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.

Advertisements

Anxiety – It’s not a ‘real’ disease until it is

“I feel awful, doc”, one man said to me today. “I’m never going to call a cold ‘the flu’ again”, he said as he shivered away under three jumpers, aching and mildly delirious.

It’s the middle of winter here in Australia, and Influenza A is cutting a swathe through the community. Everyone who walks in with a stuffy nose thinks they have ‘the flu’, that is, until they actually get Influenza and they realise just how atrocious having the real flu is.

It’s the same with mental health and illness. So many people think think that anxiety or depression aren’t real diseases. They think that everyone gets a bit sad at times, or gets a bit stressed, so depression and anxiety aren’t real diseases, they’re just normal emotions, or what weak people experience because they don’t have the inner strength to cope.

Such stigma isn’t helped when people who like to think they’re experts in mental health write blogs which declare that “anxiety is a signal that we need to listen to, not an illness we need to manage. It is a reaction to life’s challenges, not a biological disease to be treated.”

Yes, that’s right people, pretend experts are quick to tell you that the debilitating condition you’re experiencing isn’t a real disease.

Saying “Anxiety isn’t a real disease, it’s just a warning sign, a normal part of life” is a bit like saying, “You don’t really have Influenza, you just have a cold. Harden up princess … you don’t need to be ventilated in ICU, it’s just a virus. I took some Vitamin C and I was better in just a couple of days. What’s wrong with you?”

Part of the problem is because of how we use the word “anxiety”, which can mean different things to different people. To a lot of people, being anxious is the same as being a little frightened. To others, it’s being really scared, but with good reason (like if you were confronted by a very venomous snake).

Medically speaking, anxiety isn’t just being frightened or stressed. After all, it’s normal to be frightened or stressed. A little bit of fear is protective. There are dangers all around us, and our brain is our “don’t get killed” organ. If we had no fear at all, we’d end up becoming road kill. A little bit of fear, in the right amount, for the right reason and in the right place and time, is actually very protective.

But to label all anxiety as normal, or to claim that anxiety is not a mental illness is obnoxious and ignorant.

That’s because anxiety at the wrong time and in the wrong amount can disrupt our day-to-day tasks and make it hard to live a rich and fulfilling life. At the extreme, anxiety disorders are as debilitating as any major illness.

There are six main disorders that come under the “anxiety disorders” umbrella, reflecting either an abnormal focus of anxiety or an abnormal intensity:
1. Panic Disorder (abnormally intense anxiety episodes)
2. Social Anxiety Disorder (abnormal anxiety of social interactions)
3. Post-traumatic Stress Disorder (abnormally intense episodes of anxiety following trauma)
4. Obsessive-Compulsive Disorder (abnormally intense and abnormally focussed anxiety resulting in compulsive behaviours)
5. Specific phobias (abnormally focussed anxiety on one particular trigger), and
6. Generalised Anxiety Disorder (abnormal anxiety of everything)

The common underlying theme of anxiety is uncertainty. Clinical psychologists Dan Grupe and Jack Nitschke from the University of Wisconsin wrote in Nature Reviews Neuroscience that “Anxiety is a future-orientated emotion, and anticipating or ‘pre-viewing’ the future induces anxiety largely because the future is intrinsically uncertain.” [1]

The fear of uncertainty that defines anxiety comes from genetic changes that affect the structure and function of the brain, primarily in the regions of the amygdala and the pre-frontal cortex. As a result of these changes, the brain processes information incorrectly.

For example:
> the brain thinks that threats are more likely and will be worse than they are,
> the brain spends more time looking for possible threats,
> the brain fails to learn what conditions are safe, which is aggravated by avoidance, and
> the brain assumes that unavoidable uncertainty is more likely to be bad than good.

It’s important to understand at this point that anxiety disorders aren’t the result of poor personal choices. They’re the result of a genetic predisposition to increased vulnerability to early life stress, and to chronic stress [2]. The other way of looking at it is that people who don’t suffer from anxiety disorders have a fully functional capacity for resilience [3,4].

