%.

Dr Leaf doesn’t offer any proof that “Our expectations change the nature of our biology” but she does allude to “recent research” which suggests that “just fearing that you will get Alzheimer’s can potentially increase your chance of getting it by up to 60%”.  She doesn’t reference that either.  She could be referring to the research from Yale which she alludes to later in her post, although that research by Levy and colleagues didn’t mention anything about the risk of Alzheimer disease increasing by 60 percent [18].  In fact, given certain methodological weaknesses, it didn’t conclusively prove that negative beliefs about aging did anything to the brain, but that’s a topic for another day.

Dr Leaf made several attempts throughout the rest of the blog to portray Alzheimer disease as a disease related to toxic thoughts and poor lifestyle choices.  For example:

There is now a growing body of research that approaches the question of Alzheimer’s and the dementias as a preventable lifestyle disease, rather than a genetic or biological fault.  More and more scientists are looking at Alzheimer’s and the dementias as the result of a combination of factors, including how toxic stress and trauma are managed, the quality of someone’s thought life, individual diets and exercise, how we can be exposed to certain chemicals and toxic substances, the impact of former head injuries, and the effect of certain medications.

That statement is just a big furphy.  Yes, Alzheimer disease is the result of a complex interaction of genes and environmental factors.  Yes, there is some evidence looking at the interactions of diet and exercise, environmental exposures and former head injuries (although there’s very mixed evidence for the role of brain trauma in Alzheimer disease.  It’s not clear cut [19]).  But there is no ‘growing body of research’ that claims Alzheimer disease is not strongly genetic or biological, and there’s certainly no real scientist dumb enough to call Alzheimers a “preventable lifestyle disease”.

The evidence is pretty clear, that there are very strong genetic factors for developing Alzheimer disease.  Yes, some of them can be modified by environmental factors, but it’s foolhardy to claim that Alzheimer disease can be entirely prevented, based on the current evidence I outlined earlier.  Dr Leaf is rushing in where angels fear to tread.

Dr Leaf’s baseless exaggerations don’t stop there.

It is therefore unsurprising that professor Stuart Hammerhoff of Arizona University, who has done groundbreaking research on consciousness and memory, argues that the kind of thinking and resultant memories we build impacts our cell division and can contribute to the development of Alzheimer’s and the dementias.

Dr Leaf includes a hyperlink which when clicked, takes you to this article: https://www.theglobeandmail.com/life/health-and-fitness/health/conditions/new-theory-targets-different-origins-of-alzheimers/article4210442/.

It’s not a scientific paper, but a newspaper article which is more than seven years old.  The only thing it says about Professor Stuart Hameroff is this:

One of the co-authors, Stuart Hameroff at the Center for Consciousness Studies at the University of Arizona, has argued that microtubules may also be involved in consciousness.

That’s it.  There’s nothing else in the article about Prof Hameroff at all, nothing to back up Dr Leaf’s wild claim that our thinking and our memories alters cell division and contributes to the development of Alzheimers and dementia.  Dr Leaf is just confabulating.

Dr Leaf also claims that:

One of the many studies that have come out of this research, done by the Buck Institute for Research on Aging, showed dramatic improvement in patients diagnosed with Alzheimer’s and the dementias when they were put on an individualized lifestyle-based program that includes diet, exercise and learning.

Again, that’s a gross exaggeration.  The “research” that Dr Leaf is alluding to is a paper written by Bredesen [20].  It’s a narrative paper which describes a total of ten cases. That’s it – just ten cases. That’s nowhere near enough information to draw even the weakest of conclusions, but it gets worse.  The paper only gives a formal description of three patients and their treatments, the rest were listed in a table.  So there is even less data to draw any definitive conclusions from.  The other serious weaknesses of the paper were that the patients self-identified, and most of them didn’t have dementia at all, but instead had “amnestic mild cognitive impairment” or “subjective cognitive impairment”.  In other words, they were a little forgetful, or they only thought they were forgetful. The one subject that did have Alzheimer disease continued to rapidly deteriorate in spite of the program.

If you took Dr Leaf at her word, you would think that this treatment program was working miracles and clearly proved that Alzheimer disease could be cured by lifestyle treatment.  The study showed anything but.

Again, Dr Leaf is proving herself untrustworthy – either she knew that the study failed to demonstrate significant results and she was deliberately deceptive, or she didn’t understand that the results of the study were not conclusive, in which case she’s too ignorant to be treated as an expert.

In the same vein, Dr Leaf writes:

Another famous study, known as the “Nun Study,” followed a number of nuns over several years, showing that, although extensive Alzheimer’s markers were seen in their brains during autopsy (namely neurofibrillary plaques and tangles), none of them showed the symptoms of Alzheimer’s and the dementias in their lifetime. These nuns led lifestyles that focused on disciplined and detoxed thought lives, extensive learning to build their cognitive reserves, helping others and healthy diet and exercise, which helped keep their minds healthy even as their brains aged!

