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.

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.

Can you really Think and Eat Yourself Smart?

Posted on August 19, 2016 by cedwardpitt

Today I’m in Sydney, a vibrant, bustling city which centres on one of the most beautiful harbours in the world. When I booked my flights in April, I was originally going to spend the day attending Dr Caroline Leaf’s Australian Think and Eat Yourself Smart workshop. Dr Leaf and her minions revoked my ticket a few weeks later. She also changed the workshop twitter hashtag from #thinkandeatsmart to just #eatsmart, so perhaps Dr Leaf doesn’t want free thinking at the workshop.

It’s such a shame really, because I was looking forward to being part of the history of Dr Leaf’s first workshop on Australian soil. But no matter … why waste a perfectly good plane ticket when I can have a day to sightsee, take photos, and catch a few Pokemon here and there as well.

And as a special something for all the people who’re attending the workshop today with Dr Leaf, I thought I’d pen a blog in their honour … something for them to ponder as they listen to Dr Leaf’s presentation, and maybe even provide them with a nidus of a question to pose to her during the day. So here goes …

As the name would suggest, the Think and Eat Yourself Smart workshop is based on Dr Leaf’s book, Think and Eat Yourself Smart. Does the book (and the subsequent workshop) deliver what it promises? That is, can you really think and eat yourself smart? It’s all well and good for Dr Leaf to espouse her fringe opinions on the food industry and modern farming, and to recycle nutritional information that doctors and dieticians have been promoting for years, but if her book can’t deliver on its titular promise, then it’s just an unoriginal rehash.

To support her thesis that we can think and eat ourselves smart, Dr Leaf declares that what you think affects what you eat, and what you eat affects what you think. It’s on these intertwined ideas that Dr Leaf’s book stands or falls. Let’s look at those statements in more detail.

Statement number 1 – “What you think affects what you eat”

Dr Leaf has a broad approach with this premise. She suggests that the mindset that you have will not only determine what you consume, but also how your body will process it.

For example, she said on page 84 of Think and Eat Yourself Smart, “Research shows that 75 – 98 percent of current mental, physical, emotional and behavioural illnesses and issues come from our thought life; only 2 – 25 percent come from a combination of genetics and what enters our bodies through food, medications, pollution, chemicals, and so on. These statistics show that the mindset behind the meal – the thinking behind the meal – plays a dominant role in the process of human food related health issues, approximately 80 percent. Hence the title of this book: you have to think and eat yourself smart, happy and healthy.”

She goes on to say, “If we do not have a healthy mind, then nothing else in our life will be healthy, including our eating habits.”

We can break down these statements to assess their validity.

First of all, this statement is predicated on her 98 percent myth, something which I’ve previously proven to be implausible, but which Dr Leaf continues to use despite the overwhelming evidence against it. To arrive at this conclusion, Dr Leaf has over-extrapolated, paraphrased, and exaggerated a handful of sources that were either out-of-date, clearly biased, or irrelevant. She even had the gall to ascribe a made-up figure to an article which, ironically, twice contradicted her. If you want to know more, see Chapter 10 in my book (http://www.debunkingdrleaf.com/chapter-10/)

This means that Dr Leaf’s statement, and indeed, her entire book, is built on gross misrepresentations of illegitimate resources. Genetics and our external environment actually play a much greater role than she is willing to give credit for. The mindset behind the meal is largely irrelevant – nowhere near 80 percent as Dr Leaf suggests.

But for the sake of argument, let’s take a couple of well-known medical conditions that are often associated with lifestyle and compare the research examining the difference that thinking and food make to them. After all, if your mindset really is responsible for more than 80 percent of our health, then these two very common conditions should improve by more than 80 percent when thought patterns are changed.

Example 1: Hypertension.

Hypertension is also known as high blood pressure. First, a brief explanation of what the numbers mean when talking about blood pressure so we’re on the same page: Blood pressure is measured in units of millimetres of mercury (or mmHg). The old sphygmomanometers were hand pumps attached to a rubber bladder and a column of liquid metal mercury. The blood pressure reading was however high the column of mercury rose at the two ends of the cardiac cycle. There are always two numbers, expressed as ‘number 1 over number 2’ and written as N1/N2, like 120/80 or ‘one hundred and twenty over eighty’. The top number is the maximum pressure in the arterial system when the heart pumps the blood into the arteries. The bottom number is the pressure left over in the arterial system just before the heart beats again. A blood pressure of 120/80 is the gold-standard physiological reference of normal blood pressure. A blood pressure consistently above 140/90 is considered high.

Primary hypertension, which accounts for about 95 percent of all cases, has a strong genetic component. According to eMedicine, “Epidemiological studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%.” (http://emedicine.medscape.com/article/241381-overview#a4) Environmental causes account for nearly all of the rest. Secondary hypertension is related to a number of different diseases of the arteries, kidneys, hormone system and many others. Diet is clearly part of those environmental causes. Psychological stress is in there too, but the question is, how important is it? If Dr Leaf is right, it should be 80 percent.

According to medical research, reducing alcohol intake to one standard drink per day or less reduces the systolic blood pressure (the top number) by between 2 and 4 mmHg. Reducing salt to less than 6g a day decreases the systolic blood pressure by between 2 and 8 mmHg. At best, that’s a 12mmHg reduction. The DASH diet is as close to Dr Leaf’s macrobiotic tree-hugging anti-MAD diet as one could reasonably get, relying not just on cutting out salt, but also consuming low fat milk and lots of fruit and vegetables. At best, the DASH diet could shave another 6mmHg from the standard low salt diet. So that’s a grand total of 18mmHg with even the most optimistic of expectations.

