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

Posted on July 21, 2019 by cedwardpitt

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

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.

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.

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.

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].

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?

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.

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.

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.

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 connections, which 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.

The lost art of joy – Move!

Posted on December 17, 2017 by cedwardpitt

What’s your vision of bliss? Massage? Sitting by the beach with a pina colada? Enjoying a sumptuous dinner with friends?

Most relaxation fantasies don’t involve sweat.

So it’s almost a bit counter-intuitive that exercise is one of the most frequently associated habits of happy people. Although maybe it’s not so counter-intuitive, as there is strong anecdotal evidence of the “runner’s high” – the feeling of euphoria that some people feel after a session of vigorous exercise, the “endorphin buzz” that ironically doesn’t have anything to do with endorphins!

Endorphin buzz or no, exercise is certainly one way of enhancing the joy in your life. I previously wrote about the work of George MacKerron from the University of Sussex, who used an app he created to map the correlation of happiness to activity and location. Using the hundreds of thousands of data points from the tens of thousands of users, he found that the times that people recorded the highest levels of happiness and life satisfaction were during sexually intimate moments (on a date, kissing, or having sex). Number two was during exercise.

Physical fitness is good for us. I’ve never seen a study that shows exercise to be a bad thing. Ultimately, it’s not how fat you are that’s important for your longevity, it’s how fit you are, and the way to get fit is to exercise. Physical exercise isn’t just good for the body but good for the brain as well. While the exact pathways are still being determined, there’s good evidence that moderate regular physical activity improves the balance of pro- and anti-inflammatory mediators in the body and in the brain. In the brain, this improves the overall function of our brain cells. Exercise is also thought to increase the production of a growth factor called BDNF which helps the brain cells grow new branches and improves their ability to form new pathways, which in turn, has been shown to improve mood disorders like anxiety and depression.

Exercise is great, but not everyone is ready to suddenly get up and run a half-marathon, me included. These days, I’m like a walrus on tranquillisers. I’m certainly not about to jump up and go for a jog. Some people have physical injuries or conditions that limit their capacity for physical exercise.

So how do you find the balance between maximising the joy-enhancing effects of exercise while not pushing yourself so far and causing yourself some unhappiness?

Simply, move more.

Where are you at with you’re level of exercise right now? If you could turn it into a scale from 1 to 10 (where 1 is completely sedentary, and 10 is your ideal version of regular exercise), what would you rate? The next question is, what’s one thing you could do to go one point closer to 10? So let’s just say that you walk 200m from your house to the bus stop in the morning, and the same on the way home at night. For you, that might be a 3/10. What else could you do to make that 3 turn into a 4?

You don’t have to go for vigorous two-hour walks or run up every set of stairs you come across to be happy. Just move, and move that little bit more. That will help build joy in your life.

The lost art of joy – Beauty

Posted on December 15, 2017 by cedwardpitt

Cottesloe Beach, Western Australia, at sunset

I like to flirt with photography.

There’s a particular ambience about taking photos, especially landscape photography, at either dawn or dusk. The softer light, the interplay of shadows, all make the end of the day a great time to wander around and take some photographs. I’ve always lived on the east coast of Australia, so I don’t ever get to see the sunset over the ocean, but late last year I was at a conference in Perth, Western Australia, so I thought I would seize the moment. I analysed the weather forecasts, and on the only sunny day of my trip, I skipped the afternoon workshops and went to Cottesloe Beach. There, I sat in front of the Indiana Tea House, the chill of the icy gale creating a stunning contrast to the majesty of the sun dipping into the sea, then the pink and orange glow fading beyond the expansive horizon.

It was a moment of profound beauty, a moment of aesthetic richness in the vast tapestry of the earth’s natural grandeur.

I remember that moment as one of joy. I was cold, and I was tired and I was hungry, but those aren’t the feelings that I’ve tagged to my memory of that event. The joy of beauty trumped my usual hangriness.

That bond between beauty and joy has been confirmed in broader studies. George MacKerron, now a lecturer at the University of Sussex, used an app he created to map the correlation of happiness to activity and location. He has tens of thousands of users and hundreds of thousands of data points. The times that people recorded the highest levels of happiness and life satisfaction were during sexually intimate moments (on a date, kissing, or having sex) and during exercise. The next three types of moments where people recorded the highest levels of happiness were all related to beauty: when at the theater, ballet, or a concert; at a museum or an art exhibit; and while doing an artistic activity (e.g. painting, fiction writing, sewing).

But what about beauty links it to happiness?

I think it’s a complex answer to a simple question.

Some people believe that physical beauty, especially of people, is related to happiness of those people. The more beautiful you are, the happier you are. That might seem true, but like beauty itself, the assumption is superficial.

Beauty is not specifically related to the usual markers of happiness (colloquially known as the “Big Seven”: wealth, family relationships, career, friends, health, freedom, and personal values). It’s not something that meets our material needs or aspirations. So the observation that beauty is associated with joy means there must be something deeper to it.

Stendhal, a French writer in the 18th century, wrote, “Beauty is the promise of happiness.”

I think that’s closer to the money.

It may be that our appreciation of beauty is because it is able to encourage the feelings we associate with happiness: calmness, connection (to history or to the divine), wealth, reflection, appreciation, hope.

Beauty offers a portal directly to our emotions. It transcends conscious thought and speaks directly to our soul. It communicates in a language that can never be described in just words.

I travelled from one side of Australia to the other but you don’t have to travel 5,000 kilometres to experience beauty. Beauty is usually all around us, but so often we aren’t paying attention. Mindfulness, being in the present moment, paying attention to what’s around you, can help you unlock the beauty that’s all around you, if you take the time to appreciate it.

See if you can experience something beautiful in your every day life, and unlock the joy it contains.

Dr Caroline Leaf on Drugs

Posted on March 22, 2017 by cedwardpitt

We all have a drug problem.

Well, we do according to communication pathologist and self-titled cognitive neuroscientist-come-health guru, Dr Caroline Leaf. She’s pretty chirpy for a woman with essentially no health credentials. She did a PhD two decades ago on a specialized area of educational psychology, but she has no medical training or experience. Essentially she is the Christian equivalent of the health and relationships section of a tabloid newspaper. Her information lurches between unfounded and the bleeding obvious.

Today’s e-mail newsletter, “Mental Health News March 2017” is a mixture of both. It’s more moderate than usual in its tone, but it’s still inspired by her open rejection of pharmaceuticals, especially medications for mental health which she has railed against many times.

