Is sunshine healthy again?

  • New study claims avoiding the sun is as dangerous as smoking
  • Study found women in Sweden who had greatest sun exposure had lowest risk of dying from heart disease/stroke and death overall
  • But study failed to consider exercise as possible cause of improved health in cohort
  • UV exposure clearly linked to cancer risk
  • Safe sun exposure for most people still a few minutes of sunlight to face, arms and hands in the morning and evening

I live in Queensland.  Queensland is the Sunshine State, so named because we boast about having the most hours of sunshine than any other state in Australia (we actually don’t have the most sunshine in Australia, but we like to remain pleasantly deluded).

We’re blessed with temperatures that vary from pleasantly warm to oppressive and humid, but with an outdoor climate and a coastline that boasts some of the world’s most beautiful beaches, traditionally, Queenslanders have enjoyed lots of time in the sun.

In the 1960’s and 70’s, it was fashionable, and even considered healthy, to have a deep brown tan, even if that meant burning yourself to a lobster-red colour in order to achieve it.  Then in the 1980’s, we had a rethink because of the large number of skin cancers that were appearing.  I remember being at school in the 1980’s and being indoctrinated with the “Slip Slop Slap” mantra, “Slip on a shirt, slop on some sunscreen, and slap on a hat”.

Now, in the mid twenty-teens, the trend in sun avoidance behaviour has almost led us back to the Victorian era of full body swimsuits, enormous hats and constant shade seeking.  Tan’s are considered unhealthy, and if you get burnt enough to peel, everyone tells you that you’re going to die of melanoma.

If the trend continues, the next generation will be anaemic zombies whose only light exposure will be from LED devices.  Actually, come to think of it, that IS the current generation …

Given our carcinophobic sun-avoidance, I was surprised to see an article come across my social media feed entitled, “Avoiding sun as dangerous as smoking”.

Oh my goodness, was this another thing we’ve been get wrong all these years?  Should I start promoting tans again?  Should I be in my backyard in my underwear trying to get one myself?

As it turns out, I can keep my clothes on, much to the relief of my neighbours.

The study in question is a 20 year follow up of nearly 30,000 women in Sweden [1].  They measured their sun exposure habits at entry to the study, and throughout the two decades of follow up, and they found a nice linear relationship between their sun exposure and their overall mortality.

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The authors stated that, “Nonsmokers who avoided sun exposure had a life expectancy similar to smokers in the highest sun exposure group, indicating that avoidance of sun exposure is a risk factor for death of a similar magnitude as smoking.”

This is sometimes where reading medical literature can be confusing.  I can imagine some people thinking, “Well, that means if I want to spend all day on the beach, I can protect myself by taking up smoking.”  So let’s take a step back here before we swap our sunblock for a packet of ciggies.  We have to be careful in how we apply this information from this study.

For a start, this research was done on women living in Sweden, where the climate is slightly different from living in the tropics.  There isn’t much sun in Sweden, and when it does come out, it’s not very intense.  That’s a big different from living in climates like Queensland where standing in the sun for an hour does to us what my microwave does to my leftovers.

We know that UV radiation is bad for us.  Tanning beds increase the risk of melanoma [2] and sunscreen decreases it [3].  When the current study broke down their numbers, the all-cause mortality related to sun-exposure was lower, but the cancer risk was higher.

Despite the risk of cancer increasing with sun-exposure, the cardiovascular causes of death were much lower, but this may be nothing to do with sun-exposure at all, but may be all to do with exercise, something the study failed to account for as an independent variable.  Time outside is usually going to be active time – exercising, gardening, walking, etc., and it may simply have been that those women who had the most sun exposure also did the most exercise or were the most active, which is common sense.

So the article isn’t able to prove that the health benefits which they ascribe to sunlight aren’t from something else.  Their cohort of subjects also doesn’t allow for a broad application of the results given their lack of UV intensity in their climate compared to other parts of the world.

I don’t think this study is enough to reverse the current wisdom about sun exposure.  It’s ok to have a few minutes of exposure to sunlight on your face, arms and hands most of the year, although some people in areas of higher latitudes (closer to the poles than the Equator) may need some more sun exposure in winter.  Look at information from a cancer council in your area for locally appropriate information.

So, keep your pants on, and the rest of your clothes for that matter.  We don’t need to expose ourselves and get a tan to live a longer life.