Compared to diet, the best improvement in blood pressure from mind control is 5mmHg at best (and given the size and quality of the studies, that’s being generous) (Anderson et al, 2008; Barnes et al, 2008).

So for hypertension, changing your thinking has, at best, only about a quarter as powerful as changing your diet, not four times more powerful as Dr Leaf would have us believe. One more nail in in the coffin for Dr Leaf’s theories.

Example 2: Dyslipidaemia.

Dyslipidaemia is medical jargon for cholesterol behaving badly. Cholesterol is a waxy substance that’s found as a component of the fats in our diet. To simplify a complex process, we need cholesterol to make our cell membranes, and cholesterol is also an essential building block for most of our hormones. Cholesterol is usually carried around the body on protein transports called lipoproteins. If there’s over-production of these lipoprotein particles or they’re not cleared by the liver properly, then the cholesterol they carry can get up to mischief. The pathways and means of lipid metabolism in the human body reflect complex processes, and genetics, certain medical conditions, medications, and environmental factors can change how the lipoproteins behave.

So how much does thinking affect our cholesterol? Well, there isn’t a lot of research looking at the subject, but a few studies have looked at cholesterol (specifically triglycerides, one of the lipids in the cholesterol ‘team’) and ‘mind-body practices’ (such as self-prayer, meditation, yoga, breathing exercises, or any other form of mind-body related relaxation technique or practice). In a cross-sectional analysis of a cohort from the Rotterdam Study, Younge and colleagues examined the association between mind-body practices and the blood levels of triglyceride. They found that mind-body practices were associated with a triglyceride level 0.00034 mmol/L less than those who did not perform mind-body practices (Younge et al, 2015). That’s nearly imperceptible, possibly an artefact. In fact, the average effect of placebos (the fake pills given as a control in therapeutic drug trials) are far greater – 0.1 mmol/L on average (Edwards and Moore, 2003). Dietary interventions such as low carbohydrate diets decreased triglycerides by 0.26 mmol/L compared to low fat diets (Mansoor et al, 2016), and low fat diets up to 0.27 mmol/L lower than standard diets (Hooper, 2012). Statins, the lipid-lowering medications, reduce triglycerides by between 0.2-0.4 mmol/L depending on the specific drug studied (Edwards and Moore, 2003).

The point of all this isn’t so much the specific numbers but the obvious difference between the (lack of) power of thought over an important lifestyle condition compared to the effectiveness of diet and medications. If thinking was four times more important to the process of human food related health issues as Dr Leafs proposes, then thought-related ‘mind-body’ interventions should be at least four times more effective than any other intervention. But the numbers don’t reflect that – ’Mind-body’ interventions are 1000 times weaker than dietary or drug interventions.

So Dr Leaf’s pronouncement that “the mindset behind the meal – the thinking behind the meal – plays a dominant role in the process of human food related health issues, approximately 80 percent” is complete bunkum. There is no evidence to support the 98 percent myth which forms her statements underlying premise, and the examples of hypertension and dyslipidaemia, two common lifestyle conditions with proven genetic and dietary links, prove that thought based interventions are much, much weaker than dietary or drug interventions.

Therefore Dr Leaf’s claim that what you think affects what you eat is entirely baseless.

Statement number 2 – “What you eat affects what you think”

Dr Leaf writes, “Although your brain is only 2 percent of the weight of your body, it consumes 20 percent of the total energy (oxygen) and 65 percent of the glucose – what you eat will directly affect the brain’s ability to function on a significant scale. Your brain has ‘first dibs’ on everything you eat. I call this the ’20 percent factor’ or the eating behind the thinking, and it underscores the fact that how and what we eat affects our mind, brain and body.” (p84-5)

On face value, the statement seems to hold some weight. Food does have an impact on how our brain works. It certainly isn’t the only factor though – demands in the environment, our oxygen levels, our hormones, the function of our major organs, infections or injury, and our levels of sleep, all play a significant role on how our brain functions too. But strictly speaking, what we eat does have an impact on how we think – if we haven’t eaten, or if we don’t consume enough calories, especially carbohydrates, our body slows some of our bodily functions down to preserve energy, including some of our cerebral functions. So when you hear people complain that they can’t think because they have low blood sugar, that may in fact be true. On the other hand, a pure glucose load can shift the balance of the amino acid tryptophan in our body, which enables the brain to produce more of the neurotransmitter serotonin, which can lift our mood. Or ingesting food or drinks with stimulants like caffeine, such as my morning espresso, also improves how we think by making us more alert.

Unfortunately, Dr Leaf’s application of this premise goes several steps too far. Later on page 85, Dr Leaf says, “if you eat while emotional, your body does not digest your food correctly.”

Well, that statement may contain an element of truth but only because it’s so hazy and indefinite that it’s applicable in the broadest sense. Technically, we’re always emotional to one degree or another. Even if I assume that Dr Leaf’s is meaning ‘angry’ when she says ‘emotional’ then it’s not so much that our body digests food incorrectly, but just differently. When you’re highly aroused (physiologically, not sexually, just to clarify), your body goes into fight or flight mode. The body diverts blood away from your intestines and towards your muscles, heart and lungs, so that you have the energy to handle the crisis. The food in your stomach and guts isn’t going anywhere, and your body leaves it where it is to come back to it later when the crisis has been averted. This is a normal physiological response. The body still digests the food and absorbs it correctly, things are just delayed a little (Kiecolt-Glaser, 2010).