Her second paragraph is a specific case in point. “Although many medications have saved lives and can help us, we cannot have a quick-fix-pop-a-pill mentality for everything in life, and we should not denigrate alternative methods of health and healing, such as diet, exercise, human relationship, love, compassion and therapy, particularly when it comes to mental health.”

She’s right – we shouldn’t have a quick-fix-pop-a-pill mentality, but she overstates her case. Most people don’t want pills for everything – people want good care and good treatment. Sometimes that involves a pill, sometimes it just involves reassurance. This is bread and butter for any good GP, and I’d love to show Dr Leaf what the front-line of medicine looks like if she ever wanted to see (seriously, the offer’s open).

And who’s denigrating diet and exercise? Diet and exercise aren’t “alternative” health, they’re mainstream. Is Dr Leaf so out of touch that she can’t see this?

Her bias against pharmaceuticals is more obvious in their third paragraph. Pharmaceutical medications are not a major cause of death. According to the Centre of Disease Control, the top ten causes of death in the US are:

* Heart disease
* Cancer (malignant neoplasms)
* Chronic lower respiratory disease
* Accidents (unintentional injuries)
* Stroke (cerebrovascular diseases)
* Alzheimer’s disease
* Diabetes
* Influenza and pneumonia
* Kidney disease (nephritis, nephrotic syndrome, and nephrosis)
* Suicide

Notice how medications do not feature on that list. Dr Leaf is so biased against medications that she is willing to ignore official government data in favour of her own bias.

But the truth is, pharmaceutical grade medications have revolutionised our lives. When used in the right way, for the right people, they improve our quality and quantity of life. They give people independence. They give people choice. They help people work, spend time with their family and care for others where that may not have been possible otherwise.

Do medications have side effects? Can people feel worse sometimes while taking them? Of course! We need to be realistic. Pharmaceutical medications are powerful agents and we have to use them respectfully. Prescription drugs are like power tools. In the right hands they can do wonders, but they can also be very dangerous when used incorrectly. But while medications can be used incorrectly, using that as a reason why we should use less drugs is like arguing that we should use less knives because sometimes they cut people, or that we should drive less cars because there are car accidents.

Oh, and what was that about the widespread manipulation of data and results in the world of science? Dr Leaf would never misrepresent the results of her studies, or misrepresent the results of other people’s research, in order to make her products look better than they are?

Lifestyle is important, and in some cases, lifestyle is more important than medication, but there is much more nuance involved. You need different tools for different jobs. Imagine a surgeon going into surgery and the scrub nurse passed over a nerf scalpel. It wouldn’t be particularly helpful would it. Or what if the scrub nurse passed over a butter knife? The surgeon might get the job done but with great difficulty, without the precision needed.

What a surgeon needs to perform surgery is an extremely sharp stainless steel scalpel blade. It is more effective and more precise. It might occasionally do some unintentional harm, but it will be a lot more effective than a butter knife (and a nerf scalpel!)

There are three different levels of treatment in health – “alternative” medicines, lifestyle treatments, and pharmaceuticals. “Alternative” medicines are, by definition, useless. As comedian Tim Minchin says, “Do you know what they call alternative medicine that’s been proven to work? Medicine.” Alternative medicines are probably not going to cause a lot of harm other than making their user poorer for wasting their time, but they’re highly unlikely to do any good.

Lifestyle treatments are the equivalent of the butter knife. They work, but their effect is non-specific and cumulative. Hear me right, “non-specific and cumulative” is not code for “ineffective”. Exercise is one of the most effective non-pharmacological health strategies with clearly proven benefits, but like all lifestyle changes, the effect is fairly general, and the benefit accumulates.

And sometimes, despite doing everything right, people still get sick, and this is where pharmaceuticals have their place. They are like the scalpel – they might have some unwanted effects, but in the right hands, when used correctly, they make a specific and tangible difference to a person’s life and health.

Dr Leaf then goes on to assert that “Changing your lifestyle and, significantly, the way you THINK can have dramatic effects on your health”. That’s a furphy. Thoughts make no difference to our health (I’ve shown how little difference thought makes to our health in my review of Dr Leaf’s book “Think and Eat Yourself Smart”). Some scientists may have recommended produce over Prozac, but that doesn’t mean to say they’re right.

And Dr Leaf has trotted out the same worn, tired old factoid about loving and serving others that I’ve shown to be inaccurate as well.

If you want to improve your health without medications, then start walking. Eat vegetables. Drink water. Don’t waste your time and money buying into Dr Leaf’s inaccurate teaching.

Dr Caroline Leaf and osteoporosis – Brittle facts on brittle bones

Posted on February 23, 2017 by cedwardpitt

In the fifteenth chapter of his gospel account, Matthew described a conversation that Jesus had with his disciples. Jesus had just reprimanded the Pharisees for their hypocrisy, and the disciples came back to Jesus to report that the Pharisees weren’t very happy about it.

“Then the disciples came to him and asked, ‘Do you know that the Pharisees were offended when they heard this?’ He replied, ‘Every plant that my heavenly Father has not planted will be pulled up by the roots. Leave them; they are blind guides. If the blind lead the blind, both will fall into a pit.’” (Matthew 15:12-14)

When it comes to many subjects, Dr Leaf is a blind guide. Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. She’s not a medical doctor – her title is academic, an award for her PhD in communication pathology over twenty years ago. She has no medical training whatsoever, which makes it a little offensive when she feels she’s qualified to lecture people about medical conditions like osteoporosis.

In an episode of her TV show broadcast this week, Dr Leaf offered a B-grade attempt at mimicking Dr Oz by trying to use her biased ideology to explain a serious medical condition, and in so doing, gave a performance laden with droll irony, a example of the Dunning-Kruger effect in its purest form.

Her co-host was Dr Avery M. Jackson III, a neurosurgeon in Michigan, who Google confuses with Dr Jackson Avery of Grey Sloan Memorial Hospital fame. Dr Jackson has an impressive bio which is replete with advanced work on osteoporotic crush fractures of the spine. One wonders why a specialist of such high regard would associate himself with a scientific philistine who doesn’t understand how genes work, and who regularly contradicts her own position.

Or why he would allow Dr Leaf to publicly associate him with claims like:
“Osteoporosis can be caused by bad thinking and bad eating”,
“Not only is it considered a silent epidemic, but (osteoporosis) has its roots in mind and lifestyle choices”, and
“much can be done on a preventative level like diet and starting young with lifestyle choices and the way we use our minds. Mind is involved in everything!”

Actually, the biggest contributors to the risk of osteoporosis are genetics, ageing and the loss of gonadal function (menopause or low testicular function). Which of these are controlled by the mind, Dr Leaf? It’s not that lifestyle has no influence on osteoporosis, but Dr Leaf overstates the case.