The main point of this post is simply this – pretend experts are everywhere, and they are usually various combinations of ignorant, stupid or lazy. They might try and tell you that your debilitating anxiety isn’t really a mental illness, but they’re usually the ones who have never experienced just how atrocious a true anxiety disorder is. Don’t listen to them, no matter how many equally ignorant followers they have on social media. Just like Influenza can make you really sick but there is treatment, so it is with an anxiety disorder – the anxiety disorder may be much harder to get through, but with the right treatment and support, you can get through it.

~~~

If you are struggling with anxiety or depression, help … real help … is available. See your general practitioner or psychologist, or if you’re in crisis and you need to talk to someone urgently:

In Australia
> you can call either Lifeline on 13 11 14, or
> BeyondBlue provides a number of different support options
> the BeyondBlue Support Service provides advice and support via
>> telephone 24/7 (call 1300 22 4636)
>> daily web chat (between 3pm–12am) and
>> email (with a response provided within 24 hours) via their website https://www.beyondblue.org.au/about-us/contact-us.
In the US
> call the National Suicide Prevention Lifeline by calling 1-800-273-TALK (8255).
In New Zealand
> call Lifeline Aotearoa 24/7 Helpline on 0800 543 354
In the UK
> Samaritans offer a 24 hour help line, on 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

References
1. Grupe DW, Nitschke JB. Uncertainty and anticipation in anxiety: an integrated neurobiological and psychological perspective. Nature reviews Neuroscience 2013 Jul;14(7):488-501.
2. Duman EA, Canli T. Influence of life stress, 5-HTTLPR genotype, and SLC6A4 methylation on gene expression and stress response in healthy Caucasian males. Biol Mood Anxiety Disord 2015;5:2.
3. Wu G, Feder A, Cohen H, et al. Understanding resilience. Frontiers in behavioral neuroscience 2013;7:10.
4. Russo SJ, Murrough JW, Han M-H, Charney DS, Nestler EJ. Neurobiology of resilience. Nature neuroscience 2012 November;15(11):1475-84.

Dr Caroline Leaf and Zombie Chemical Imbalance Myth

Sometimes if you tell a story often enough, people forget that it’s just a story and it takes on a life of its own. It’s like a zombie … the story isn’t real but it continues to wander around eating people’s brains and it’s very hard to kill off.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. She also believes that reading a few blogs from fringe psychologists entitles her to call herself a mental health expert. She is the Christian church’s pin-up girl for the Dunning-Kruger effect.

Dr Leaf recently posted a blog on “The Chemical Imbalance Myth”. It’s a zombie. She’s posted on this before (on the 26th of October 2015 to be precise) but her blog post in 2015 was so inaccurate that she later took it down, only for it to resurface later on her website (in the section dubiously titled “Scientific FAQ”).

And like every good zombie, it’s resurfaced again. Dr Leaf hasn’t changed any of the inaccuracies that forced her to take down the original post, but instead added a couple of extra bits in, mixed it up a little and then just served it up, like a reheated bowl of rancid Christmas scraps.

I won’t go through each and every point like I did with her previous iteration of this blog, although if you want to review my more in-depth analysis of this subject, then please feel free to read my previous blog post: https://cedwardpitt.com/2015/10/26/dr-caroline-leaf-and-the-myth-of-chemical-imbalances-myth/. But I thought it was worth highlighting a couple of key things from this year’s fetid reincarnation which are so flawed that not even a B-grade science fiction writer would seriously entertain them.

THE MIND AND THE BRAIN

Dr Leaf says:

“In other words, mental ill-health is a thought disorder based in the mind, which changes the brain physiologically and is a response to the complex and multifaceted challenges of life.” This is based on her underlying assumption that the brain doesn’t control the mind, but instead the mind controls the brain.

However, she also says that “Psychotropic drugs can directly affect our health, with side effects such as an increased risk of suicide, loss of sexual ability, potential brain shrinkage, agitation, insomnia, weight gain and obesity-related diseases like diabetes, lethargy, mental fog, emotional apathy, homicide”.

This statement is really ignorant and prejudiced; psychiatric drugs don’t make people into murderers for a start.