The biggest problem with Dr Leaf’s ‘eating behind the thinking’ argument is that it directly undermines her previous teaching.

Dr Leaf has made multiple social media posts claiming that the mind is separate from the brain and controls the brain. She’s written much the same sentiment in her books. Take a meme she posted to social media in May 2016. It said, “As triune beings made in God’s image, we are spirit, mind (soul) and body – and our brain being part of the body does the bidding of the mind …”, and “God has designed the mind as separate from the brain. The brain simply stores the information from the mind and your mind controls your brain.”

So the obvious question is, “If God designed our mind (our thinking) to be separate from the brain and to control the brain, then how can the food we eat make any difference to what we think? My diet affects my brain through the amount and timing of glucose I ingest, but can my diet can’t affect my thinking if the mind is separate to the brain and controls the brain?

Either the mind is separate to the brain, or it’s not. It can’t be both. If the mind is separate to the brain, then what you eat can’t affect what you think and the book becomes an emaciated shadow of rhetoric. If the mind is dependent on the brain then the book and seminar maintain some semblance of validity, but the rest of Dr Leaf’s ministry crumbles like a well-made cheesecake crust, since the entirety of Dr Leaf’s ministry rests on her idea that the mind is separate from the brain and controls the brain, not the other way around (https://cedwardpitt.com/2016/05/30/dr-caroline-leaf-and-the-mind-brain-revisited/).

At the very least, this must be embarrassing for Dr Leaf, and if she keeps shooting herself in the foot, people will eventually notice that she’s limping.

So other than the free-range, fair-trade, grass fed, organic agro-ecologically produced kale and spinach root muffins and the chia and dandelion broth, it appears that the attendees at Dr Leaf’s workshop today may not be getting what they signed up for. What you think does not radically change your health, or influence what your food does to your body, and the food you eat does not significantly change how you think. Our diet is important to our health, but we can’t think and eat ourselves smart.

To all the attendees at the workshop, I hope you got something valuable out of the workshop. While you were all sitting in a small room, listening to Dr Leaf and snacking on lemon and quinoa stuffed free-range quail giblets, Sydney was outdoing itself. Not that I’m rubbing it in or anything, but see for yourself …

Dr Mary Booth lookout

Milsons Point

Milsons Park, Neutral Bay

Cremorne

Point Piper

Macquarie Lighthouse

Blues Point Reserve

References

Anderson JW, Liu C, Kryscio RJ. Blood pressure response to transcendental meditation: a meta-analysis. Am J Hypertens 2008 Mar;21(3):310-6

Barnes VA, Pendergrast RA, Harshfield GA, Treiber FA. Impact of breathing awareness meditation on ambulatory blood pressure and sodium handling in prehypertensive African American adolescents. Ethn Dis 2008 Winter;18(1):1-5

Edwards JE, Moore RA. Statins in hypercholesterolaemia: a dose-specific meta-analysis of lipid changes in randomised, double blind trials. BMC Family practice. 2003 Dec 1;4(1):1.

Hooper L, Abdelhamid A, Moore HJ, Douthwaite W, Skeaff CM, Summerbell CD. Effect of reducing total fat intake on body weight: systematic review and meta-analysis of randomised controlled trials and cohort studies. Bmj. 2012 Dec 6;345:e7666.

Kiecolt-Glaser JK. Stress, food, and inflammation: psychoneuroimmunology and nutrition at the cutting edge. Psychosomatic Medicine. 2010 May;72(4):365.

Mansoor N, Vinknes KJ, Veierød MB, Retterstøl K. Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials. British Journal of Nutrition. 2016 Feb 14;115(03):466-79.

Younge JO, Leening MJ, Tiemeier H, Franco OH, Kiefte-de Jong J, Hofman A, Roos-Hesselink JW, Hunink MM. Association between mind-body practice and cardiometabolic risk factors: The Rotterdam Study. Psychosomatic medicine. 2015 Sep 1;77(7):775-83.

Can an aspirin a day keep the psychiatrist away?

Posted on May 2, 2016 by cedwardpitt

Floating across my Facebook feed this morning was an article on the possible link between depression and inflammation. Its premise was that depression, the joyless soul-sucking disease affecting millions of people around the world, is related to inflammation. If that were true, might mean that we could cure depression with medications that stop inflammation. Maybe we should be consuming an aspirin a day to keep the doctor away, and not the proverbial apple?

Inflammation is a hot topic right now. Inflammation in the medical sense refers to a normal body process to promote healing and recovery from sickness or injury. It’s a complex dance of chemical signals which is triggered by damage to tissue. Inflammation is essential to life. Without it, we would be unable to repair our tissues if they were damaged.

When tissues are damaged, a number of local cells in the damaged area release pro-inflammatory cytokines which then trigger a cascade of responses; increase in the size of the local blood vessels to allow greater blood flow to the area, attracting pus-cells (neutrophils) to the area, and increasing the ‘leakiness’ of the blood vessels to allow the pus cells into the area. This response is governed by a number of chemical mediators throughout the body, including histamine, serotonin, complement system, kinins, substance P, prostaglandins and leukotrienes, cytokines and nitric oxide. Anti-inflammatory cytokines balance out the process, keeping the pro-inflammatory cytokines in check so that the process doesn’t spiral out of control.