If you want some useful advice on osteoporosis, I’d encourage you to get your information from reputable experts, not wannabe experts like Dr Leaf. To reduce your risk of developing osteoporosis, Osteoporosis Australia recommends
* 3-5 serves of calcium rich food daily
* adequate sunlight
* regular weight bearing exercise
(you can get more specific information here: http://www.osteoporosis.org.au/prevention. For medical advice tailored to your circumstances, see your GP or physician)

Dr Leaf needs to move on from her unscientific premise that the mind is in control of everything. It’s patently false, and it terminally biases nearly everything she says. She needs to open her scientific eyes rather than staying blind to the truth.

Dr Caroline Leaf – Rogue Notion

Posted on February 12, 2016 by cedwardpitt

According to a new study by Rutgers University, “Learning new cognitive skills can help reduce overwhelming negative thoughts”. So said Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist. She also advised that “Intentionally bringing those rogue thoughts under control is essential to mind health! And learn something new every day – develop your mind!”

So … negative thoughts are what, like an evil spy organisation, running around causing wanton destruction, overwhelming your capacity to function?

If that’s the case, then new cognitive skills must be like Tom Cruise, running, jumping, shooting and kicking their way through the negative thoughts, saving the world and getting the girl.

It’s a popular concept. As I discussed in my previous post, the power of positive thinking is culturally sanctioned Western folk psychology. We implicitly accept the idea that we have to harness positive thoughts and stop negative thoughts if we’re to overcome life’s obstacles.

However, the only rogue notions here are Dr Leaf’s.

Dr Leaf’s post sounds authoritative and sciency, but is nothing else. It’s vague, and with a bit of deeper palpation, it’s actually wrong.

Dr Leaf has gone back to her bad habit of obfuscating her references, maybe because she’s getting lost in her own hubris, or more likely, it’s much easier for her audience to see that she’s just cut-and-pasted the opening by-line of a press release again if she actually disclosed her source.

In fact, the article is about a study from Rutgers which studied two behavioural interventions (not cognitive ones), a form of mindfulness meditation and aerobic exercise. The original publication is in the journal Translational Psychiatry [1], if you want to check it out for yourself. This article isn’t about learning cognitive skills at all. Exercise and mindfulness meditation are tried and true behavioural methods of improving mood disorders like depression, which the authors combined to assess the benefit or otherwise. Neither intervention involved challenging or fighting thoughts, or suppressing ‘negative’ thoughts, or “intentionally bringing those rogue thoughts under control”.

Indeed, the mindfulness meditation used involves “the practice of attending to the present moment and allowing thoughts and emotions to pass without judgment.” [1] Mindfulness doesn’t try to control anything. Rather than supporting Dr Leaf’s declaration that intentionally bringing thoughts under control is essential to mind health, this study contradicts it.

Cutting and pasting doesn’t make you an expert. It’s easy to take a sciency-sounding tag line and put it in a pretty little graphic. Everyone does it. 90% of Instagram and Facebook posts these days are faux-authoritative pseudo-science memes that aren’t worth the bytes they’re made of.

Junk science is like junk food. If that’s all you consume, then you eventually become an intellectual blob of lard, stuffed full of mistruths and logical fallacies, and incapable of understanding scientific truth for yourself. Dr Leaf’s audience deserves better than junk science and it’s about time that Dr Leaf stopped pretending to be an expert, and started acting like one.

Reference

[1] Alderman BL, Olson RL, Brush CJ, Shors TJ. MAP training: combining meditation and aerobic exercise reduces depression and rumination while enhancing synchronized brain activity. Transl Psychiatry 2016;6:e726.

The Prospering Soul – Christians and Depression Part 2

Posted on October 11, 2015 by cedwardpitt

For most church-goers, putting the terms “Christian” and “depression” in the same sentence just doesn’t seem natural. In part 1, we looked at what depression is and why depression affects a lot more of the church than the church is aware of.

In this instalment, we’ll look at some general ways to handle depression, and what the Bible says about being depressed.

In the first blog, I explained how I understood depression as the end result of the brains capacity to deal with the demands of life. Too many demands or not enough resources overwhelms the brain and low mood is the end result.

So how do you manage depression? Well, if the system is failing because of increased demand or decreased capacity to cope, then it’s logical to manage depression by decreasing demand and increasing capacity to cope.

We can increase our capacity to cope by increasing our brains capacity to grow new nerve branches, and to make the cells more efficient at doing their job.

Increasing the growth of new nerve cell branches (in science speak – ‘synaptogenesis’) involves increasing the growth factors. BDNF has been proven to be increased by anti-depressant medications [1, 2] and by exercise [3, 4]. There may be some evidence that diet might improve depression in a similar way although the evidence is weak [5], so we should take that with a grain of salt.

The next way of managing depression is to increase the capacity to cope. The way we do that is through psychological therapies. There are several styles of psychological therapies, too many for me to discuss them all here. In the real world, most psychologists use a mix of a number of techniques that they tailor to the needs of their patient. I’m going to quickly outline the two most commonly used therapies.

Cognitive Behavioural Therapy, or CBT for short, is “based on the theory that emotional problems result from distorted attitudes and ways of thinking that can be corrected. The aim is to treat difficulties by problem solving, finding better strategies for coping, and overcoming irrational fears.” [6] Essentially it’s the combination of two different therapies, Cognitive therapy, and Behavioural therapy. Cognitive therapy, as the name suggests, assumes that people have mental health problems because of patterns of irrational thinking. Behavioural therapy is quite broad, but looks to challenge the thinking patterns with action (for example: gradual exposure to something a person is afraid of).

CBT is the most well researched form of psychotherapy, and has a lot of evidence for it’s effectiveness [7]. Though there is good evidence that it’s the behavioural arm that gives it any clout [8, 9]. Trying to change your mental health just by trying to change your thoughts is generally ineffective.

In the last couple of decades, a new wave of psychological therapies has emerged from this idea that Cognitive Behavioural Therapy is just Behavioural Therapy with bling. The most notable is Acceptance and Commitment Therapy, or ACT for short. ACT is different to CBT in that ACT doesn’t rely on the idea of changing thoughts, but on simply accepting them. ACT “is a psychological therapy that teaches mindfulness (‘paying attention in a particular way: on purpose, in the present moment, non-judgementally’) and acceptance (openness, willingness to sustain contact) skills for responding to uncontrollable experiences and thereby increased enactment of personal values.” [10]

According to ACT, you don’t have to change your thoughts, because thoughts aren’t that powerful to begin with – they’re just words. Sometimes they’re true, and sometimes they’re helpful, but if we spent all of our time trying to fight them, we miss out on experiencing the joy in the present moment, and we can lose sight of the values that guide us into our future fulfilment.