The hyperlink that Dr Leaf included was to a Wikipedia page which again, said nothing about the nuns who were apparently impervious to the effects of Alzheimers.  It did say that

Researchers have also accessed the convent archive to review documents amassed throughout the lives of the nuns in the study. Among the documents reviewed were autobiographical essays that had been written by the nuns upon joining the sisterhood; upon review, it was found that an essay’s lack of linguistic density (e.g., complexity, vivacity, fluency) functioned as a significant predictor of its author’s risk for developing Alzheimer’s disease in old age. The approximate mean age of the nuns at the time of writing was merely 22 years. Roughly 80% of nuns whose writing was measured as lacking in linguistic density went on to develop Alzheimer’s disease in old age; meanwhile, of those whose writing was not lacking, only 10% later developed the disease.

As it turns out, lots of nuns did end up with dementia after all … well that’s awkward – the page that Dr Leaf used to try and support her argument actually directly contradicted her.

Wikipedia’s entry was supported by the original journal article in the research from Riley et al [21].  And after a bit of gentle trawling of the scientific literature, I also found this article from Latimer and colleagues which said, “Interestingly, our results show very similar rates of apparent cognitive resilience (5% in the HAAS and 7% in the Nun Study) to high level neuropathologic changes” [22].

So, sure, some nuns did indeed have some plaques and tangles without showing signs of the disease, but not 100 percent of them as Dr Leaf tried to make out. In reality, it was only 7 percent of them!  And given what we know from the current research, plaques and tangles often precede clinical symptoms, so it may be that the nuns in question were on their way to cognitive impairment, but they hadn’t quite made it.  Who knows.  One thing’s for sure, the “lifestyles that focused on disciplined and detoxed thought lives” didn’t stop dementia affecting most of the nuns in the study.

Dr Leaf finishes off her post with what she thinks will help prevent Alzheimer disease. Given that she clearly doesn’t understand Alzheimer disease, we need to take what she advises with a large dose of salt.  Let’s look at what Dr Leaf suggested and see if it lines up with actual research.

Research shows that education, literacy, regular engagement in mentally-stimulating activities and so on results in an abundance of and flexibility in these neural connectionswhich help us build up and strengthen our cognitive reserves and protect our brain against the onset of Alzheimer’s and the dementias.
Like everything in life, the more you use your ability to think, the more you get better at it and the stronger your brain gets!

Rating: Half-true

Education has a small positive benefit, but the research isn’t clear if that’s cause or correlation.  So yes, stimulate your brain and see what happens.  It might not help stave off Alzheimer disease, but at least it will make the journey interesting it nothing else.

What else can you do to prevent Alzheimer’s and the dementias, or help someone already suffering cognitive decline?
1. Detoxing the brain:
I have written extensively about the importance of detoxing the brain by dealing with our thought life in a deliberate and intentional way. Our minds and brains are simply not designed to keep toxic habits and toxic trauma; we are designed to process and deal with issues. If, however, we suppress our problems, over time our genome can become damaged, which will increase the potential for cognitive decline as we age. This is why it is important to build up a strong cognitive reserves AND live a “detoxing lifestyle”, which essentially means that you make examining and detoxing your thoughts and emotions a daily habit. We want to have good stuff in our brain, yes, but we don’t want the neurochemical chaos of a bad thought life affecting our healthy cognitive reserves!

Rating: BS (“Bad Science”)

This is Dr Leaf’s favourite pseudoscientific claptrap, her neurolinguistic-programming-voodoo-nonsense that has no scientific basis whatsoever.  Skip it and move on.

2. Social connections:
Intentionally developing deep meaningful relationships can help build up our cognitive reserves against Alzheimer’s and the dementias – our brains are designed to socialize! Loneliness and social isolation, on the other hand, can seriously impact the health of our brains, making us vulnerable to all sorts of diseases, including ones associated with cognitive decline and the dementias …

Rating: Half-true

Loneliness has deleterious effects on health, but there’s nothing in the research to suggest that loneliness is a risk factor for Alzheimer disease.  Like we discussed about education and mental stimulation before, I think you should make friends and enhance your social connections.  There’s no guarantee that it will make any difference to your risk of Alzheimer disease, but it will make things fun and interesting at least.

3.  Sleep:
Dr. Lisa Genova, a neuroscientist, wrote the book Still Alice (this was also made into a movie), which describes the impact of the early onset of Alzheimer’s. She believes that buildup of plaques and tangles associated with Alzheimer’s can be averted, since it takes about 10 to 20 years before a tipping point is reached and cognitive decline becomes symptomatic. We all build plaques and tangles, but it takes at least a decade for them to actually affect our ability to remember, so there is hope!
There are things we can do to prevent this buildup, and sleep is an important one. During a slow-wave, deep sleep cycle, the glial cells rinse cerebrospinal fluid throughout our brains, which clears away a lot of the metabolic waste that accumulates during the day, including amyloid beta associated with the dementias. Bad sleeping patterns, however, can cause the amyloid beta to pile up and affect our memory. Essentially, sleep is like a deep cleanse for the brain!

Rating: What?

Dr Leaf’s advice here isn’t necessarily BS, it’s just plain confusing as she takes two unrelated chunks of information and tries to conflate them.

I don’t know if Dr Lisa Genova is a neuroscientist, or if she thinks the build-up of plaques and tangles can be averted or not.  The science as I outlined earlier in the post shows that the rise in plaques and tangles predate clinical symptoms, so you don’t know if you have them or not.  If that’s the case, how can you hope to reverse them.  Science is working on it, but it’s not there yet.