Despite the literal plethora of chemical reactions going on simultaneously, most of the time the reaction eventually runs out of noxious agents, the anti-inflammatory cytokines dampen down the reaction, and the tissue returns to either normal, or at least functional. Though inflammation isn’t just limited to repairing damage but also preparing for damage –psychological stress prepares the inflammation system for potential damage. Physical stress triggers the inflammation system to repair any damage.

Chronic inflammation occurs when the acute illness or injury does not fully resolve and continues to smoulder, the natural healing pathway is obstructed, or the body remains in a psychological state in which it is always expecting a fight. In chronic inflammation, the processes of active inflammation, tissue destruction and attempts at healing occur simultaneously. In terms of cytokines, the anti-inflammatory cytokines can’t balance out the excess pro-inflammatory cytokines.

There’s a theory about depression which is gaining momentum within the scientific community, that depression and a number of other psychiatric and neurodegenerative conditions are the result of chronic inflammation which occurs because of chronic stress.

Remember when I said before that psychological stress readies the inflammatory system for potential damage? Well, what if that damage never comes? If there’s chronic psychological stress, the system is constantly being worn down, and never getting a chance to recover. This seems to make sense – chronic stress reduces new nerve cell production and growth, and may interfere with the action of nerve growth factors like BDNF and neurotransmitters like serotonin. Hence why this article by Feelguide seems to ring true.

But is it true? Is depression fundamentally an inflammatory disease, and if so, can we treat it with medications that decrease inflammation, like aspirin?

Let’s go through the various statements made in the Feelguide article and see what the medical evidence says.

First, a necessary correction to avoid confusion. The Feelguide article says that, “New research is revealing that many cases of depression are caused by an allergic reaction to inflammation.” Depression is not an allergic reaction. A true allergy is an antibody response which releases a chemical called histamine from cells called mast cells. If the current theory about depression and inflammation is true, then depression is related to cytokines, chemicals that are entirely different to histamine. It may be really annoying to sneeze like you’re demon possessed if a cat’s been in the same room a week ago, but it’s not going to make you depressed.

Is inflammation caused by obesity, high sugar diets, high quantities of trans fats, unhealthy diets in general? There’s limited evidence that the foods you eat result in inflammation. Most of the positive data comes from observational studies which are relatively weak. Better, stronger studies generally give conflicting information [1]. For example, if high fat, sugary foods were really the cause of low grade inflammation, then diets like the Palaeolithic diet, which replace sugary, fatty processed foods with a bucket load of vegetables should improve inflammation. Yet there have been no statistically significant changes in inflammatory markers recorded in subjects following the Palaeolithic diet [2].

The Feelguide article claims that, “By treating the inflammatory symptoms of depression – rather than the neurological ones – researchers and doctors are opening up an exciting new dimension in the fight against what has become a global epidemic”, but let’s not get too excited. Again, there’s precious little evidence that medications or supplements reported to reduce inflammation make any difference to depression. For example, the article mentions omega-3 and curcumin as having some benefit in the treatment of depression, which is half-right. There’s some evidentiary support that EPA-predominant omega-3 supplements may have some effect on depression, but none at all for DHA omega-3’s [3] or curcumin [4].

When it comes to other medications with an anti-inflammatory effect, the results are similarly mixed. The issue seems to be the specific cellular action of the medication on a particular immune cell in the brain called the microglial cell. For example, normal anti-inflammatory medications like aspirin and other Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) increased the activity of these special microglial cells which resulted in an increase in depressive symptoms in otherwise healthy individuals, whereas a medication called minocycline has been noted to decrease the activity of these microglia, and reduced the risk of depressive symptoms (in animal studies at least) [5].

So we really can’t say whether medications believed to have an anti-inflammatory effect really have any significant benefit. As neuroscientists, Dr Dora Brites and Dr Adelaide Fernandes wrote,

“Nevertheless, we should be cautious in believing that depression can be treated by therapies targeting inflammation. Further studies are required to evaluate whether a combined therapy with anti-inflammatory compounds and antidepressants will result in additional clinical benefits.” [5]

That’s really because we don’t know whether inflammation causes depression, or if depression causes inflammation. The article by Feelguide seem pretty confident, but the science is still a long way from being settled.

The final word is this:
1. Depression is complicated and still poorly understood.
2. It may be related to inflammation, but please don’t rely on herbs or medications that claim to have anti-inflammatory or “immune boosting” properties.
3. If you really want to try and treat your depression without pharmaceutical medications, take some EPA Omega 3 supplements by all means, although I’d encourage you to exercise and engage with a good psychologist too, both of which have more evidence of benefit overall.

References

[1]        Minihane AM, Vinoy S, Russell WR, et al. Low-grade inflammation, diet composition and health: current research evidence and its translation. The British journal of nutrition 2015 Oct 14;114(7):999-1012.
[2]        Pitt CE. Cutting through the Paleo hype: The evidence for the Palaeolithic diet. Aust Fam Physician 2016 Jan-Feb;45(1):35-8.
[3]        Hallahan B, Ryan T, Hibbeln JR, et al. Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression. The British journal of psychiatry : the journal of mental science 2016 Apr 21.
[4]        Andrade C. A critical examination of studies on curcumin for depression. J Clin Psychiatry 2014 Oct;75(10):e1110-2.
[5]        Brites D, Fernandes A. Neuroinflammation and Depression: Microglia Activation, Extracellular Microvesicles and microRNA Dysregulation. Front Cell Neurosci 2015;9:476.