The common link between good psychotherapy is that their therapeutic effect comes from improving skills in different areas that the patient lacks. That is, psychological therapies increase the capacity of the patient to cope with things that would have otherwise wouldn’t have handled well and would have caused distress.

The last way to manage depression is to limit the excessive demands that have been placed on the system in the first place, or in other words, reduce the unnecessary stressors. People who are depressed tend to be bad at this, but there are a few basic skills that are common to all stress management techniques that can form the platform of ongoing better skills in this area. The full list will be a blog for another time, but the simplest technique is to breathe!

It’s really simple. Sit in a comfortable position. Take slow, deep breaths, right to the bottom of your lungs and expanding your chest forward through the central “heart” area. Count to five as you breathe in (five seconds, not one to five as quickly as possible) and then count to five as you breathe out. Keep doing this, slowly, deeply and rhythmically, in and out. Pretty simple! This will help to improve the efficiency of your heart and lungs, and reduce your stress levels.

Remember, B.R.E.A.T.H.E. = Breathe Rhythmically Evenly And Through the Heart Everyday.

To recap, there are three main ways to manage depression – increase the brains ability to process the incoming information, increase the capacity to cope, and decrease the amount of stress that our brains have to process.

The fourth way to help manage depression is prayer. There is limited scientific information on the effects of prayer on depression, although a small randomised controlled trial did show that prayer with a prayer counsellor over a period of a number of weeks was more effective than no treatment [11]. But the Bible encourages us, “Do not be anxious about anything, but in every situation, by prayer and petition, with thanksgiving, present your requests to God. And the peace of God, which transcends all understanding, will guard your hearts and your minds in Christ Jesus.” (Philippians 4:6-7)

And Jesus himself called to those heavy in heart, “Come to me, all you who are weary and burdened, and I will give you rest. Take my yoke upon you and learn from me, for I am gentle and humble in heart, and you will find rest for your souls. For my yoke is easy and my burden is light.” (Matthew 11:28-30)

One final thought. It’s sometimes hard to understand how strong Christians can become depressed in the first place. After all, the Bible says that the fruit of the Spirit is joy (Galatians 5:22). 1 Peter 1:8 seems to suggest that every Christian should be “filled with an inexpressible and glorious joy.”

So when you’re filled with the opposite, it makes you feel like a faithless failure, and Christians without depression assume a similar thing for Christians they know who are suffering from depression. It’s the logical conclusion to draw after all – if the fruit of the Spirit is joy, and you are not filled with joy, then you mustn’t be full of the Spirit.

But when you look through the greatest heroes in the Bible, you see a pattern where at one point or another in their lives, they went through physical and emotional destitution. Sure, their lives had some pretty amazing highs, but they often experienced some amazing lows as well. Moses spent forty years in the wilderness, and when God appeared to him in the burning bush, he argued with God about how weak and timid he was (Exodus 3 and 4).

In 1 Kings 18, Elijah had just seen God rain down fire to supernaturally consume his sacrifice, capture and kill four hundred and fifty prophets of Baal, and watched God break the drought over Israel. At the height of this run of amazing connection to God, Jezebel the evil queen threatened him, and he ran for his life in a panic and asked God to kill him, twice, over the period of a couple of months (1 Kings 19).

Peter had spent three years with Jesus, the Messiah himself, hearing him speak and watching him perform miracle after miracle after miracle. Peter even saw the empty tomb first hand on the very first Easter Sunday, but still, he gave up on life with God and went back to his former occupation, which turned out to be lots of hard work for very little reward (John 21:1-3).

The same pattern is also seen in King David, Gideon, and a number of other great leaders through the Bible. The take home message is this: it’s human nature to suffer from disease and dysfunction. Sometimes it’s physical dysfunction. Sometimes it’s emotional dysfunction. It’s not a personal or spiritual failure to have a physical illness. Why should mental illness be treated any different?

As the stories of Moses, Elijah and Peter testify, being a strong Christian doesn’t make you impervious to low mood or emotional fatigue. Hey, we’re all broken in some way, otherwise why would we need God’s strength and salvation! Having depression simply changes your capacity to experience the joy and love of God. Closing your eyes doesn’t stop the light, it just stops you experiencing the light. Being depressed makes it hard to experience God’s love, but it doesn’t stop God’s love.

In the 80’s and 90’s, a popular Christian musician was a man named Carmen. One of his best known songs had these words,

“When problems try to bury you and make it hard to pray, it may seem like Friday night, but Sunday’s on the way!”

It’s really hard when you’re afflicted by the dank darkness of depression. But nothing will separate us from the love of God (Romans 8:35-39), including depression. You may not feel it, but God’s love is there, and Sunday’s on the way.

Remember:

Depression is a common mental health condition that can have prolonged and devastating consequences. Depression is characterised by either a sadness or a lack of joy which are abnormal in their intensity and their duration, but also affects sleep, appetite and motivation. It’s caused by abnormalities in genes which affect the brains ability to grow new nerve cell branches, and which also affect in-built coping mechanisms, so stress is both more likely to occur in people who are more prone to depression, and the stress is then handled poorly, overloading their emotional capacity.

The management of depression is three-pronged: to improve the brains ability to grow new nerve cells through exercise and/or medication, to learn new ways to cope with distress, and to decrease the amount of stress in the first place.

Christians are not immune from depression, and it’s important for Christians to understand that Christians suffering from depression are not weak, or failing in their spiritual walk, or are unloved by God. The love of God is always present, even if they are unable to process it properly. As dark and dismal as depression can become, there is hope. It may seem like Friday night, but Sunday’s on the way.