Irrespective, Dr Leaf doesn’t present any evidence to support her statement that sleep clears amyloid proteins.  And neither is there any evidence that sleep has a significant impact on the development of Alzheimer disease.

I think it’s good general advice to try and get a reasonable amount of good quality sleep so you can wake up refreshed.  Whether it changes your Alzheimer disease risk, who knows.

2. Diet:
We can now say with a good degree of certainty that consuming highly processed, sugar-, salt-, and fat-laden foods contributes to increased levels of obesity, cardiovascular disease, diabetes, stroke, allergies, autism, learning disabilities, and autoimmune disorders and Alzheimer’s! Some of the ways modern, highly processed and refined foods can contribute to Alzheimer’s and the dementias include added, highly-processed sugars, which cause your insulin to spike and the enteric nervous system of your gut to secrete an abnormal amount of amyloid protein. This will start destroying the blood-brain barrier, and can contribute to the formation of the amyloid plaques of Alzheimer’s disease. Some researchers now even refer to Alzheimer’s as type III diabetes!

Rating: Complete and utter BS

High sugar and high fat foods is certainly a contributing factor to obesity and to diabetes, and indirectly to cardiovascular disease and stroke. That’s where the intelligence in Dr Leaf’s statement comes to a grinding halt.  The rest of it is just a stream of fictitious nonsense without any basis in reality.

The western diet does not contribute to allergies, and it’s scientifically impossible for it to contribute to autism since autism is a genetic condition which expresses itself during foetal development, and I am yet to see a foetus chow down on a cheeseburger.  But wait, there’s more – learning disabilities, and autoimmune disorders too, and of course, Alzheimer disease.  Who cares that there’s no definitive trials to clearly prove that Alzheimer disease is in any way connected to our diets.

But apparently it’s the evil sugar which causes insulin to make the gut nervous system secrete amyloid proteins which destroy the blood brain barrier. When you put enough medical terms in a sentence, you would fool about 99 percent of people.  But looking past the random string of medical jargon, it’s clear that Dr Leaf is deluded.  The structural damage in Alzheimer disease comes from the nerve cell’s poor lipid metabolism, most of which comes from a gene which codes for a lipid carrying protein. Lipids have nothing to do with sugar. Besides, who cares if the enteric nervous system secretes amyloid … the enteric nervous system is in the gut [23], not the brain.  Even her inconsistencies are inconsistent.

Dr Leaf’s throw-away line at the end, “Some researchers now even refer to Alzheimer’s as type III diabetes!” is ignorant or intentionally misleading.  We’ve already established that the name “Type 3 diabetes” referred to the fact that scientists have recognised a metabolic disease with overlapping molecular mechanisms shared between diabetes and Alzheimer disease, not that Alzheimer disease is a metabolic disorder. Alzheimer disease is not because of too much sugar or bad lifestyle choices.

5. Exercise:
There is extensive research on the importance of exercise as a preventative tool against Alzheimer’s and the dementias. A number of studies show that people who exercise often improve their memory performance, and show greater increase in brain blood flow to the hippocampus, the key brain region that deals with converting short-term memory to long-term memory, which is particularly affected by Alzheimer’s disease.

Rating: Plausible

I don’t know what the state of the research is, but the study discussed earlier in the post about lifestyle changes did show improvement in risk for those who exercised.  And out of all of Dr Leaf’s pronouncements, at least this one has scientific plausibility.

Exercise promotes a growth factor in the brain called BDNF.  BDNF does stimulate the growth of new nerve cell branches.  Growth of new nerve cell branches results in improved mood.  It’s not entirely implausible to think that it would help with new memory formation and an enhanced hippocampus.

How much it really prevents Alzheimer disease is not clear, but given that exercise is universally good for you, I think it should be first on the list, not the last.

Dr Leaf – in a tangle

So in summary, Alzheimer disease is a complex multifactorial disease with a number of factors that affect its development, some of which can be changed, while others cannot.

Dr Leaf doesn’t understand this.  Her reading of the literature about Alzheimer disease is limited and skewed by her biased assumptions about toxic thinking and lifestyle.  Sure, there are some risk factors for Alzheimer disease which may be related to lifestyle and which may be modifiable, but Dr Leaf has failed to synthesise that information into the broader understanding of Alzheimer disease.

So some of her advice is helpful.  Most of it is not.  If you’re concerned that you or a loved one might have early memory loss, please don’t listen to Dr Leaf – see a real doctor instead and get the right advice.

References

[1]        Alzheimer’s A. 2018 Alzheimer’s disease facts and figures. Alzheimers Dement 2018;14(3):367-429.

[2]        Area-Gomez E, Schon EA. On the Pathogenesis of Alzheimer’s Disease: The MAM Hypothesis. FASEB J 2017 Mar;31(3):864-67.

[3]        Eid A, Mhatre I, Richardson JR. Gene-environment interactions in Alzheimer’s disease: A potential path to precision medicine. Pharmacol Ther 2019 Jul;199:173-87.

[4]        Toepper M. Dissociating Normal Aging from Alzheimer’s Disease: A View from Cognitive Neuroscience. J Alzheimers Dis 2017;57(2):331-52.

[5]        Dai MH, Zheng H, Zeng LD, Zhang Y. The genes associated with early-onset Alzheimer’s disease. Oncotarget 2018 Mar 13;9(19):15132-43.