Book review: “Think and Eat Yourself Smart” by Dr Caroline Leaf

Posted on April 26, 2016 by cedwardpitt

Think and Eat Yourself Smart
Dr Caroline Leaf
328 pages, Published by Baker Books USA

My rating: 2 / 10

As a society, we are obsessed with food. With copious food blogs, celebrity chefs and reality cooking shows, food has become more about our social status and self-identity than about nourishment.

Food has always been intimately connected to our health and well-being, and the modern food obsession has taken that to extreme levels as well. Organic, paleo, sugarless, raw food, cleansing and other popular diets have morphed into ‘movements’, the polite shorthand way of describing popular obsessions that are borderline cults.

Trying to cash in on this wave of cultural orthorexia is Dr Caroline Leaf with her latest book, “Think and Eat Yourself Smart”, published in early April by Baker Books.

Dr Leaf describes the book as “an attempt to reintroduce a culture of thinking and effort back into eating, one based on diligently stewarding the body and world God entrusted to us. In the spirit of renewing the mind, it is a lifestyle book that seeks to reimagine what we eat within an integrated spirit, mind and body framework.”

And that would be fine in theory, though in practice, Dr Leaf uses the book more as a vehicle for divulging her personal food preferences and her socio-political ideology while recycling most of her dubious brain science.

But before we go any further, let me issue a disclaimer: There’ll be some who will look this review and assume I’m being critical of Dr Leaf’s book for the sake of being critical. I recognise that I’m not Dr Leaf’s number one fan, however, I want to say from the outset of this review that I have approached this as dispassionately and objectively as I can.

“Think and Eat Yourself Smart” is certainly not all bad. Dr Leaf raises some legitimate issues. For example, she’s critical of the vitamin and supplement industry and the staggering cost of supplements compared to their very limited benefits. She discusses the previous dietary advice regarding low-fat foods, and how the misguided attempt to reduce our dietary fat intake lead to a compensatory increase in starch and sugars. She also discussed the current concerns about too much sugar and refined carbohydrates, and raises the very real problem of food waste and food security. The recipes at the back of the book contain the usual over-rated hipster foodie ingredients like dandelion, kale, quinoa and chia seeds to maintain Dr Leaf’s foodie creds, although some of the recipes themselves sound alright.

Unfortunately, every truth is outweighed by a multiplex of factoids and misrepresentations. Dr Leaf clearly favours organic food, which despite her claims, have not been shown to be better tasting, more nutritious, less toxic, and better for the environment. She’s clearly against genetically modified organisms (or GMO’s), a stance which is more populist than scientific.

Dr Leaf’s underlying premises are also deeply flawed. It’s clear that she’s been heavily influenced by the work of Michael Pollan and other post-modern food gurus of the same ilk. She’s critical of modern food systems including all food processing, food transportation, and supermarkets, claiming that modern agriculture and food processing destroys all nutrients and taste. Dr Leaf claims that “Real food is food grown the way God intended: fresh and nutritious, predominantly local, seasonal, grass-fed, as wild as possible, free of synthetic chemicals, whole or minimally processed, and ecologically diverse.” (p29)

Dr Leaf’s definition of “real food” is nothing more than a romanticised post-modern social construct, and claiming it’s God’s idea doesn’t make it any less misleading. Of course we want our food to be fresh, and we also want it to be nutritious. But fresh and nutritious are not dependent on being local, seasonal, ecologically diverse (whatever that means), grass-fed and wild. In fact, how something can be grass-fed and wild seems contradictory. Processing food makes it safer, and in most cases, more nutritious that the unprocessed farm gate versions. There’s virtually no pesticide residues left on conventional produce either, so that’s a moot point.

In fact, modern food is actually easier to eat and digest, more nutritious, tastier, safer, and longer lasting than ever before in human history. Today’s canned and frozen foods are infinitely healthier than in the past, and in some cases, more nutritious than the vegetables straight off the farm (canned tomatoes, for example, because nutrients are more easily absorbed from cooked tomatoes). Dr Leaf’s idealised view of our agrarian past is false, and the notion that we should return to it is inane.

Dr Leaf also spends a great deal of time trying relate our nutritional health to our thinking. I discussed this in the pre-review of the book, here. She claims that “Research shows that 75 to 98% of current mental, physical, emotional and behavioural illnesses and issues come from our thought life; only 2 to 25% come from a combination of genetics and what enters our bodies through food, Medication, pollution, chemicals, and so on. These statistics show that the mindset behind the meal – the thinking behind the meal – plays a dominant role in the process of human food related health issues, approximately 80 percent.” (p84)

Again, this is a false premise based on bogus science. 75 to 98% of current mental, physical, emotional and behavioural illnesses and issues do not come from our thought life. What you think and how you feel makes no difference to how your body processes the nutrients you put into it.

This excessive focus on the power of thought is a segue back to her previous teaching, a justification as to why she as a self-titled cognitive neuroscientist should be writing about food. Unfortunately, the information contained in the second part of the book makes it obvious that she’s not an expert on either.

Sure, Dr Leaf discusses responsibility and choices which are important to what we put in our mouths, but there are so many other variables that are more intrinsic to our individual diets than just personal responsibility. Like, poverty, income, education, cooking skills or geographic location for example.

Dr Leaf claims that how you think changes how you eat, and how you eat changes how you think. Except the last part of that statement is mutually exclusive to her premise that the mind is separate to the brain and controls the brain. What you put in your mouth might change the function of your brain, but how can that change the way you think if the mind is separate to the brain?