References

[1]        Duman RS, Li N. A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists. Philosophical transactions of the Royal Society of London Series B, Biological sciences 2012 Sep 5;367(1601):2475-84.
[2]        Anderson I. Depression. The Treatment and Management of Depression in Adults (Update). NICE clinical guideline 90.2009. London: The British Psychological Society and The Royal College of Psychiatrists, 2010.
[3]        Karatsoreos IN, McEwen BS. Resilience and vulnerability: a neurobiological perspective. F1000prime reports 2013;5:13.
[4]        Rimer J, Dwan K, Lawlor DA, et al. Exercise for depression. The Cochrane database of systematic reviews 2012;7:CD004366.
[5]        Lai JS, Hiles S, Bisquera A, Hure AJ, McEvoy M, Attia J. A systematic review and meta-analysis of dietary patterns and depression in community-dwelling adults. The American journal of clinical nutrition 2014 Jan;99(1):181-97.
[6]        NowOK. Cognitive Behavioural Therapy. Dictionary of Psychotherapy 2015 [cited; Available from: http://www.dictionary.nowok.co.uk/cognitive-behavioural-therapy-cbt.php
[7]        Ruiz FJ. Acceptance and Commitment Therapy versus Traditional Cognitive Behavioral Therapy: A Systematic Review and Meta-analysis of Current Empirical Evidence. International journal of psychology and psychological therapy 2012;12(3):333-58.
[8]        Longmore RJ, Worrell M. Do we need to challenge thoughts in cognitive behavior therapy? Clinical psychology review 2007 Mar;27(2):173-87.
[9]        Dobson KS, Hollon SD, Dimidjian S, et al. Randomized trial of behavioral activation, cognitive therapy, and antidepressant medication in the prevention of relapse and recurrence in major depression. Journal of consulting and clinical psychology 2008 Jun;76(3):468-77.
[10]      Smout M. Acceptance and commitment therapy – pathways for general practitioners. Aust Fam Physician 2012 Sep;41(9):672-6.
[11]      Boelens PA, Reeves RR, Replogle WH, Koenig HG. A randomized trial of the effect of prayer on depression and anxiety. Int J Psychiatry Med 2009;39(4):377-92.

If you’re suffering from depression or any other mental health difficulties and need help, see your GP or a psychologist, or if you’re in Australia, 24 hour telephone counselling is available through:

Lifeline = 13 11 14 – or – Beyond Blue = 1300 22 4636

Seven Elements of Good Mental Health: 4. Show some SSAS – The Prospering Soul

Posted on June 23, 2015 by cedwardpitt

Life shouldn’t just be about avoiding poor health, but also enjoying good health. Our psychological health is no different.

Before we take a look at poor mental health, let’s look at some of the ways that people can enjoy good mental health and wellbeing. This next series of posts will discuss seven elements that are Biblically and scientifically recognised as important to people living richer and more fulfilling lives.

These aren’t the only ways that a person can find fulfilment, nor are they sure-fire ways of preventing all mental health problems either. They’re not seven steps to enlightenment or happiness either. But applying these principles can improve psychosocial wellbeing, and encourage good mental health.

4. Show some SSAS

SSAS stands for Supple, Strong and Skilful. This applies physically and mentally.

Physical fitness is good for us. This isn’t the main point of the blog, but I have never seen a study that shows exercise to be a bad thing. Ultimately, it’s not how fat you are that’s important for your longevity, it’s how fit you are [1, 2]. And the way to get fit is to exercise.

Physical exercise is not just good for the body but good for the brain as well. While the exact pathways are still being determined, there’s good evidence that moderate regular physical activity improves the balance of pro- and anti-inflammatory mediators in the body and in the brain. In the brain, this improves the overall function of our brain cells and their ability to form new pathways, which in turn, has been shown to improve mood disorders like anxiety and depression [3].

But being SSAS isn’t just about what being physically fit and active can do for your mood, but it also relates to being psychologically flexible and using psychological skills to leverage your strengths rather than just fighting with your weaknesses. One of the keys here is acceptance. Remembering your values that we spoke about in key 1 as your guide, exploit the things that you’re good at, using them to gain some self-confidence and momentum. Accept the things that can’t be changed in your life. Then when you have some momentum, learn some new skills to increase your resilience and strengthen your weaknesses.

I say this because sometimes we spend so much time focussing on all the bad things in our lives that we forget about the good things that we already have or can already do. It would be like an athlete spending all their time in the gym, getting really fit and strong, but never getting onto the field or court. It’s important that we courageously challenge ourselves to turn our weak points into strong points, but it’s more important to do what we can to help others around us.

References

[1]        Barry VW, Baruth M, Beets MW, Durstine JL, Liu J, Blair SN. Fitness vs. fatness on all-cause mortality: a meta-analysis. Progress in cardiovascular diseases 2014 Jan-Feb;56(4):382-90.
[2]        Lavie CJ, McAuley PA, Church TS, Milani RV, Blair SN. Obesity and cardiovascular diseases: implications regarding fitness, fatness, and severity in the obesity paradox. Journal of the American College of Cardiology 2014 Apr 15;63(14):1345-54.
[3]        Moylan S, Eyre HA, Maes M, Baune BT, Jacka FN, Berk M. Exercising the worry away: how inflammation, oxidative and nitrogen stress mediates the beneficial effect of physical activity on anxiety disorder symptoms and behaviours. Neuroscience and biobehavioral reviews 2013 May;37(4):573-84.

Fats and Figures: Re-examining saturated fat and what’s really good for your heart

Posted on January 28, 2015 by cedwardpitt

A Facebook friend forwarded me an article a few weeks back and asked for my humble medical opinion.

The article was entitled, “World Renowned Heart Surgeon Speaks Out On What Really Causes Heart Disease”. It was written by a man who said he was a heart surgeon, and who claimed to be coming clean on the real reason why our world has an epidemic of obesity and heart disease despite the low fat advice of the medical profession.

It’s a highly controversial topic right now. For decades, the western world was under the impression that fat was tobaccos right hand man in a war on good health. Standard medical dogma was that high cholesterol was bad, and that saturated fat was its main source. Evil butter was replaced with angelic margarine. Fatty red meat was always served with a generous side portion of guilt. Low fat became high fashion.

Today, the pendulum of public opinion has swung back with such amazing ferocity, it’s become more like a wrecking ball. Fat has returned to the fold as friend instead of foe. The once mighty cholesterol lowering medications called statins have become seen as another example of pharmaceutical company profits-before-patients. Sugar has become the new villain, and along with it, the nebulous concept of “inflammation” as the key mechanism of heart disease and strokes, and nearly every other medical ailment.

What started off as a three-paragraph reply on Facebook has evolved into a short eBook, which you can download for free from Smashwords (https://www.smashwords.com/books/view/514719)

In today’s post, I want to look at six things that, over the years, have been touted as contributing to or preventing heart disease, and see what the evidence says. The results may be surprising!

1. Is saturated fat bad? Is polyunsaturated fat good?

According to a meta-analysis of observational studies on dietary fats by Chowdhury et al. (2014), relative risks for coronary disease were 1.02 (95% CI, 0.97 to 1.07) for saturated fats, 0.99 (CI, 0.89 to 1.09) for monounsaturated, 0.93 (CI, 0.84 to 1.02) for long-chain n-3 polyunsaturated, 1.01 (CI, 0.96 to 1.07) for n-6 polyunsaturated, and 1.16 (CI, 1.06 to 1.27) for trans fatty acids. The total number of patients in all of the trials was more than half a million. This is pretty convincing evidence that saturated fats aren’t as bad as first believed.