But the most striking flaw of all is that Dr Leaf is contradicting herself. She confidently asserts that psychotropic medications and their terrible chemical imbalances have ghastly side effects on emotional and cognitive functions such as “mental fog” and “emotional apathy”. But how can that be? After all, if the brain does not control the mind as she says, then the medications affecting the brain would not have any effect on the mind.

Dr Leaf can’t have it both ways – either her entire ministry is built on a false premise (the brain really controls the mind after all) or her dire assertions about psychiatric medications are unfounded (chemical imbalances in the brain can’t cause effects on the mind).

One way or the other, Dr Leaf has a serious problem in her reasoning.

Real science has clearly demonstrated that the mind is a product of the brain. Things that alter the structure of the brain (trauma, tumours) or the function of the brain (medications like ropinirole, every day drugs like caffeine, or illicit drugs like LSD) can all cause changes in how the mind functions with resulting changes in behaviour.

If Dr Leaf isn’t able to get the basics of science right and make even the most basic cogent argument then how can she be trusted to speak to more complicated issues surrounding mental health and illness.

DR LEAF’S RESEARCH

Dr Leaf has never been one to undersell her scientific work. Accordingly, in her blog post she says:

Following a similar research path, I have also demonstrated, using my research on the power of mind-action in changing the brain, that mental disorders are primarily based in the mind …

I have researched the effectiveness of mind action techniques (which are thought-based) in overcoming the negative effects of neurological issues such as TBI, dementias, movement disorders, autism, aphasia, and learning disabilities, emotional trauma as well as various cognitive, emotional and mental health issues …

My Geodesic Learning Theory has been shown not only to be effective in mental health care, but also treating physical damage to the brain that occurs in Traumatic Brain Injury (TBI), learning disabilities and to improve learning techniques in both schools and the corporate world …

my research and experience indicated that many of these conditions were influenced by, or originated in, a disorder of the mind that was either caused by a trauma or negative thinking patterns. In other words, mental ill-health is a thought disorder based in the mind, which changes the brain physiologically and is a response to the complex and multifaceted challenges of life.

And yet the reality is that Dr Leaf only did one PhD in South Africa, and has not done any other university based research since. Her PhD did not look at “the power of mind-action in changing the brain”. In fact, her research didn’t focus on mental health or illness at all, and it certainly didn’t focus on dementias, movement disorders, autism, aphasia, and learning disabilities, emotional trauma, cognitive, emotional or mental health issues.

Her PhD was the evaluation of her Geodesic Learning Theory on a group of very normal students in a South African School. None of them had dementia. None of the other conditions were mentioned either. The overall results were likely due to chance, and in some cases, her intervention made the students grades worsen. The only other research that Dr Leaf performed was a similar intervention in come schools in Dallas, but the results were much the same as her PhD and given the unflattering results, this study was never published in a peer-reviewed journal.

Dr Leaf should know what she studied for her own research, and yet her description in her current blog post is so strikingly different from what is on the public record. So again, this begs the question – how can someone who is so wrong about her own research be trusted with any level of authority in any other subject?

PREJUDICE AGAINST MENTAL ILLNESS

For someone who claims to be an expert on mental health, Dr Leaf is extremely callous and dismissive of those people who suffer from mental illnesses. She repeatedly uses quotation marks to refer to mental illnesses, like ‘“diseases” like depression’ as if to suggest that they aren’t illnesses at all. Can you imagine if this same level of disrespect was applied to someone with a physical disability? That people in wheelchairs have the “disability” of paraplegia, for example. It’s extremely disrespectful and intolerant whether it is speaking about a physical disability or a mental illness.