[6]        Cupples LA, Farrer LA, Sadovnick AD, Relkin N, Whitehouse P, Green RC. Estimating risk curves for first-degree relatives of patients with Alzheimer’s disease: the REVEAL study. Genet Med 2004 Jul-Aug;6(4):192-6.

[7]        Nordestgaard LT, Tybjaerg-Hansen A, Rasmussen KL, Nordestgaard BG, Frikke-Schmidt R. Genetic variation in clusterin and risk of dementia and ischemic vascular disease in the general population: cohort studies and meta-analyses of 362,338 individuals. BMC medicine 2018 Mar 14;16(1):39.

[8]        Altmann A, Tian L, Henderson VW, Greicius MD, Investigators AsDNI. Sex modifies the APOE‐related risk of developing Alzheimer disease. Annals of neurology 2014;75(4):563-73.

[9]        Larsson SC, Traylor M, Malik R, et al. Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis. Bmj 2017 Dec 6;359:j5375.

[10]      Rantanen K, Strandberg A, Pitkälä K, Tilvis R, Salomaa V, Strandberg T. Cholesterol in midlife increases the risk of Alzheimer’s disease during an up to 43-year follow-up. European Geriatric Medicine 2014;5(6):390-93.

[11]      Ott A, Stolk R, Van Harskamp F, Pols H, Hofman A, Breteler M. Diabetes mellitus and the risk of dementia: The Rotterdam Study. Neurology 1999;53(9):1937-37.

[12]      Huang C-C, Chung C-M, Leu H-B, et al. Diabetes mellitus and the risk of Alzheimer’s disease: a nationwide population-based study. PloS one 2014;9(1):e87095.

[13]      de la Monte SM. Type 3 diabetes is sporadic Alzheimer׳s disease: mini-review. European Neuropsychopharmacology 2014;24(12):1954-60.

[14]      Scarmeas N, Luchsinger JA, Schupf N, et al. Physical activity, diet, and risk of Alzheimer disease. JAMA : the journal of the American Medical Association 2009 Aug 12;302(6):627-37.

[15]      Hu N, Yu J-T, Tan L, Wang Y-L, Sun L, Tan L. Nutrition and the risk of Alzheimer’s disease. BioMed research international 2013;2013.

[16]      Heymann D, Stern Y, Cosentino S, Tatarina-Nulman O, Dorrejo JN, Gu Y. The Association Between Alcohol Use and the Progression of Alzheimer’s Disease. Curr Alzheimer Res 2016;13(12):1356-62.

[17]      Wu YC, Lin YC, Yu HL, et al. Association between air pollutants and dementia risk in the elderly. Alzheimers Dement (Amst) 2015 Jun;1(2):220-8.

[18]      Levy BR, Ferrucci L, Zonderman AB, Slade MD, Troncoso J, Resnick SM. A culture-brain link: Negative age stereotypes predict Alzheimer’s disease biomarkers. Psychol Aging 2016 Feb;31(1):82-8.

[19]      Kokiko-Cochran ON, Godbout JP. The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease. Front Immunol 2018;9:672.

[20]      Bredesen DE. Reversal of cognitive decline: a novel therapeutic program. Aging (Albany NY) 2014 Sep;6(9):707-17.

[21]      Riley KP, Snowdon DA, Desrosiers MF, Markesbery WR. Early life linguistic ability, late life cognitive function, and neuropathology: findings from the Nun Study. Neurobiology of aging 2005 Mar;26(3):341-7.

[22]      Latimer CS, Keene CD, Flanagan ME, et al. Resistance to Alzheimer Disease Neuropathologic Changes and Apparent Cognitive Resilience in the Nun and Honolulu-Asia Aging Studies. J Neuropathol Exp Neurol 2017 Jun 1;76(6):458-66.

[23]      Costa M, Brookes SJH, Hennig GW. Anatomy and physiology of the enteric nervous system. Gut 2000;47(suppl 4):iv15-iv19.

Thinking about suicide

Do you think about dying? I do, quite often.

In an article published last week in the Sydney Morning Herald, Daniel Mezrani wrote about his father’s suicide. Daniel’s tone was honest and heartfelt. His message was sobering. Daniel’s father was an emergency physician, highly respected, with “three teenage children, dozens of enamoured colleagues and an innumerable network of people he had touched with his generosity, humour and passion for social justice”, yet he ended his life.

Throughout the article, Daniel approaches suicide through a social framework. “I don’t think that suicide should be viewed as a purely psychiatric issue” he writes. “The idea that suicide is always the consequence of a definable mental illness continues to dominate the public consciousness despite a growing consensus among the academic community that there is much more at play.”

“We know that isolation significantly increases suicide risk, as do other social stressors such as unemployment and relationship failure. A new paradigm in suicide prevention emerges – if we begin to see people in context, we become privy to external factors that may be causing them distress and can thus look out for more subtle cues that they may be at risk.”

He’s not incorrect. Social factors are important to a person’s risk of suicide, though mental health is very important too.

“There is no simplicity in this conclusion, but there is promise. It means that anything we do to address stigma, discrimination and hardship at a systemic level has the potential to bring down our national suicide rate. If we really want to stop people dying in this most horrific way, we need to make it easier for them to live.”