References

[1]        Lindqvist PG, Epstein E, Nielsen K, Landin-Olsson M, Ingvar C, Olsson H. Avoidance of sun exposure as a risk factor for major causes of death: a competing risk analysis of the Melanoma in Southern Sweden cohort. Journal of internal medicine 2016 Mar 16.
[2]        Boniol M, Autier P, Boyle P, Gandini S. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. Bmj 2012;345:e4757.
[3]        Green AC, Williams GM, Logan V, Strutton GM. Reduced melanoma after regular sunscreen use: randomized trial follow-up. Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2011 Jan 20;29(3):257-63.

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The truth about ADHD

ADHD is always a popular topic … and an apoplexic topic. Any mention of ADHD seems to induce everyone within ear-shot to uncontrollably expectorate their half-baked opinion on the subject, like the Tourette’s syndrome of ignorance.

I’ve heard them all over the years …

ADHD is over diagnosed.
ADHD is just a label for bad parenting.
ADHD is caused by sugar.
ADHD is caused by food colouring / preservatives / gluten / (any other fad ‘toxin’)
ADHD is cured by diet / meditation / supplements / swiss balls.
ADHD medication (Ritalin) is overused / irresponsible / lazy parenting / harmful / ungodly.
ADHD doesn’t exist in France.
ADHD doesn’t exist at all.

I could go on, but if I do, I’m just going to get myself in a tizz.

ADHD is the new AIDS. There is so much misinformation and discrimination surrounding ADHD in our modern enlightened society that the stigma is worse than the actual illness, which really says something about how badly ADHD is treated in our communities.

One of the cruellest aspects of the cultural mismanagement of ADHD is the fact that it maligns the sufferers while simultaneously isolating them from much needed support. Saying that children with ADHD should just behave themselves, or parents of children with ADHD should just have better parenting skills is victim blaming at its worst.

In order to counter the prevalent ignorance of ADHD, even just a little, I want to give a crash course on the science so that at least somewhere on the searchable web, there is a counterbalance to the thousands of misinformed arm-chair ‘experts’ whose only experience with ADHD is reading the misguided perspectives of other so-called ‘experts’.

ADHD stands for Attention Deficit Hyperactivity Disorder.

The current formal definition that must be matched to have a diagnosis of ADHD is:

  1. Inattention: Six or more symptoms of inattention for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of inattention have been present for at least 6 months, and they are inappropriate for developmental level:
    * Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
    * Often has trouble holding attention on tasks or play activities.
    * Often does not seem to listen when spoken to directly.
    * Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., loses focus, side-tracked).
    * Often has trouble organizing tasks and activities.
    * Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
    * Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
    * Is often easily distracted
    * Is often forgetful in daily activities.
  1. Hyperactivity and Impulsivity: Six or more symptoms of hyperactivity-impulsivity for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for the person’s developmental level:
    * Often fidgets with or taps hands or feet, or squirms in seat.
    * Often leaves seat in situations when remaining seated is expected.
    * Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
    * Often unable to play or take part in leisure activities quietly.
    * Is often “on the go” acting as if “driven by a motor”.
    * Often talks excessively.
    * Often blurts out an answer before a question has been completed.
    * Often has trouble waiting his/her turn.
    * Often interrupts or intrudes on others (e.g., butts into conversations or games)

In addition, the following conditions must be met:
– Several inattentive or hyperactive-impulsive symptoms were present before age 12 years.
– Several symptoms are present in two or more setting, (e.g., at home, school or work; with friends or relatives; in other activities).
– There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.
– The symptoms do not happen only during the course of schizophrenia or another psychotic disorder.
– The symptoms are not better explained by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder.

(http://www.cdc.gov/ncbddd/adhd/diagnosis.html)

In Australia, ADHD cannot be formally diagnosed by anyone other than a paediatrician or a psychiatrist. So even as an experienced GP, I can’t officially diagnose it. The school counsellor or local naturopath can’t diagnose it. You can’t just pluck it out of the air. The diagnosis can only come from a medical specialist with at least a decade of university level training.

The official prevalence rate of ADHD (the number of people with a current diagnosis) is only 5%. According to some US based community surveys, nearly a half of those children are not on medication for it (http://www.cdc.gov/ncbddd/adhd/data.html). So much for Ritalin being overprescribed.

Stimulants vs nothing

ADHD is a predominantly genetic disorder which leads to specific structural deficiencies in the brain. Children with ADHD have a significant global reduction in the volume of grey matter, most prominently in a part of the brain called the right lentiform nucleus. These changes usually improve with age and improve with stimulant medication. There is also evidence of changes to the shape and size of other brain structures such as the amygdala and the thalamus (areas of the brain integral to sensory and emotional processing). Early evidence also exists which suggests changes in the white matter pathways connecting a number of critical brain regions. Studies investigating brain development have estimated that the frontal lobe development of ADHD children lags that of normal children by an average of about three years.