The other thing which is highly inappropriate is her scare-mongering about psychiatric treatments. Psychiatric patients are not imprisoned, drugged, locked in solitary confinement and compelled to “live their days marinating in their own excrement.” I doubt whether Dr Leaf has ever set foot in a psychiatric facility. She is simply regurgitating the information fed to her by alarmist groups such as Mad In America, a group of psychologically trained rogue extremists – the Taliban of the world of psychiatry. It’s propaganda in it’s purest form, but Dr Leaf takes it at face value and repeats it no matter how inaccurate it actually is.

Dr Leaf’s criticism of modern psychiatry is breathtaking in it’s ignorance, especially in the face of published science, but what makes it more concerning is that it is internally inconsistent her own teaching, and this isn’t the first time that she’s contradicted herself.

Dr Leaf should take down this ignorant, inaccurate and intolerant post. This particular zombie myth needs to be buried once and for all.

Kintsukuroi Christmas

Have you ever opened a Christmas present to find it wasn’t quite what you expected?

I confess, I hate Secret Santa. I’ve been scarred more than once. One time a group of my friends decided it would be good to do a Secret Santa. I spend an hour or two making sure that I found a present for my secret santa that was good quality, something small but meaningful. After all, no one wants to get some dud present. In the end I bought this person a small sampler of some good quality chocolates – something discreet, tasteful and universally enjoyed.

In return, I got a tin of cat food … and not even good quality cat food, but the cheapest generic cat food from the worst supermarket chain.

Stunned, I remember stammering, “But … I don’t have a cat …” (For the record, my friends were very unsympathetic and thought it was extremely hilarious).

Another time for a workplace Secret Santa, I had to buy for one of my receptionists. Again, I thought about something that would be discreet, tasteful and universally enjoyed, and I tracked down a small gift box from the Body Shop.

In return, I got batteries, and again, not good batteries, but the cheap variety that have lost half their charge before you even take them from the packet. To rub salt into that particular wound, my secret santa revealed himself as one of the other doctors in the practice, who proudly said, “You’ve got kids, so I thought batteries would be a great present for all of the toys they’re going to get.”

Dude, I’ve got Asperger’s, and even I know that was a sucky present! So, uh, thanks?

Ever since the first Christmas more than two thousand years ago, Christmas is a time of giving gifts. In the description of the first Christmas in the Bible, the three magi (or wise men) brought the baby Jesus three gifts – gold, frankincense and myrrh. Interestingly, history suggests that these gifts were extraordinarily precious which in ancient times made them standard gifts to honour a king or deity. Gold as we know is a precious metal. Frankincense was used as perfume or incense and myrrh was used as an anointing oil. These same three items were apparently among the gifts, recorded in ancient inscriptions, that King Seleucus II Callinicus offered to the god Apollo at the temple in Miletus in 243 B.C.E.

Christmas presents have come a long way since then, and even more so in the last century. My father was born in a poor part of northern England at the end of the great depression, the youngest child of a family of ten children. He would tell me of his Christmases growing up and how his brothers and sisters looked forward to getting an apple, an orange and some nuts in their Christmas stockings. When I was a pre-teen in the 80’s, I got books and clothes, cricket gear and matchbox cars (hey, they were cool back in the day). This Christmas, all my tween and teen children want is electronic consoles (my son has his heart set on a Wii Switch). I don’t dare think what my grandchildren will be asking for at Christmas time in twenty or thirty years’ time.

Whether you get presents fit for a king or you end up with the booby prize of generic cat food, we at least expect our presents to work. No one wants a broken present after all. So imagine if when you opened your Christmas present, it was cracked, or chipped, or broken. What would you do? Would you keep it, or hope that the person who gave it to you kept the receipt?

There’s an ancient Japanese tradition that would not only keep things which were broken, in repairing them, would make them even more precious. For more than 400 years, the Japanese people have practiced kintsukuroi. Kintsukuroi (pronounced ‘kint soo koo ree’) is the art of repairing broken pottery with gold or silver lacquer, and the deep understanding that the piece is more beautiful for having been broken.