What does all this mean? In statistical terms, a relative risk is the incidence of disease in one group compared to the incidence of disease in another. The risk of the disease in the two groups is the same if the relative risk = 1. A relative risk of 7.0 means that the experiment group has seven times the risk of a control group. A relative risk of 0.5 would mean the experiment group has half the risk of the control group. The confidence interval is a range of numbers in which there is a 95% chance that the true relative risk is in the interval. A result is “statistically significant” when the confidence interval (CI) does not cross the number 1.

So going back to the study by Chowdhury et al. (2014), only 2% more patients in the group with the highest saturated fat consumption had heart disease compared to the lowest saturated fat consumption. The confidence interval crossed 1, so that result may have been due to chance alone. For trans fatty acid consumption, 16% more people had heart disease in the higher consumption group compared to the lower consumption group, which was probably a real effect and not due to chance (the confidence interval did not cross 1). Simply put, trans-fats are bad. Saturated fats probably aren’t.

The same meta-analysis by Chowdhury et al. (2014) also reviewed supplementation with PUFA’s on the overall risk of heart disease. They found that in 27 randomised controlled trials with more than 100,000 people, relative risks for coronary disease were 0.97 (CI, 0.69 to 1.36) for alpha-linolenic acid supplements, 0.94 (CI, 0.86 to 1.03) for long-chain n-3 polyunsaturated acid supplements, and 0.89 (CI, 0.71 to 1.12) for n-6 polyunsaturated fatty acid supplements. In this case, there was a trend in favour of supplementation with omega-3 and omega-6 supplements, but it was small, and may have been due to chance. This is confirmed by other reviews (Rizos, Ntzani, Bika, Kostapanos, & Elisaf, 2012; Schwingshackl & Hoffmann, 2014)

So it appears that it doesn’t matter what fat you consume, saturated or polyunsaturated, or whether you supplement with fish oils or eat lots of fish, your cardiovascular risk is much the same. The only thing that’s definitely clear is that you should avoid trans-fats.

2. Is sugar bad for you?

That depends.

When we think of sugar, we think of sucrose, a carbohydrate made up of one glucose and one fructose molecule. There are many carbohydrates, which are just various combinations of different numbers of glucose/fructose molecules, sucrose being one type.

Sugar consumption is thought to be the modern scourge, it’s consumption linked to everything from cancer to gallstones. It’s been recently become the villain of cardiovascular disease as well. It’s thought to cause insulin resistance, inflammation and an increase in the fats circulating in the blood stream. So, is it as bad as they say? The evidence is surprising.

First of all, sugar doesn’t make you fat. Rather, it’s the calories you consume that make you fat. Te Morenga, Mallard, and Mann (2013) conclude their meta-analysis of dietary sugar and body weight, “Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.”

The intake of sugar and glucose don’t cause an increase in inflammation or cholesterol in healthy people. In a study on effects of sugar consumption on the biomarkers of healthy people, Jameel, Phang, Wood, and Garg (2014) found that consumption of sucrose and glucose actually decreased cholesterol. Fructose increased cholesterol, though interestingly, the Total:HDL ratio (which is prognostic for heart disease) did not change significantly with the consumption of any form of sugar. They also found that fructose was associated with an increase in inflammation, but glucose and sucrose reduced inflammation.

On the other hand, a study by Isordia-Salas et al. (2014) showed a small but significant association between those with high blood glucose level and inflammation, though they also found an association between inflammation and BMI (the body-mass index), so it’s not clear what the causal factor is.

There seems to be a clearer association between blood glucose after meals in those who have abnormal glucose metabolism. In patients with pre-diabetes, higher levels of blood glucose two hours after eating were associated with increased risk of death from cardiovascular disease and all causes (Coutinho, Gerstein, Wang, & Yusuf, 1999; Decode Study Group, 2003; Lind et al., 2014).

To melt your brain a little more, just because high glucose levels are associated with higher mortality doesn’t mean the lower the glucose, the better. In the study by the Decode Study Group (2003), low blood glucose had a higher mortality than normal glucose levels, and a meta-analysis by Noto, Goto, Tsujimoto, and Noda (2013) showed that low carbohydrate diets have a 30% increase in all-cause mortality.

How do you pull all of these seemingly contradictory studies together? The bottom line appears to be, according to the evidence so far, that consumption of sugar does not cause inflammation or significantly increase the risk of heart disease in healthy people who are able to metabolise it properly.

In those people who have abnormal glucose metabolism, the higher the glucose is after a meal (a measure of how well the body processes glucose), then the higher the risk is of inflammation, heart disease, and all-cause mortality.

The distinction between who has normal glucose metabolism and who has dysfunctional glucose metabolism is probably related to genetics. A study by Sousa, Lopes, Hueb, Krieger, and Pereira (2011) showed that genetic information was able to predict 5-year incidence of major cardiovascular events and overall mortality in non-diabetic individuals, even after adjustment for the persons blood sugar. Those without diabetes but who had a high genetic risk had a similar incidence of cardiovascular events compared to diabetics. So if you have the genes, your body doesn’t process the glucose properly and your risk is increased, even if you aren’t bad enough to have a diagnosis of diabetes.

Thus it appears that sugar is not the bad guy that everyone makes it out to be. Excess sugar will make you fat, but so will excess everything-else. It probably won’t kill you unless you’re genetically pre-disposed to handle it poorly. And there’s the rub, because we don’t have the capacity to test for that clinically yet.

So the last word on sugar is that it’s a sometimes food. You may be lucky enough to handle large amounts of sugar, but the best advice at this time is don’t tempt fate by eating large quantities of it.

3. Is obesity bad for you?

Again, that depends.

It used to be thought that obesity posed a linear risk, that is, the fatter you were the higher your risk of heart attacks, cancer, diabetes, everything. Then in 2013, a meta-analysis by Flegal, Kit, Orpana, and Graubard (2013) showed that people who were overweight (but not obese) had better survival than those who were normal weight.

Later in 2013, Kramer, Zinman, and Retnakaran (2013) published a meta-analysis which showed that metabolically unhealthy people of normal BMI were at greater risk of cardiovascular disease than metabolically healthy obese people.

Last year a paper by Barry et al. (2014) showed that those who were unfit were twice as likely to die compared to people who were fit, irrespective of their BMI.