These changes in the brain are not caused by the child’s behaviour, since other studies have shown the same changes in the brains of unaffected first degree relatives (brothers or sisters), just to a milder degree.

Modern functional imaging techniques show that the brains of children with ADHD have abnormally low functioning in most of the brain structures related to attention and planning (numerous areas of the frontal cortex as well as the basal ganglia, thalamus and parietal cortices). At the same time, there is extra activity in portions of the brain related to the Default Mode Network (the day-dreaming part of your brain). So children with ADHD have brains in which the ‘day-dreaming’ network activity persists into, or emerges during, periods of task-related activity. This takes processing power away from the competing task-specific processing causing a deficit in performance. Studies show that Ritalin normalises this dysfunction.

The best evidence suggests that dopamine is the main neurotransmitter involved in ADHD. Other neurotransmitters are likely to be involved but the evidence is still being confirmed. Medications like Ritalin improve ADHD symptoms by increasing the amount of dopamine that the nerve cells have access to, improving the clarity of the signal between them.

Underlying all of these neural changes are genetics. While there have been no specific genes discovered in research thus far, twin studies have demonstrated a heritability of ADHD of up to 76%. The most significant environmental factors that are responsible for the remainder of the influence on ADHD are not nutritional factors such as sugar or food additives, but are low birth weight/prematurity and exposure to smoking during pregnancy.

Are there any better treatments for ADHD other than stimulants like Ritalin? Other non-stimulant medications are available although at this stage, Ritalin and Dexamphetamine still out-perform them. Cognitive therapies may mimic some of the brain changes of Ritalin but it is not clear whether the effectiveness of cognitive therapies are equal to or better than the stimulant medications. What is clear is that Ritalin doesn’t lead to a euphoric state (a “drug high”) when given orally. So children can not get addicted to Ritalin when used responsibly.

In summary, ADHD exists. It’s caused by the interaction of a number of genes and some environmental factors such as those related to prematurity, low birth weight and maternal smoking, which alter the growth and development of the brain, specifically the grey matter of the frontal cortex, the basal ganglia and thalamus, and the pathways which connect them. These structural changes cause the day-dreaming part of the brain to be more active and the attention and planning parts of the brain to be less active.

ADHD is not caused by food additives or sugar. There is no evidence that autoimmunity plays a significant part. Forcing your child to consume bone broth or stop eating gluten will not cure them.

ADHD is not caused by bad parenting. Ritalin is not evil. Medications like Ritalin and Dexamphetamine have been shown to improve the functioning of children with ADHD and improve their underlying neurological deficits.

It’s time to cut the crap. Our culture needs to stop victimising the child with ADHD and their parents, who already suffer enough from the ADHD without ignorant busy-bodies and self-titled experts chiming in and making their suffering even more pronounced. It’s time to stop judging those who choose the best for their child by medicating them, who do so in spite of the unfair and ill-informed criticism of everyone from their mother-in-law to the milkman when they do. It’s time to remove the stigma from one of the most common psychiatric disorders of childhood so that every child has an equal chance of growing into an adult that can realise their full potential.

That’s the truth about ADHD.

Bibliography:

Cortese, S. (2012). The neurobiology and genetics of Attention Deficit/Hyperactivity Disorder (ADHD): what every clinician should know. Eur J Paediatr Neurol, 16(5), 422-433. doi: 10.1016/j.ejpn.2012.01.009

Dr Caroline Leaf and the obesity overstatement

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Caroline Leaf is on the nutritional warpath.

Our society isn’t the best when it comes to eating right. Fast food and junk food are more attractive options than fresh food, and nearly everyone knows it. Today, the internet is flooded with celebrity chefs and self-titled experts attempting to leverage some profit by advocating their own brand of diet or herb as the simple solution to what is a deceptively complex problem.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. In recent times she has also jumped on to the nutritional bandwagon, advocating organic gluten free recipes through food-selfies, and reposting Jamie Oliver quotes.

Today’s meme follows a similar line, where she has reposted an image which fits with her personal cognitive bias – a picture of french-fries in a cigarette packet, accompanied by the tag line, “THE OBESITY DEATH RATE IS OVERTAKING CIGARETTE SMOKING. Consume with caution”.