The edges of the broken fragments are coated with a glue made from Japanese lacquer resin and are bonded back into place. The joints are rubbed with an adhesive until the surface is perfectly smooth again. After drying, more lacquer is applied. This process is repeated many times, and gold dust is also applied.

In kintsukuroi, the gold lacquer accentuates the fracture lines, and the breakage is honoured as part of that piece’s history.

In the practice of kintsukuroi, we see the principle that whilst all things have the capacity to be broken, they also have the capacity for redemption.

Sometimes I feel very, very broken … hopeless, useless, like I’m just a broken present. Sometimes I wish I could be returned, but I didn’t come with a receipt and sometimes I feel like no one would want me back anyway. Sometimes I feel like I’m good for nothing but the scrapheap.

Whether it’s mental illness, family stress, financial hardship or just the daily grind wearing us down, we can all find ourselves feeling a bit broken at times.

Christmas reminds us of the gift of redemption. Jesus’ life was one of fixing that which was broken, of giving people a second chance. The gospels tell story after story of how Jesus helped people back on to their feet; forgiving, healing and restoring hope. Even his life before his ministry was that of a carpenter, creating new things and fixing that which was broken.

It’s easy to feel broken in this broken world, but remember, whilst all things have the capacity to be broken, they also have the capacity for redemption. No one is beyond repair. Like objects fixed with kintsukuroi, being broken isn’t the end, but we can become even better – more beautiful and more honoured for having been broken.

I hope that this Christmas, you can find hope and redemption, and that you get some good gifts worthy of a king, not worthy of a cat.

Merry Christmas and Happy New Year to everyone. See you in 2019.

The Conundrum of Developmental Dysplasia of the Hip

I know I’m old.

I know I’m old because the bits of me that used to be supple and strong are now weak and stiff, and the bits of me that used to be stiff are now flaccid.

I also know I’m old because I’m now regaling medical students with stories, usually starting with the words, “Back in my day …”

Back in my day, we didn’t have the internet and had to to go to the library to get actual books!

Back in my day, we couldn’t go on-line, we had to stand in lines …

Back in my day, we were taught about congenital dysplasia of the hip, and learning the nuances of the Barlow and Ortolani manoeuvres was one of the most important skills a young paediatric house officer could possess.

While age has made me go soft and stiff in all the wrong places, it does give the benefit of hindsight.  And with hindsight and further research, it turns out that my view of Congenital Hip Dysplasia was all wrong.

It’s not that hip dysplasia isn’t really important – it is.  A child with moderate to severe hip dysplasia is destined for a lot of physio and possibly surgery to try and help them walk and run and play normally.

It’s more that congenital dysplasia of the hip isn’t necessarily congenital, and the tests we were taught to perform to diagnose it really aren’t that helpful after all.

Developmental dysplasia of the hip (DDH), as explained in layman’s terms on the Kids Health Info website, is “an abnormal development of the hip joint. In children with DDH, the ball at the top of the thigh bone (called the head of the femur bone) is not stable within the socket (called the acetabulum). The ligaments of the hip joint that hold it together may also be loose. Sometimes, the hips can dislocate early in life and this may not be noticed until your child starts to walk.”[1]

More formally, the condition and its definition are more nuanced.  As per eMedicine: “The definition of DDH is not universally agreed upon. Typically, the term DDH is used in referring to patients who are born with dislocation or instability of the hip, which may then result in hip dysplasia. More broadly, DDH may be defined simply as abnormal growth of the hip … This condition may occur at any time, from conception to skeletal maturity.”[2]

Although there are some inconsistencies in the literature regarding incidence of DDH, it is generally accepted that approximately 1 in 100 infants will be identified as having some hip instability at birth, and 1 – 2 in 1000 infants will be born with a dislocated hip.[3]