True again. More suicides are prevented through decisions at a systems and government level than through direct personal intervention.

He concludes by saying, “They are tangible reminders that things can get better, and that we are never, ever alone.”

It’s a lovely way of rounding out an article on a very difficult topic, I give him credit for that. And for the average person, it seems like a very reasonable thing to say … things do get better, no one is ever truly alone.

Except that’s not how someone who’s suicidal will see it.

Daniel succinctly encapsulated the essence of suicide earlier on in his article: “The final common pathway is not neurochemical disturbance or a discrete socioeconomic stressor, it is an anguish that feels otherwise inescapable; hopelessness manifest.”

I’ve battled with depression for a long time now, the chronic latent adversity of pathological hopelessness. Most of the time it sits on me like an emotional weight vest, making the simplest tasks feel like so much more of an effort, subtly stealing my energy, tempering my sense of joy. But there are times when I feel like I’m being crushed by a tonne of wet sand and I can’t move or breath or see. There are other times where I feel like someone has ripped out my heart and is pouring battery acid into my chest, and all I can feel is pain.

I think about suicide. Depending on where my mood is, there are times when I think about it a lot. The recurrent theme connecting all those times is hopelessness.

Shame brings isolation, inequality brings inertia, but it is hopelessness that finally destroys.

Most people have never felt the depths of despair that true hopelessness brings, and I hope they never do. Unless you’ve been there, it’s impossible to truly understand how overwhelming it is. The only way I think I could describe it would be to imagine that you’re out to sea and your boat sinks, leaving you stranded in the middle of the ocean at night in the middle of a storm – it’s dark, it’s disorientating, numbingly cold, fighting to try and keep your head above the water when the swells and the currents are constantly dragging you down.

Things can get better, and we are never alone, but when overwhelmed by deep existential despair, you can’t see it.

It might sound like I’m against addressing stigma, discrimination and hardship, but I’m not. The purpose of this article isn’t to advocate for one solution or another. I certainly don’t pretend to know all, or maybe any of, the answers. The purpose of speaking out like this is simple … I want to add to the conversation.

At the opening plenary of the conference I attended this weekend, Dr Geoff Toogood, a doctors mental health advocate, spoke about his own personal journey with mental illness as a way of starting the conversation. It’s a hard conversation, but it’s one we have to have, and it needs to be authentic if it’s going to have any real resonance. It would be much easier to simply hide away, masking the pain, pretending it’s not there, but lets face it, we’ve tried that strategy already and it’s killing us.

I can’t offer answers, but I do promise authenticity.

I also wanted to broach the key issue of hope. How do we give people hope? Hope doesn’t come from a pill or a program, but where does it come from? Can we mobilise hope? Can we give hope to the hopeless, and if so, how do we communicate hope to those who struggle the most to hear it?

I know there will be people reading this who have thought about, or might even be thinking about suicide. I know what you’re feeling. I know how hard it is.

Again, I don’t pretend to know all the answers. All I can say is that you’re not the only one, and you’re not alone. I know it’s not easy, but find even the faintest glimmer of hope – in your family, in your job, in people around you, in a faith. Hold on to it. The storm will pass and day will break.

Sometimes even the simplest connection to another person can help. If you need to talk to someone, there are always people that can help. In Australia, call Lifeline ~ 13 11 14, BeyondBlue ~ 1300 22 4636 or https://www.beyondblue.org.au/about-us/contact-us or the Suicide Callback Service ~ 1300 659 467 or https://www.suicidecallbackservice.org.au. In the USA, call the National Suicide Prevention Lifeline ~ 1-800-273-TALK (8255). In New Zealand, call Lifeline Aotearoa 24/7 Helpline ~ 0800 543 354. In the UK, call Samaritans ~ 116 123. For other countries, Your Life Counts maintains a list of crisis services across a number of countries: http://www.yourlifecounts.org/need-help/crisis-lines.

Kudos to Daniel Mezrani. It’s shattering to lose someone you love so much, and it takes a special kind of person to turn that tragedy into something that will help other people. I wish him and his family all the best as they continue on their difficult journey.

Stigma, discrimination and hardship do need to be addressed at a systemic level if we are going to help lower our nation’s suicide rate.

We also need to better understand hope, how to foster it in those whose hope is dormant, and how to help those who have lost all hope to find it again.

We need to keep talking too. The conversation is extremely challenging, but without an open and authentic dialogue, many will continue to suffer, silent and alone, instead of getting the help they deserve.

More love, not less guns?

Wow.

Just … wow.

Dr Caroline Leaf is no stranger to ignorance and controversy – she thinks that our minds can create matter, that our thoughts can control our genetic expression, and that psychiatric medications are a leading cause of death. So it should come as no surprise when she proves the Dunning-Kruger Effect over and over again.

Still, I found her podcast and meme today utterly breathtaking.

Dr Leaf, communication pathologist and self-titled cognitive neuroscientist-cum-life-guru continues to weigh in on the gun debate every time there’s a mass shooting. I wouldn’t if I were her, but fools rush in.

At least Dr Leaf has finally stopped blaming mental illness or psychiatric medication for causing such mass murders. That said, there’s still more twisting and contorting in her statement than at a pretzel convention.