So obesity doesn’t seem to be the problem after all, rather it’s a persons ability to handle blood sugar, cholesterol and blood pressure that’s the problem. It seems that more people with obesity have these metabolic problems, but correlation does not equal causation. There’s probably a undetermined factor that links obesity and metabolic dysfunction.

I’m not suggesting that we should all get fatter. Obesity has problems of its own, unrelated to metabolic issues, that make it problematic. We should still be careful about our weight. The take-home message is that skinny does not necessarily mean healthy and that focusing on what the scales are saying may be distracting us from the real problem.

4. Is meat bad for you? Should we be vegetarians?

In a word, no.

In the two available meta-analyses of the studies on red meat consumption (Larsson & Orsini, 2014), and red meat vs white meat vs all meat (Abete, Romaguera, Vieira, Lopez de Munain, & Norat, 2014), there was a statistical but moderate increase in death and heart disease from processed meats.

There was a trend towards a higher death rate in those who ate the most red meat, but the trend wasn’t statistically significant (i.e.: may have been related to chance). There was no trend associated with white meat consumption. So it appears that as long as it’s not processed meat, red meat isn’t as bad as people first thought.

Meat might not be particularly bad, but are vegetarian diets better? Again, probably not. The meta-analysis by Huang et al. (2012) shows that there’s a positive trend for vegetarian diets, though again, that might be attributable to chance as the results are not statistically significant.

The take-away message? Even though the trends may be related to chance, the trend is favourable for vegetables and not as favourable for red meat. So eat more veggies, eat less red meat, but don’t let some sanctimonious vegan convince you that meat is noxious and vile.

5. Is alcohol good for you?

A different meme recently came around my Facebook feed, entitled, “Is Drinking Wine Better Than Going To The Gym? According To Scientists, Yes!” For a while there, I had fantasies about giving my membership card back to the gym and heading down to the local bottle shop for my daily workout instead.

Disappointingly, it turns out that red wine isn’t better than exercise according to the research that I uncovered. However, my research did suggest that the daily exercise of wine drinking is still beneficial, and not just red wine, but alcohol of any form. Ronksley, Brien, Turner, Mukamal, and Ghali (2011) showed about two standard drinks of alcohol daily conferred a 25% reduction in deaths from heart disease (relative risk 0.75 (0.68 to 0.81)), and a small but statistically strong reduction in death from all causes of 13% (relative risk 0.87 (0.83 to 0.92)). The risk reduction of coronary heart disease from alcohol was also confirmed in a more recent study by Roerecke and Rehm (2014), who showed that death from heart disease was reduced by 36% for those who consistently consumed less than three standard drinks a day (relative risk 0.64 (0.53 to 0.71)).

The effect applies to consistent daily consumption, not to drinking in a cluster pattern (binging or weekend-drinking only, for example). And there’s a gender difference, women having the maximum beneficial effect at about one drink a day, and two drinks a day in men.

6. Is exercise good for you?

In a word, yes!

I’ve never seen a study that showed exercise was harmful. Exercise improves overall metabolism, decreases cardiovascular disease, improves mood and memory and increases your lifespan, amongst many other things. If exercise came in pill form, it would be labelled a wonder-drug.

As discussed earlier, fit people have a better rate of survival compared to unfit people, whether they’re obese or not (Barry et al., 2014). And the key to fitness is exercise. In a large meta-analysis by Samitz, Egger, and Zwahlen (2011), 80 studies involving more than 1.3 million subjects in total were analysed, showing that the highest levels of exercise had an all cause mortality reduction of 35% (relative risk 0.65 (0.6 to 0.71)).

There’s always debate about what form of exercise is best. Are you better to do weights, do interval training, or run for hours? Honestly, it probably doesn’t matter that much in the end. What is important is that you work hard enough to elevate your heart rate and break a sweat. If you aren’t very fit, it won’t take much exercise to do that. If you are very fit, it probably will. But for the average person, you don’t have to jump straight into a boot camp style program and work so hard that you’re puking everywhere, and so sore afterwards that you can’t move for a week. Common sense prevails!

References

Abete, I., Romaguera, D., Vieira, A. R., Lopez de Munain, A., & Norat, T. (2014). Association between total, processed, red and white meat consumption and all-cause, CVD and IHD mortality: a meta-analysis of cohort studies. Br J Nutr, 112(5), 762-775. doi: 10.1017/S000711451400124X

Barry, V. W., Baruth, M., Beets, M. W., Durstine, J. L., Liu, J., & Blair, S. N. (2014). Fitness vs. fatness on all-cause mortality: a meta-analysis. Prog Cardiovasc Dis, 56(4), 382-390. doi: 10.1016/j.pcad.2013.09.002

Chowdhury, R., Warnakula, S., Kunutsor, S., Crowe, F., Ward, H. A., Johnson, L., . . . Di Angelantonio, E. (2014). Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med, 160(6), 398-406. doi: 10.7326/M13-1788

Coutinho, M., Gerstein, H. C., Wang, Y., & Yusuf, S. (1999). The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95,783 individuals followed for 12.4 years. Diabetes Care, 22(2), 233-240.

Decode Study Group, E. D. E. G. (2003). Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases? Diabetes Care, 26(3), 688-696.

Flegal, K. M., Kit, B. K., Orpana, H., & Graubard, B. I. (2013). Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA, 309(1), 71-82. doi: 10.1001/jama.2012.113905

Huang, T., Yang, B., Zheng, J., Li, G., Wahlqvist, M. L., & Li, D. (2012). Cardiovascular disease mortality and cancer incidence in vegetarians: a meta-analysis and systematic review. Ann Nutr Metab, 60(4), 233-240. doi: 10.1159/000337301

Isordia-Salas, I., Galvan-Plata, M. E., Leanos-Miranda, A., Aguilar-Sosa, E., Anaya-Gomez, F., Majluf-Cruz, A., & Santiago-German, D. (2014). Proinflammatory and prothrombotic state in subjects with different glucose tolerance status before cardiovascular disease. J Diabetes Res, 2014, 631902. doi: 10.1155/2014/631902

Jameel, F., Phang, M., Wood, L. G., & Garg, M. L. (2014). Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation. Lipids Health Dis, 13(1), 195. doi: 10.1186/1476-511X-13-195

Kramer, C. K., Zinman, B., & Retnakaran, R. (2013). Are metabolically healthy overweight and obesity benign conditions?: A systematic review and meta-analysis. Ann Intern Med, 159(11), 758-769. doi: 10.7326/0003-4819-159-11-201312030-00008

Larsson, S. C., & Orsini, N. (2014). Red meat and processed meat consumption and all-cause mortality: a meta-analysis. Am J Epidemiol, 179(3), 282-289. doi: 10.1093/aje/kwt261