There are a number of generally accepted risk factors associated with developmental dysplasia of the hip[4](although their validity is controversial[5]):

  • Breech Presentation
  • Family History of developmental dysplasia of the hip (especially if in parent or sibling)
  • Female Baby (developmental dysplasia of the hip is four times more likely to occur in a female infant)
  • Large Baby > 4kg
  • Overdue > 42 weeks
  • Oligohydramnios
  • Associated with Plagiocephaly, Torticollis and foot deformities
  • First born baby or multiple pregnancies

Of these risk factors, the most significant are breech presentation and family history[6].

Traditionally, all newborns are screened for DDH a number of times throughout their first year of life using the Barlow and Ortolani manoeuvres.

In the Barlow manoeuvre, “gentle backward pressure is applied to the head of each femur in turn, and a subluxable hip is suspected on the basis of palpable partial or complete displacement”.

In the Ortolani manoeuvre: “the examiner applies gentle forward pressure to each femoral head in turn, in an attempt to move a posteriorly dislocated femoral head forwards into the acetabulum. Palpable movement suggests that the hip is dislocated or subluxed, but reducible.”[7]

In older infants, the Galeazzi test may be performed: “Hips are flexed to 90° and placed in neutral adduction/abduction, with knees in flexion. In this position, the vertical level of the knees can be assessed for asymmetry.”[8]

Limited hip abduction is also a test used to attempt to elicit developmental dysplasia of the hip[9].  Asymmetrical gluteal and thigh skinfolds have also been considered signs of developmental dysplasia of the hip[10].  (A video demonstrating Barlow, Ortolani and Galeazzi signs is here: https://youtu.be/iKfoovi5gvI)

All this is well and good, but the effectiveness of clinical hip screening programmes internationally have been disputed in the published literature[11].  The U.S. Preventive Services Task Force gives screening for developmental dysplasia of the hip an “I” rating (insufficient evidence to recommend for or against screening) while the American Academy of Family Physicians endorses this “I” rating[12].  This is partly because the tests and manoeuvres for developmental dysplasia of the hip have very limited capacity to correctly detect a positive finding, and/or have a limited impact on significant clinical outcomes.

For example, the Ortolani test has a sensitivity[13]of 0.6 and the Barlow manoeuvre has a positive predictive value of just 0.22[14].  The Barlow and Ortolani manoeuvres fail “to identify two thirds of the hips which subsequently need surgical treatment and has made little or no difference to the number coming to surgery.”[15]

Hip abduction “is a relatively insensitive and nonspecific marker of DDH in early infancy but becomes more accurate after 3 to 6 months of age and with more severely affected hips.”[16]  Also, “physical examination findings sometimes linked to DDH include asymmetrical gluteal and thigh skinfolds, and leg-length discrepancy. No studies from the past 40 years were identified that assessed the value of these findings in diagnosing DDH.”[17]

So if clinical screening is next to useless, what about universal screening for DDH with ultrasound? Well, a Cochrane review showed that universal ultrasonography (versus clinical examination alone) resulted in a higher rate of detected developmental dysplasia of the hip and a higher rate of treatment, but it did not reduce the rate of missed (late-diagnosed) developmental dysplasia of the hip or the need for surgery.[18]

Why?  I’m not going to pretend to be an expert, but I think the key is that DDH isn’t fixed and stable, but is actually a dynamic condition in which the hip abnormality may improve or deteriorate with growth[19].  Paton wrote, “The term Congenital Dislocation of the Hip (CDH) was superseded by the new name of Developmental Dislocation of the Hip (DDH) in 1989. This was in recognition of the fact that not all cases of pathological hip conditions associated with DDH were present at birth.”

So, to screen or not to screen?  A generally accepted view is that screening with physical examination, compared with no screening or universal ultrasonography screening, would result in fewer adults having osteoarthritis of the hip at 60 years of age.[20] However, there is no published statistical difference in outcome measures of developmental dysplasia of the hip when comparing the various combinations of screening utilising clinical examination and ultrasonography.[21]