Dr Leaf has relinquished one over-simplistic solution in favour of another. Yes, mass shootings aren’t related to mental illness, but can you really say with a straight face that mass shootings occur because of a lack of love? So we should all hold hands and sing Kumbayah? Have a few more hugs? Dr Leaf’s suggestion is childish and inane.

Since 1996, Australia’s number of mass shootings has been zero. Australia’s gun-related homicide and suicide rate also fell. Why? It’s not because we all started loving each other more down here after 1996. It’s because, amongst other reasons, the Australian government introduced gun law reform, drastically reducing the number of guns available within the general population.

Perhaps living in Texas has rubbed off on her, or perhaps Dr Leaf is an NRA sympathiser. I honestly don’t know why Dr Leaf is so afraid to speak directly to the problem. Most of the US and the entire rest of the world can see the issue for what it is. If it wasn’t so tragic, her dance around the issue would be comical.

Dr Leaf is welcome to her opinion, but she can not claim any level of moral or professional authority on this issue. Her “years of experience in the mental health field” are zero, as is her credibility as an expert. Encouraging more love with the same number of handguns and semi-automatics on the street is not going to prevent more casualties.

Stop mislabelling labels.

The last time I looked through the supermarket, I bought some baked beans. How did I know the can I took off the shelf was full of baked beans and not freshly harvested sheep’s innards? Because the label on the can said so.

Labels aren’t perfect of course. Every now and then, a can of something has the wrong label applied in the factory. Usually it’s nothing too sinister – no accidental swaps of some goat entrails instead of your tinned salmon. Instead, it’s usually something similar – tuna gets labelled as salmon and vice versa, and the worst that happens is that the tuna mornay you’ve just made had an unexpected flavour.  Even these sorts of mild mix ups are rare. Overall, we trust that the labels are guides and the information they provide us helps us make an informed decision about what do to with that particular can and its contents.

It would be pretty silly for some random person to preach out the front of the supermarket, ranting about how all labels for a particular thing are all wrong.

“Uh, just because the occasional can of tuna was accidentally filled with cat food doesn’t mean to say that all labels are wrong. And just because one person had a bad experience with the wrong label, the supermarket shouldn’t stop using them … otherwise how else is anyone supposed to manage their cans effectively without labels? Honestly, stop looking like a fool by preaching about labels and let the rest of us finish our shopping.”

Dr Caroline Leaf, communication pathologist, self-titled cognitive neuroscientist, and a self-elected champion of irrelevant mental health advocacy, has come out all guns ablazin’ over ADHD labels again. She needs to give it a rest – she’s just like the crazy person standing in front of the supermarket.

“Labels for ADHD are bad”, she says. “Look at Avery Jackson, who was labeled ADHD but did not accept the label. He went on to earn multiple degrees and become one of the top neurosurgeons in the U.S!”  The underlying message – labelling a child with ADHD will lock then into a life of pathetic excuses and they won’t ever reach their full potential until they renounce the curse of their ADHD label.

For every scary anecdote about the evils of ADHD and the mental prison that everyone with such a label is supposed to find themselves in, there are ten more where the ADHD label helped them.  There are so many more people where the ADHD label helped them to finally understand their condition and receive the correct treatment, enabling them to reach their potential and improve their life in leaps and bounds.

Take, for example, one of my patients called Little Jimmy (not his real name). When Little Jimmy was in the early primary school grades, he was a bit of a fidgeter and couldn’t concentrate well enough at school or at home to complete his homework tasks. His mother took him to a naturopath who told him he had a disorder of “pyrolles disease”. Thankfully, mum brought him to see me, and after a careful history and a long chat, Little Jimmy went to see a specialist who diagnosed him with ADHD and commenced him on stimulant medications. Before his label, Little Jimmy’s reading levels were languishing at the bottom off his class after two years of stagnation.  He was more than a year behind in reading levels and going nowhere fast.  Two weeks after getting his label and the right medication, he went to the top three reading levels in the class.  His mother told me of the massive gains he made, and the flow-on effect this had to his self-esteem and confidence in other areas of his school work and school life. She cried as she recounted his story, and then I cried too.

So perhaps Avery Jackson became an orthopaedic surgeon because he chose to ignore his label of ADHD and worked hard anyway.  Good for him.  Little Jimmy got a label of ADHD and because of it, he learnt to read. Now he’s got the chance to follow in Avery Jackson’s footsteps, BECAUSE of his label.

Labels are important. Without them, we wouldn’t know how to know who needs which treatment. Labels can help people overcome some of the strongest barriers and connect with others for support.

And let’s face it, if someone really wanted to, they don’t need a label of ADHD to find excuses in life.

So labels are not a hinderance, but rather, they are a guide to help you know what’s going on so informed choices can be made. In Dr Leaf’s mind, those kids with ADHD are just naughty children, with bad parents, who are using the label of ADHD to cover their poor parenting and their bad behaviour. Clearly all they need to do is to stop their toxic thinking and they wouldn’t need their medications, but they would be cured.

Dr Leaf is wrong … she can stand and scream blue murder about labels and ADHD all she wants.  But just like the crazy random person screaming about labels in front of the supermarket, it means very little. It’s not helping her cause, and if anything, it’s sewing distrust in an system that, despite it’s flaws, works very well, and has helped thousands of children and adults alike to achieve their potential.