This paradox is the death-knell to her books credibility and usefulness. Not that it makes any difference to Dr Leaf, who conveniently forgets this central tenet of her teaching whenever it suits her.

The advice she provides is also off-track. The answer to processed food isn’t to plant your own garden, or raise your own chickens, or join a local agro-economic food co-op. That sort of advice is impractical for the vast majority of her audience. It excludes everyone who lives in a modern city, or who, like me, has an uncanny ability to kill all but the hardiest of plants. Even her exhortation to eat “real food” is unnecessarily complicated.

Ultimately, Dr Leaf’s advice isn’t dangerous, but just old and confusing. Most of the useful information she gives is obscured by the plethora of unnecessary and irrelevant opinions and factoids. It’s also nothing new. There have been countless books and blogs written by real nutritionists and dieticians that say the same essential things in much simpler ways. Even John Oliver did a better job of explaining problems associated with sugar and our modern food systems (* Warning * – Strong language and adult themes). He’s an agnostic satirical comedian who doesn’t pretend to be a scientific expert, and he still get’s the message across more effectively than Dr Leaf.

To conclude, if you want sound nutritional advice, I’d suggest you head for books by actual dieticians. Professor Rosemary Stanton is one author I would recommend. She’s a Professor of Nutritional Science and Visiting Fellow of the School of Medicinal Sciences at the University of New South Wales. She’s published hundreds of academic and consumer articles including 33 books on good nutrition. She’s been lecturing and writing about good food for longer than I’ve been alive.

In contrast, Dr Leaf’s book “Think and Eat Yourself Smart” is a repackaging of stale opinion and dubious science by an author who isn’t a nutritionist, or even a cognitive neuroscientist for that matter. There might be some helpful advice in there, but it would be difficult for an average reader to pick out what’s beneficial and what’s bogus.

To that end, “Think and Eat Yourself Smart” is a lot like a frozen microwave dinner. It looks good on the packaging, but what you get on the inside isn’t the same. There’s a few nutritional morsels, to be sure, but most of it is just offal and gristle that’s been homogenised to an unrecognisable mush and then reassembled.

If you’re a Dr Leaf devotee, or you’re interested in her socio-political views, then by all means, buy this book. If you want sound nutritional advice, look elsewhere.

“Think and Eat Yourself Smart”: a pre-review

Posted on March 31, 2016 by cedwardpitt

Update: Read my full review of “Think and Eat Yourself Smart” here.

They say, “Never judge a book by its cover.” What about judging it by its marketing?

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. She’s also a wannabe nutritionist. Her latest book is “Think and Eat Yourself Smart”, due for official release at the end of April.

I haven’t read her book yet so I’m not really sure what she’s going to say. It might be a well reasoned and soundly researched discussion about healthy eating, except there are some conflicting ideas that are appearing in Dr Leaf’s own marketing of the book, so I’m not holding out much promise.

For example, yesterday Dr Leaf suggested that “the mindset behind the meal – the thinking behind the meal – plays a dominant role in the process of human food related health issues, approximately 80 percent.”

This is bogus science. It doesn’t matter if I’m convinced that eating a half gallon tub of ice cream is nutritious or not, it’s going to have the same nutritional effect on my body (namely, none). It’s not 80 percent healthy because I believe it’s healthy.

Dr Leaf has made this assertion based on other bogus science – “How does thinking affect eating, and how does eating affect thinking? Research shows that 75 to 98% of current mental, physical, emotional and behavioural illnesses and issues come from our thought life; only 2 to 25% come from a combination of genetics and what enters our bodies through food, Medication, pollution, chemicals, and so on.”

Dr Leaf’s assertion that “75 to 98% of current mental, physical, emotional and behavioural illnesses and issues come from our thought life” is a favourite factoid of hers that forms the basis of most of her teaching. Except that it’s wrong. It has no basis in fact. I’ve discussed this at length in several blogs and in my book (see here for a more detailed explanation of Dr Leaf’s 98% myth).

It’s unclear just how much of her book Dr Leaf has based on this false assumption, but the fact that it’s there in the first place sets a bad precedent for the rest of the book.

Only time will tell, of course. I’d like to be proven wrong, but unfortunately, Dr Leafs latest book seems to be plagued with the same poor science as her other tomes.

Watch this space …

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

Aspartame. Is it more ‘Die’ than ‘Diet’?

Posted on May 5, 2015 by cedwardpitt

A link came around tonight on my Facebook feed about aspartame: “Aspartame is linked to Leukemia and Lymphoma in new Landmark Study on Humans” (http://worldtruth.tv/aspartame-is-linked-to-leukemia-and-lymphoma-in-new-landmark-study-on-humans/)

I’ve seen these sorts of articles come around on social media before, usually in the form of an alternative health website hysterically exaggerating an irrelevant or pseudoscientific study, trying to prove some point about the evils of western medicine or society, or get more internet traffic through sensationalist click-bait.

And I’d heard the whole aspartame-causes-cancer thing before. I’d heard that there was maybe some evidence in animal studies, but that there was no definitive link in humans.

So just from the title, before I’d even read the article, my sceptical mind was primed to expect the opposite of the articles eye-catching headline. I started searching the literature to see if there was any evidence to prove me right.