Lind, M., Tuomilehto, J., Uusitupa, M., Nerman, O., Eriksson, J., Ilanne-Parikka, P., . . . Lindstrom, J. (2014). The association between HbA1c, fasting glucose, 1-hour glucose and 2-hour glucose during an oral glucose tolerance test and cardiovascular disease in individuals with elevated risk for diabetes. PLoS One, 9(10), e109506. doi: 10.1371/journal.pone.0109506

Noto, H., Goto, A., Tsujimoto, T., & Noda, M. (2013). Low-carbohydrate diets and all-cause mortality: a systematic review and meta-analysis of observational studies. PLoS One, 8(1), e55030. doi: 10.1371/journal.pone.0055030

Rizos, E. C., Ntzani, E. E., Bika, E., Kostapanos, M. S., & Elisaf, M. S. (2012). Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis. JAMA, 308(10), 1024-1033. doi: 10.1001/2012.jama.11374

Roerecke, M., & Rehm, J. (2014). Alcohol consumption, drinking patterns, and ischemic heart disease: a narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers. BMC Med, 12(1), 182. doi: 10.1186/s12916-014-0182-6

Ronksley, P. E., Brien, S. E., Turner, B. J., Mukamal, K. J., & Ghali, W. A. (2011). Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ, 342, d671. doi: 10.1136/bmj.d671

Samitz, G., Egger, M., & Zwahlen, M. (2011). Domains of physical activity and all-cause mortality: systematic review and dose-response meta-analysis of cohort studies. Int J Epidemiol, 40(5), 1382-1400. doi: 10.1093/ije/dyr112

Schwingshackl, L., & Hoffmann, G. (2014). Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression. BMJ Open, 4(4), e004487. doi: 10.1136/bmjopen-2013-004487

Sousa, A. G., Lopes, N. H., Hueb, W. A., Krieger, J. E., & Pereira, A. C. (2011). Genetic variants of diabetes risk and incident cardiovascular events in chronic coronary artery disease. PLoS One, 6(1), e16341. doi: 10.1371/journal.pone.0016341

Te Morenga, L., Mallard, S., & Mann, J. (2013). Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ, 346, e7492. doi: 10.1136/bmj.e7492

Drink up or work out? Is alcohol really better than exercise?

Posted on January 13, 2015 by cedwardpitt

An article came through my Facebook feed today which grabbed my attention. Entitled, “Is Drinking Wine Better Than Going To The Gym? According To Scientists, Yes!“, the article suggested that red wine with it’s particular blend of anti-oxidants was in fact proven by scientists to be more beneficial to you than slogging it out at the gym.

I tend to prefer drinking red wine to going to the gym, as do a lot of other people it seems, given the viral-esque proliferation of this article through social media. If it were true that red wine was equivalent to exercise then I needed to rescind my newly acquired gym membership and swap it for a wine club membership post-haste. If it were true …

Even though my aching legs wanted it to be true, my sceptical brain held sway. I needed to find the answer to this vital question. If it were true, it would be a good excuse to enjoy a glass of red on a more regular basis. I could even come up with my own little euphemism for it … yes … I would call it “my daily workout”! My thighs would be much happier.

I took a deep breath and started to have a look through the published medical literature, looking to see if there were large studies or meta-analyses on red wine, exercise and all cause mortality. Interestingly there were a few studies on red wine, but mostly looking at its anti-oxidant effects, and not on the overall health benefit. However, there were a number of papers on the effects of alcohol consumption more broadly and its effect on heart disease and deaths from any cause. The study by Ronksley, Brien, Turner, Mukamal, and Ghali (2011) showed about two standard drinks of alcohol daily conferred a 25% reduction in deaths from heart disease (relative risk 0.75 (95% Confidence Interval 0.68 to 0.81)). The study also showed a small but statistically strong reduction in all-cause mortality of 13% (relative risk 0.87 (0.83 to 0.92)). The risk reduction of coronary heart disease from alcohol was also confirmed in a more recent study by Roerecke and Rehm (2014), who showed that death from heart disease was reduced by 36% for those who consistently consumed less than three standard drinks a day (relative risk 0.64 (0.53 to 0.71)). So far so good … “my daily workout” was looking promising.

What about exercise? Well, a meta-analysis by Samitz, Egger, and Zwahlen (2011) analysed 80 studies involving more than 1.3 million subjects in total, and found that the highest levels of exercise had an all cause mortality reduction of 35% (relative risk 0.65 (0.6 to 0.71)). Damn! 35% beats 13% … I couldn’t give up in the gym just yet. I could feel my legs silently groaning.

In fairness, the article by Samitz and colleagues found that 150 minutes per week of moderate to vigorous exercise a week had a relative risk of mortality of 0.86 (0.8 to 0.92), so that’s comparable to the benefit conferred by 2 standard drinks a day in the study by Ronksley et al. Strictly speaking, the numbers aren’t directly analogous as each study is limited by the vagaries of the statistics they pooled. Red wine isn’t better than going to the gym as the Facebook article suggested, but they are probably comparable.

So, what to do with this information? I’ve decided that I need to adopt two daily workouts. Two standard drinks of alcohol a day is more than likely going to reduce my mortality, as will 25-30 minutes or more a day of moderate intensity exercise. I’m not exactly sure what the combined effect of both workouts will be on my longevity, but I’m pretty sure it won’t make things worse.

Cheers!

References

One note of caution: Roerecke and Rehm (2014) note that the relative risk from alcohol is a J-shaped curve. More than three standard drinks a day increases the risk from alcohol, especially for women, which is in keeping with the Australian national guidelines for alcohol consumption (http://www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/guide-adult).

If you’re concerned about your drinking and you want help, talk to your local GP, local community health service, call the alcohol helpline in your state (for Australian state-based helplines, see http://www.alcohol.gov.au/internet/alcohol/publishing.nsf/Content/guide-adult) or visit the DrinkWise website https://www.drinkwise.org.au/drinking-and-you/support-services-adults/#

Dr C. Edward Pitt

Faith, Hope, Love, Science.

Tag Archives: exercise

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Seven Elements of Good Mental Health: 4. Show some SSAS – The Prospering Soul

Fats and Figures: Re-examining saturated fat and what’s really good for your heart

1. Is saturated fat bad? Is polyunsaturated fat good?

2. Is sugar bad for you?

3. Is obesity bad for you?

4. Is meat bad for you? Should we be vegetarians?

5. Is alcohol good for you?

6. Is exercise good for you?

Drink up or work out? Is alcohol really better than exercise?