What does it mean medico-legally?  Some commentators believe it’s a very important point. Paton again, “If some hip joint conditions that are stable at birth deteriorate and are diagnosed at a later date as an irreducible hip dislocation, they cannot be considered to be ‘missed’ cases following negative neonatal clinical hip screening by a competent screener.”[22]

Lomax writes, “Medico-legally, if a clinical screening test is undertaken by an individual who has been properly trained and assessed as competent in the clinical test and a late irreducible dislocation occurs, this should not be considered negligent due to the poor sensitivity and positive predictive value of the tests.”[23]

For mine, I think the key is to remain vigilant.  It may not make a massive difference to the eventual outcome, but given that Barlow, Ortolani and Galeazzi tests are easy to learn and very cheap to do, I think we should continue to perform them.  Having said that, we should remain vigilant and not ignore an infant who has limited hip abduction or a limp at any age.

I think that’s sage advice no matter how young or old you are!

Summary points:

  • Developmental dysplasia of the hip refers to patients who are born with dislocation or instability of the hip or more broadly as an abnormal growth of the hip
  • DDH is a dynamic condition which may occur at any time from conception to skeletal maturity
  • The most significant risk factors for DDH are breech presentation and family history
  • The most common tests for diagnosis of DDH are Barlow, Ortolani and Galeazzi signs
  • However, the tests and manoeuvres for developmental dysplasia of the hip have very limited capacity to correctly detect a positive finding, and/or have a limited impact on significant clinical outcomes
  • Universal ultrasonography resulted in a higher rate of detection and reatment, but no reduction in missed (late-diagnosed) DDH or surgery
  • Consensus is that screening with physical examination, compared with no screening or universal ultrasonography screening, would result in fewer adults having osteoarthritis of the hip at 60 years of age.
  • However, there’s no published statistical difference in outcome measures of DDH comparing various combinations of screening utilising clinical examination and ultrasonography.

References

[1]Kids Health Info, “Developmental dysplasia of the hip (DDH)” Royal Children’s Hospital, Melbourne, 2018. https://www.rch.org.au/kidsinfo/fact_sheets/Developmental_dysplasia_of_the_hip_DDH_treatment_and_hospital_stay/ (Accessed 12/4/2018)

[2]eMedicine, “Background / Developmental Dysplasia of the Hip” https://emedicine.medscape.com/article/1248135-overview Updated: Feb 26, 2018 Accessed: 12 Apr 2018

[3]”Screening, Assessment and Management of Developmental Dysplasia of the Hip. Clinical Practice Guideline: Resource Manual 5/05/2011″ Hunter New England Local Health District – Children, Young People & Families, NSW Health http://www.hnekidshealth.nsw.gov.au/client_images/1287736.pdf Accessed 12/4/2018

[4]ibid

[5]Paton RW. Screening in Developmental Dysplasia of the Hip (DDH). Surgeon 2017 Oct;15(5):290-96.

[6]”Screening, Assessment and Management of Developmental Dysplasia of the Hip”, 2011.

[7]Payne, J. “Developmental Dysplasia of the Hip” Patient https://patient.info/doctor/developmental-dysplasia-of-the-hip-pro Updated: 23 Sep 2016 Accessed 12/4/2018

[8]”Screening, Assessment and Management of Developmental Dysplasia of the Hip”, 2011.

[9]ibid

[10]Shipman SA, Helfand M, Moyer VA, Yawn BP. Screening for developmental dysplasia of the hip: a systematic literature review for the US Preventive Services Task Force. Pediatrics 2006 Mar;117(3):e557-76

[11]Paton RW. Screening in Developmental Dysplasia of the Hip (DDH). Surgeon 2017 Oct;15(5):290-96.

[12]Jackson JC, Runge MM, Nye NS. Common questions about developmental dysplasia of the hip. Am Fam Physician 2014 Dec 15;90(12):843-50

[13]Sensitivity is the probability of being test positive when the condition is present, or the ability of a test to correctly classify an individual as ′diseased′.  The positive predictive value is the percentage of patients with a positive test who actually have the disease ~ Parikh R, Mathai A, Parikh S, Chandra Sekhar G, Thomas R. Understanding and using sensitivity, specificity and predictive values. Indian J Ophthalmol 2008 Jan-Feb;56(1):45-50

[14]Paton, 2017

[15]Robinson R. Effective screening in child health. BMJ: British Medical Journal 1998;316(7124):1.

[16]Shipman et al, 2006

[17]ibid

[18]Shorter D, Hong T, Osborn DA. Cochrane Review: Screening programmes for developmental dysplasia of the hip in newborn infants. Evid Based Child Health 2013 Jan;8(1):11-54.