The image is a case study in overstatement. According to the most recent Global Burden of Disease data (currently 2010), the death rate associated with cigarette smoking is currently 91.4 per 100,000 population while the death rate associated with a high BMI is only 48.1 per 100,000 population. Even extrapolating the figures to the current year, the predicted rates would still be 89.1 vs 51.9 respectively, which are still a long way apart. On the current trends, obesity won’t overtake smoking as a global cause of death until 2055. So saying the obesity death rate is overtaking cigarette smoking is like saying that Christmas is coming – it’s technically true, but it’s still a long way off.

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There are a couple of reasons why deaths associated with obesity are rising while the deaths associated with cigarette smoking are falling. The most obvious is that cigarette smoking is decreasing, but treatments for smoking related illnesses are also concurrently improving, so less people are getting sick from cigarette smoking and those that do are less likely to die.

Of course, it’s no secret that more people, especially in the western world, are getting fatter. The old assumption was that obesity contributed to metabolic syndrome which then caused heart disease and type 2 diabetes and a concomitant rise in deaths. However, new evidence casts serious doubt over these assumptions.

In a meta-analysis of the association of mortality to BMI, Flegal, Kit, Orpana, and Graubard (2013) showed that overweight people have a slightly lower death rate than normal weight people, those with mild obesity have the same risk of death as normal weight people, and that the overall risk of all classes of obesity was small (relative risk 1.18 (95% CI, 1.12-1.25)). As a comparison, the risk of death from cigarette smoking is up to 2.66 (Shavelle, Paculdo, Strauss, & Kush, 2008)**.

The key to understanding this paradox is found in another meta-analysis, by Kramer, Zinman, and Retnakaran (2013) They showed that obesity and metabolic dysfunction are separate entities, with metabolically healthy obese people having the same risk of death as metabolically healthy people of normal weight (RR 1.19 (95% CI 0.98 to 1.38)) while metabolically unhealthy people with a normal weight had a risk three times that (RR 3.14 (95% CI, 2.36 to 3.93)).

So the key isn’t whether someone’s obese or not, the key is whether someone’s metabolically healthy or not (which is another blog for another time). According to the latest scientific evidence, the obesity death rate probably isn’t related to obesity after all.

Dr Leaf might be on the nutritional warpath with the right intentions, but her lack of expertise and willingness to fact-check is showing with every meme. If she wants to continue portraying herself as an expert in the area of food and nutrition, she needs to move away from her personal biases and start promoting proper science.

References

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

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

Shavelle, R. M., Paculdo, D. R., Strauss, D. J., & Kush, S. J. (2008). Smoking habit and mortality: a meta-analysis. J Insur Med, 40(3-4), 170-178.

Graph data: Institute for Health Metrics and Evaluation (IHME). GBD Database. Seattle, WA: IHME, University of Washington, 2014. Available from http://www.healthdata.org/search-gbd-data. Accessed 15/1/2015

** This means that a smoker is more than twice as likely to die compared to a non-smoker, but an obese person’s risk is only about one fifth more likely to die compared to a person with a normal body mass index.

Fat checking … sorry, fact checking

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As I was living vicariously on Facebook again this afternoon, I came across a forwarded page from nutritionist Christine Cronau. She was previewing tonight’s (Australian) ABC episode of Catalyst, on the topic of the low fat diet.

It’s not that she or the ABC are necessarily wrong about low fat diets. Some scientists have been sceptical of the evidence for low fat diets every since they were proposed in the late 1970’s [1]. Often, low fat foods have been manufactured with extra sugar to make them palatable again [2]. So while western consumers have been thinking they’ve been doing the right thing, they’ve probably been making the problem worse.

We’re also a society of carnivores, and the meat consumed in modern society is much higher in saturated fat. Plant and seafood based diets contain a high number of poly-unsaturated fatty acids (omega-3 and omega-6) which has also been a recommendation for our heart health, however a study in JAMA in 2012 suggested that high levels of omega-3 PUFAs did not protect from cardiovascular disease or reduce all cause mortality [3]. On the other hand, it appears that reviews of scientific research have suggested that saturated fat doesn’t pose a significant risk for cardiovascular disease or all-cause mortality either [4].

So it’s true that we may have to review exactly why plant based diets are good for us. What I raised an eyebrow at was her suggestion that, “What in the world did we do before cholesterol-lowering meds? Oh, that’s right, before we started mass producing sugar and back when we enjoyed plenty of saturated fat, heart disease was pretty much non-existent.”