The first research article I came across that wasn’t on rats was from the American Journal of Clinical Nutrition in 2012, “Consumption of artificial sweetener – and sugar-containing soda and risk of lymphoma and leukemia in men and women” [1]. It was an impressive study in terms of its numbers and its quality. It was drawn from the data of the Nurses Health Study and the Health Professionals Follow-Up Study, which were both prospective studies (which follow a large number of subjects over a long time to see who gets the disease in question, rather than starting with who has the disease in question and trying to work backwards trying to ascertain causes, which is much less reliable). Both studies also had a large number of subjects which increased their statistical power, and made their findings more robust.

The results didn’t look very good for aspartame. There was a clear-cut increase in the risk of Non-Hodgkins Lymphoma for men who consumed two or more serves per day of diet drinks containing aspartame (Relative Risk: 1.69; 95% Confidence Interval: 1.17, 2.45; P-trend = 0.02) and Multiple Myeloma for men who consumed one or more serve per day of diet drinks containing aspartame (RR: 2.02; 95% CI: 1.20, 3.40). However, there was no change in the risks for women who consumed aspartame.

The results certainly caught me a little off guard. Perhaps there was some truth to the alternative website’s assertions after all. Interestingly enough, the study that the worldtruth.tv site reviewed was the same article I’d found. I was guilty of making a snap judgement, and I had to remind myself not to always jump to conclusions.

Still, even though the article wasn’t sensationalist click-bait, some unanswered questions remained. Why was the risk only found in men? Was there a real association, and if so, why the difference. Should we extrapolate this finding like worldtruth.tv did and justifiably ask “will future, high-quality studies uncover links to the other cancers in which aspartame has been implicated (brain, breast, prostate, etc.)?”

In terms of the gender difference, the authors of the original study did have a theory: “We hypothesized that the sex differences we observed may have been due to the recognized higher enzymatic activity of alcohol dehydrogenase type I (ADH) in men, which possibly induced higher conversion rates from methanol to the carcinogenic substrate formaldehyde.” In support of this theory, they looked at the risk of leukaemia and lymphoma in those aspartame users who were drinkers vs the aspartame users who weren’t. Ethanol stops the metabolic conversion of aspartame to formaldehyde, so if their theory was on the right track, those aspartame users who also drank alcohol would have a lower risk. As it turns out, their data was supportive, with aspartame non-drinkers having an increased risk for Non-Hodgkins Lymphoma (RR: 2.34; 95% CI: 1.46, 3.76; P-trend = 0.004) compared with aspartame users who also drank (RR: 0.96; 95% CI: 0.48, 1.90; P-trend = 0.99) [1].

However, despite the findings of Schernhammer et al, a more recent large prospective trial published in the Journal of Nutrition last year found there was no association between soft-drinks of any variety and blood cancers, including those containing aspartame [2].

So the jury is still out on aspartame. Based on what we currently know, if you’re a woman, then there’s no risk of developing leukaemia or lymphoma from drinking diet drinks. If you’re a man, there’s also probably no risk, but a glass or two of alcohol a day would probably make sure of that. Although the best advice is probably to not bother drinking diet drinks at all. The best diet drink is still plain old water, which has virtually no associated risks, is much cheaper, and probably tastes a whole lot better.

References

Schernhammer, E.S., et al., Consumption of artificial sweetener- and sugar-containing soda and risk of lymphoma and leukemia in men and women. Am J Clin Nutr, 2012. 96(6): 1419-28 doi: 10.3945/ajcn.111.030833
McCullough, M.L., et al., Artificially and sugar-sweetened carbonated beverage consumption is not associated with risk of lymphoid neoplasms in older men and women. J Nutr, 2014. 144(12): 2041-9 doi: 10.3945/jn.114.197475

Gluten mad!

Posted on February 24, 2015 by cedwardpitt

Tonight as I was browsing Facebook again, I came across an article a person had posted on gluten. The article claimed that gluten is connected to depression, and indeed, nearly every other neurological disorder for good measure.

Gluten is a protein found in certain grains like wheat, barley and rye. Gluten also makes foods taste better and improves their texture, so it’s often added to everything else.

The “gluten is toxic” meme is a very catchy one that’s doing the rounds again. I first heard of the idea that gluten is the cause of nearly every disease when I was in medical school, when every person I knew who’d seen a naturopath was told they had gluten intolerance and were conned into an unappetising and restrictive diet which didn’t make any of them better.

The same meme is now making it’s way back around again now that the low-fat, sugar-free, zucchini broth-type diet fads are waning.

The proposed link between depression, anxiety and gluten is a new twist to the old story. But with depression becoming a preeminent disease in the 21st century, the link doesn’t surprise me.

So what does the evidence say? Is gluten the culprit behind the modern scourge of mental illness?

I certainly don’t think so, at least according to my interpretation of the medical literature. As far back as 2001, researchers studying the mental health of patients with coeliac disease noted that coeliac disease patients had much higher levels of anxiety and depression than healthy matched controls (up to about three to six times greater in one study), and after a year on a gluten free diet, there were no changes to the rates of anxiety and depression (Addolorato et al., 2001).

In more recent times, larger studies have been performed. Hauser, Janke, Klump, Gregor, and Hinz (2010) confirmed higher levels of anxiety in German female coeliac patients who were on a gluten free diet, compared to the normal controlled population. Mazzone et al. (2011) showed that children with coeliac disease on gluten-free diets for about 7 years on average still showed an increased rate of anxiety and depression symptoms and showed higher scores in “harm avoidance” and “somatic complaints” as compared to healthy control subjects.