That’s the power of labels, and Dr Leaf would do herself and all her followers a favour if she stopped mislabelling them.

The lost art of joy – Something to look forward to

Bacon.

With only about eight hours left in 2017, I should be contemplating bigger things … the lessons learnt from the year gone by, what did I achieve, where did I fall down, what can I learn from those experiences.

Instead, I feel like bacon, so I’m cooking bacon.

Bacon is delectable. It’s one of those foods that proves God’s love. On it’s own, it’s special, but you can also add bacon to almost any other food and it will add to the gustatory experience of pleasure. The auditory and olfactory stimulation of bacon frying is distinctly pavlovian – I’m drooling just thinking about the culinary delights that await me.

As I was standing over the frypan, listening to the crackling and popping, smelling the juicy aroma and mopping up my hypersalivation, it also stimulated the rusty gears of my cognition.

Why do I drool when bacon is cooking? For all I know, the bacon could be rancid, or I could have cooked it wrong, or it could be too salty, or it could be pigeon meat in disguise.

But I have hope.

I can’t say, rationally and with certainty, that “the bacon will be good” because there are lots of reasons why it might be bad, but I have hope that the bacon will be delicious.

Hope. It is “the quintessential human delusion, simultaneously the source of your greatest strength, and your greatest weakness.
Hope is “being able to see that there is light, despite all of the darkness”. (Desmond Tutu)
Hope “smiles from the threshold of the year to come, whispering, ‘It will be happier.’” (Alfred Lord Tennyson)

Like we discussed yesterday, happiness is someone to love and something to do. Happiness is also something to look forward to.

Hope is like joy’s air. In order for joy to breathe, it has to be surrounded by hope. Without hope, joy can not survive.

Research bears this out. Numerous studies over the years have shown that those with higher levels of hope had higher academic and sports achievements. Lower levels of hope correlate to general maladjustment and thoughts of suicide. Hope is a crucial factor in dealing with major life stressors and traumas, such as cancer and old age. The impact of hope on depression and adjustment was studied in people with traumatic spinal cord injuries, and it was found that those with higher levels of hope had less depression and greater overall mental and social adjustment irrespective of how long it had been after the injury. In another study, lower levels of hope was related to higher levels of depressive symptoms in general.

Hope is applied optimism. Optimism is the general expectancy that good rather than bad will happen. Hope is “the belief that the future will be better than the present, along with the belief that you have the power to make it so.”  Hope is the ultimate fusion of acceptance, values and committed action – knowing which direction you want to go in, having a path leading in that direction and then going, not knowing what will happen but accepting that not everything will be perfect but believing that it will be better.

So what about 2018? I can’t say, rationally and with certainty, that “2018 will be a great year” because there are lots of reasons why it might be bad.

Still, I have hope that 2018 will be a great year.

Do you have hope? Do you believe 2018 will be a better year? Do you believe that you have the power to make it so? Over the last month, we’ve explored the lost art of joy; the ingredients of joy and how these can shape our lives; the things that can suffocate joy and the things that can help joy flourish. Do you believe that you can apply these principles to experience a life of greater joy, a richer life of deeper meaning and fulfilment? In all sincerity, I hope you can.

Thank you for coming on my journey with me. On the 1st of December when I had the bright idea of writing a blog post a day for a whole month, I thought it would be easy. When I got to the 5th of December, I thought I was going to run out of ideas and I should have thought twice before committing to such a huge project. Now, on the 31st of December, I’m glad I made that ill-considered commitment. It has challenged me for sure. It’s helped me to clarify concepts, to grow in knowledge and make me that little bit more proficient as a writer.

My hope is that my 31-day challenge will not just help me, but help others who are struggling to see the light and to experience the warmth of joy in their souls. “These things have I spoken unto you, that my joy might remain in you, and that your joy might be full.

Happy New Year! May you all have a safe, prosperous, and joyous 2018.

Oh, and by the way, the bacon was delicious.

The lost art of joy – Something to do

“So, what do you do?”

I don’t like that question. We all ask it as a relatively benign conversation starter, but it still makes me cringe a little. It’s not that I’m not proud of what I do, but so often the moment I tell people that I’m a doctor, they assume that I’m rich or pretentious, or that they suddenly have a segue to some free medical advice.
“Oh, you’re a doctor hey? Pleased to meet you … so, uh, can you have a quick look at this mole on my neck?”

It’s interesting that we treat someone’s occupation as the second most important thing to know about them after their name, and it shows how subliminally important our occupations are to us.

And I think that’s largely to do with the personal and social value of purpose.

It’s starts from childhood doesn’t it? “When I grow up, I want to be …”

“I want to do nothing with my life” said no kindergarten child ever. Our subject choices in through high school, and out decisions after high school, to go to University or join the military, or taking a job in a trade, come down to what we want to do, to what we want to be. We all want to be someone, to do something. We all aspire to a life of meaning through purpose, because deep down, having a life which makes a difference is much more rewarding to us than having a life than means nothing.

Happiness is someone to love like we discussed yesterday, but happiness is also something to do.

It’s well known that long-term unemployment is associated with poorer physical and mental health outcomes including increased stress and isolation, depression and anxiety, heart disease and a myriad of other illnesses.