[19]Paton, 2017

[20]Jackson et al, 2014

[21]Paton, 2017

[22]ibid

[23]Lomax A. Examination of the newborn: an evidence-based guide (2ndEd). John Wiley & Sons; 2015 Aug 17: p146

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.

Fake science is no joke

Happy Easter everyone.

I went to church this morning, and came home to get a lamb ragu going in the slow cooker, and thought I would just hop onto Facebook to see what was going on in the world. I was greeted with this:

“Your body literally treats negative thoughts like an infection.” Dr Peter Amuaquarshie

Oh dear … oh dear, oh dear, oh dear …

Easter is meant to be about redemption, about hope, about God’s great love for us. Clearly #TheDrLeafShow isn’t any of that.

Unfortunately, this is more pseudoscience from Dr Leaf and her cabal.  And while it might also be April Fools Day, fake science is no joke.

Dr Peter Amua-Quarshie has been in cahoots with Dr Leaf since the beginning of her teaching. He has supplied most of the illustrations for Dr Leaf’s ministry over the years, so I’m sure he’s profiting handsomely from Dr Leaf’s enormous sales and influence.

It’s so sad to see academics trade their integrity and sell their soul for the sake of the ill-gotten gains of popular pseudoscience.

Your body doesn’t “literally” treat negative thoughts like an infection. Our thoughts have literally no bearing on our immune function. In research work that has intentionally studied thought separately to stress, thought has not been associated with any significant changes in stress or health behaviour [1]. It’s also been confirmed that thought alone does not lead to detrimental biological changes, such as significant changes in immune function [2].

If anything, it’s the other way around – our immune system and our thoughts respond to physical changes in our bodies internal milieu. For example, an adrenaline surge causes us to feel fear and engage in fight or flight behaviours, and to respond quickly to injury, the balance of our immune system’s cells and cytokines changes to prepare for possible injury.

Another example, a physical infection from a microbe of some kind (bacterial or virus) causes a flood of chemical mediators called cytokines to float around the blood stream. This inflammatory response leads to an immune system that is better able to fight off infection, but it also changes our feelings and our thoughts – this flood of cytokines is the reason why we feel tired, achey and miserable when we’re sick.

Having “negative thoughts” is not the same as having an infection. Infections are disease states, whereas “negative thoughts” are normal and more often than not, beneficial. It’s normal to feel sad. It’s normal to feel angry. It’s normal to feel disgusted or embarrassed. These feelings are adaptive. Without them, we wouldn’t grow or change. Without them, we couldn’t have a rich, full life.

Dr Leaf claims that her goal is to “equip and empower you to use your mind to overcome labels and mental ill health (depression, anxiety, etc) to live a more fulfilled and successful life.” It’s a bit hard to do that by promoting fake science.

For his part, Amua-Quarshie should know better. He’s a teaching academic by trade and has a medical degree from the University of Ghana, after all. Unfortunately, it appears that Dr Amua-Quarshie has been exiled from mainstream academia, leaving a full-time position as an Adjunct Professor (lecturer) at the University of Wisconsin-Stout in Menomonie, Wisconsin and is now working as a lecturer in a school for chiropractors (Parker University, Dallas, Texas).

Though that’s more of an aside. The bottom line here is that Dr Leaf might claim that she wants people to overcome ‘labels and mental ill health’ but she isn’t going to do that by promoting such obvious mistruths that mislead people into fearing normal, adaptive human emotions. She isn’t promoting a more fulfilled and successful life, she’s promoting imbalance. She’s promoting false hope.

I know it’s April Fools, but believe me, this is no joke.  Fake science is misleading and harmful.  If Dr Leaf really wants people to live a more fulfilled and successful life, she should refrain from using it.

References
1. Doom, J.R. and Haeffel, G.J., Teasing apart the effects of cognition, stress, and depression on health. Am J Health Behav, 2013. 37(5): 610-9 doi: 10.5993/AJHB.37.5.4
2. Segerstrom, S.C. and Miller, G.E., Psychological stress and the human immune system: a meta-analytic study of 30 years of inquiry. Psychol Bull, 2004. 130(4): 601-30 doi: 10.1037/0033-2909.130.4.601