A larger cross sectional survey was performed in the Netherlands in 2013, on 2265 adults with coeliac disease (van Hees, Van der Does, & Giltay, 2013). That survey showed that a significantly higher proportion of those with coeliac disease, despite being on a strict gluten free diet, reporting a higher rate of anxiety and depression compared to the general population. It also showed (albeit in a smaller subgroup of respondents) that poor adherence with a gluten free diet did not affect the likelihood of depressive symptoms.

To be fair, cross sectional surveys and longitudinal cohorts aren’t necessarily the strongest form of evidence, but it is the best we’ve currently got. There was a recent randomised controlled trial, a stronger form of evidence, looking at the effect the introduction of gluten had on depressive symptoms in people who did not have coeliac disease but reported gluten sensitivity and were controlled on a gluten free diet (Peters, Biesiekierski, Yelland, Muir, & Gibson, 2014). While this showed some worsening of depressive symptoms in those subjects given gluten, the exposure was short, the effect was moderate, and the results should be considered cautiously given the small number of subjects reduced the power of the study.

Given the weight of evidence, I can’t help but be sceptical of books touting the ‘gluten = depression’ theory, books like “Grain Brain”. It’s author, American neurologist Dr David Perlmutter, attests that more than 38 different diseases are caused by gluten, including autism and depression. If you believe the celebrity chiropractor who reviewed Perlmutter’s work (http://www.glutenfreesociety.org/gluten-free-society-blog/gluten-leaky-brain-the-connection-to-depression/), increased intestinal permeability and intestinal dysbiosis (“leaky gut” and bad gut bacteria) combine to increase inflammation in the blood and in the brain, causing depression.

But correlation does not equal causation. Just because brain diseases, inflammation and gut problems tend to occur together does not prove that gut problems cause inflammation and brain problems. Rather, the evidence suggests that it’s the other way around, with all of the processes linked to genetics.

For example, autism is related to a number of genes that both reduce the proteins that help nerve cells grow branches (Won, Mah, & Kim, 2013), and at the same time, switch on a low grade form of inflammation (Onore, Careaga, & Ashwood, 2012). I believe it’s the pre-existing inflammation that adds to the cellular dysfunction of the brain and at the same time, promoting low grade inflammation of a number of organs, including the gut. It’s the pre-existing inflammation that causes the gut to become “leaky”, not the “leaky” gut causing the inflammation.

Because if gluten was the primary cause, then why do people with coeliac disease who do not eat gluten report more depressive and anxious symptoms than control groups who do eat gluten? Why would those with coeliac disease who are eating sporadic gluten be just as depressed as those patients who do not?

If you don’t have coeliac disease, then gluten free diets are just like Amway products. You really don’t need them, and you could probably do much better without them. All you’re really doing is just making someone else obscenely rich.

Not only are you wasting your money, but you might also be harming your health by eating gluten free foods, since most foods that are stripped of gluten are also stripped of most of their other nutrients.

As Nash and Slutzky (2014) summarise, “Every major change in our diet carries with it the possibility of unforeseen risks. Many readers — the general public, as well as medical professionals — accept what they read at first glance. Myths have been part of our medical lore for millennia. Those jumping on the gluten-free/high-fat bandwagon may be disappointed when their symptoms are not mitigated; more critically, they may be at increased risk for other, more dangerous ailments.”

If you really think you feel better off gluten, then talk to your doctor or registered dietician to make sure you remain healthy off it.

References

Addolorato, G., Capristo, E., Ghittoni, G., Valeri, C., Masciana, R., Ancona, C., & Gasbarrini, G. (2001). Anxiety but not depression decreases in coeliac patients after one-year gluten-free diet: a longitudinal study. Scand J Gastroenterol, 36(5), 502-506.

Hauser, W., Janke, K. H., Klump, B., Gregor, M., & Hinz, A. (2010). Anxiety and depression in adult patients with celiac disease on a gluten-free diet. World J Gastroenterol, 16(22), 2780-2787.

Mazzone, L., Reale, L., Spina, M., Guarnera, M., Lionetti, E., Martorana, S., & Mazzone, D. (2011). Compliant gluten-free children with celiac disease: an evaluation of psychological distress. BMC Pediatr, 11, 46. doi: 10.1186/1471-2431-11-46

Nash, D. T., & Slutzky, A. R. (2014). Gluten sensitivity: new epidemic or new myth? Every major change in our diet carries with it the possibility of unforeseen risks. Am J Cardiol, 114(10), 1621-1622. doi: 10.1016/j.amjcard.2014.08.024

Onore, C., Careaga, M., & Ashwood, P. (2012). The role of immune dysfunction in the pathophysiology of autism. Brain Behav Immun, 26(3), 383-392. doi: 10.1016/j.bbi.2011.08.007

Peters, S. L., Biesiekierski, J. R., Yelland, G. W., Muir, J. G., & Gibson, P. R. (2014). Randomised clinical trial: gluten may cause depression in subjects with non-coeliac gluten sensitivity – an exploratory clinical study. Aliment Pharmacol Ther, 39(10), 1104-1112. doi: 10.1111/apt.12730

van Hees, N. J., Van der Does, W., & Giltay, E. J. (2013). Coeliac disease, diet adherence and depressive symptoms. J Psychosom Res, 74(2), 155-160. doi: 10.1016/j.jpsychores.2012.11.007

Won, H., Mah, W., & Kim, E. (2013). Autism spectrum disorder causes, mechanisms, and treatments: focus on neuronal synapses. Front Mol Neurosci, 6, 19. doi: 10.3389/fnmol.2013.00019

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

Dr C. Edward Pitt

Faith, Hope, Love, Science.

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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?