By contrast, according to research done at Deakin University, engaging in activities that provided a sense of purpose was strongly associated with wellbeing. It could be paid employment although in order to increase wellbeing, the employment had to provide more than just financial security. However, any activity that provided purpose tended to increase wellbeing, such as volunteering or being a part of a club like Rotary.

Knowing what we know about joy, it’s easy to see why engaging in activities which give purpose to life also increases our joy. Like having someone to love, having something to do that provides purpose usually involves committed action to our values, incorporating psychological flexibility, kindness, giving, moving, learning laughing … the list goes on.

There are several keys to ensuring that what we do is truly purposeful, and thus provides the greatest opportunity for joy to flourish

First, “It’s not about you.” This was the first sentence in Rick Warren’s phenomenally successful book, “Forty Days of Purpose”. True purpose in life goes beyond our needs and aims to fulfil the needs of others. This is a reflection of the true interdependency of the human race. We’re social creatures by design. We can survive independently, but we thrive collectively. We’re at our most successful when we’re dependent on each other and we work together. If we focus only on ourselves and our own needs, we fail to connect with others, and we miss out on the benefits of living in community.

Second, your purpose is inseparable from your values. As we’ve talked about several times in the last month, our values are integral to living a life rich in meaning and joy. Values reflect what is most important in the deepest part of ourselves that we can access. Our values provide us with direction. If our true purpose is going to enrich our lives and enhance our joy, then it will always be built on and synchronised with our deepest values. If your purpose and your values don’t align, then you need to reconsider either or both.

There are lots of other interesting and insightful explorations of purpose in the blogosphere but I don’t want to be over-prescriptive about it. Our own individual purpose in life is as unique to use as our fingerprints. So long as we commit the best of ourselves to being part of something bigger than ourselves.

Or as George Bernard Shaw wrote, “This is the true joy in life, the being used for a purpose recognized by yourself as a mighty one; the being thoroughly worn out before you are thrown on the scrap heap; the being a force of Nature instead of a feverish selfish little clod of ailments and grievances complaining that the world will not devote itself to making you happy.”

The lost art of joy – Someone to love

In 1939, a doctor at Harvard University initiated a research study into long term health and happiness. He recruited 268 physically and mentally healthy young men who were all in their second year of study at Harvard University, including one John F. Kennedy, who went on to become US President. As the story goes, as part of the recruitment process, “the men who were chosen for the study had what the team considered a ‘masculine body build’: significant muscle mass, narrow hips and broad shoulders. The study participants were asked about masturbation and their thoughts on premarital sex. They were also measured for brow ridge, moles, penis function and the hanging length of their scrotum.”

As it turns out, the hanging length of one’s scrotum isn’t a significant factor in one’s long term health and happiness.

What is important is love.

Over the last eight decades, the study has grown to include a number of control groups, wives and children. The longer the trial has gone on, the stronger the conclusions, that “Close relationships, more than money or fame, are what keep people happy throughout their lives, the study revealed. Those ties protect people from life’s discontents, help to delay mental and physical decline, and are better predictors of long and happy lives than social class, IQ, or even genes.”

The short and intense forms of love are very strongly associated with happiness. Remember the study we discussed in earlier posts from George MacKerron, who mapped the correlation of happiness to activity and location of the users of his specifically designed mobile phone app? With hundreds of thousands of data points, he was able to show that people were happy when they were exercising, when they were at the theatre, ballet, or a concert; when they were at a museum or an art exhibit; and while doing an artistic activity (like painting etc.). Though at the top of his list, the greatest number of people were at their greatest level of happiness during “sexually intimate moments” (on a date, kissing, or having sex).

Of course, love is more than just a good snog, but it demonstrates that intimate connection with another person you love, and who loves you, is an intense and intoxicating source of joy.

Other research into the relationship between love and joy shows the same thing as the Harvard Study of Adult Development. The “Very Happy People” study showed that there was a 0.7 correlation between social support and happiness, which is higher than the connection between smoking and cancer. People with one or more close friendships are more likely to be happier, and those with few social connections are more likely to be depressed than those who have more social connections. People with strong and healthy relationships are less likely to feel stressed by challenging situations. Supportive marriage is a cause of happiness.

We always need to be careful in interpreting these sorts of conclusions, remembering that correlation does not equal causation – people don’t get depressed because they have no friends. Often times there are underlying factors contributing to both a persons depression and difficulty in forming solid friendships.

What we can safely say is that happiness and love are intimately connected. The deeper the social bond, the more likely there is to be happiness.

It’s also important to remember that it’s not quantity of the social connections that’s important, but the quality of the social connections. A hundred loose associates, or deep but unequal, unreciprocated relationships are not associated with happiness. Joy comes from sincere, committed love that gives as much as it receives.

Do those themes sound familiar? They are the same sort of themes that we have discussed on other blogs in this series, the same sort of things that are common to our personal search for joy – kindness, giving, honesty and acceptance, committed action to a deeper value. When you apply the same things that bring individual joy to a relationship, they also bring joy, but to more than just yourself.

And what else better sums up love, but sharing the best things in life with another person.

If you want to foster happiness, invest in quality connections with other people by sharing those same things that bring individual joy. Be thankful, be kind, be generous and be committed and there will be more than enough joy to go around.