This is a classic case of “two wrongs don’t make a right”. Sure, low fat diets are probably not the all-glorious panacea that they were touted to be, but suggesting that heart disease didn’t exist before the rise of sugar and low fat foods is grossly inaccurate. A quick glance at the data of the Australian Bureau of Statistics shows that heart disease peaked in the late 1960’s, which was coincidentally before we started mass producing sugar and back when we enjoyed plenty of saturated fat, and has since dropped significantly.

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Is that because of dietary guidelines recommending a low fat diet? There are many contributors to heart disease, so low fat diets can’t be singled out as the sole cause, especially in light of the reviews I discussed above. The reduction of smoking may be part of it, as smoking has dropped in the same amount of time, although a significant proportion of our population still smoke.

Whatever the reason, it isn’t a good reflection when you try and support your argument against a fallacy with a fallacy of your own. I haven’t read any of her other material, so her books maybe quite cogent. However, Ms Cronau’s Facebook post today provides a good example of how cognitive biases can sometimes blind us to facts that don’t agree with our chosen position, and why we all need to be careful when evaluating the evidence of “experts” on line.

References

  1. La Berge, A.F., How the ideology of low fat conquered america. J Hist Med Allied Sci, 2008. 63(2): 139-77 doi: 10.1093/jhmas/jrn001
  2. Malnick, E., et al. Low fat foods stuffed with ‘harmful’ levels of sugar. The Telegraph, 2014. http://www.telegraph.co.uk/health/healthnews/10668189/Low-fat-foods-stuffed-with-harmful-levels-of-sugar.html
  3. Rizos, E.C., et al., Association between omega-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis. JAMA, 2012. 308(10): 1024-33 doi: 10.1001/2012.jama.11374
  4. Hoenselaar, R., Saturated fat and cardiovascular disease: the discrepancy between the scientific literature and dietary advice. Nutrition, 2012. 28(2): 118-23 doi: 10.1016/j.nut.2011.08.017

Dr Caroline Leaf and the genetic fluctuations falsehood

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While idling away on Facebook, as is my usual pass time, I came upon Dr Leaf’s Facebook feed. There were her usual self-indulgent holiday happy-snaps and another couple of Pinterest-style fluffy inspirational posts. Then this: “Our genetic makeup fluctuates by the minute based on what we are thinking and choosing”.

Dr Caroline Leaf is a South African born and trained, US based, communication pathologist. She also claims that she’s a cognitive neuroscientist. Given the quality of the posts on her social media pages recently, no one could ever take such a claim seriously.

To make sure we’re all clear about what she just said, I’m going to say it again: “Our genetic makeup fluctuates by the minute based on what we are thinking and choosing”. It was an astonishing, if not bewildering statement, especially coming from someone with a PhD level education. If Dr Leaf were a medical doctor and publically made a statement like that, her registration would be reconsidered.

The core of the statement, which pushes it so far beyond the boundaries of rational scientific thinking, is the phrase “Our genetic makeup fluctuates by the minute.”

DNA in our cells is like an old audio cassette tape. Audio cassette tape is a long magnetic stripe, storing the code which the tape player decodes as sound. DNA is a chemical string which has a sequence of “bases” off to the side. The full DNA molecule is made of two matching strings joined by chemical bonds between the bases (hence the name, “base pairs”). Depending on what the cell needs, it runs the DNA through a decoder to either copy it, or to ‘play’ it (i.e. using the information stored in the code to build new proteins).

Like the tape in an audio cassette, the code of the DNA is incredibly stable. The rate of DNA mutation is about 1 in 30 million base pairs [1]. DNA doesn’t ‘fluctuate’, (“rise and fall irregularly in number or amount” [2]). It’s not the stock market. The number of genes in each cell of my body does not rise or fall depending on whether I’m having a good hair day.

The other part of Dr Leaf’s statement, that our DNA “fluctuates … based on what we are thinking and choosing” is also scientific nonsense. The only way that your thoughts and choices are capable of inducing genetic mutations is if those thoughts or choices involve cigarette smoking or standing next to industrial sources of ionising radiation.

I think Dr Leaf is trying to say that our thoughts and choices can change our gene expression, which is the construction of new proteins from the instructions in the DNA code. However, gene expression has nothing to do with our thoughts and choices. IVF embryos are expressing genes like crazy as they grow from one cell to an embryo in just a petri dish. It doesn’t think or choose.

More often than not, our thoughts and our choices are the result of gene expression, not the cause of it. We don’t have any specific control over the process either. The process of genetic expression is dependant on a complex series of promoters and tags on the DNA, which are controlled by other proteins and DNA within the cell, not thought or choice.

The truth is that gene expression occurs moment-by-moment, regardless of what we think or don’t think, do or don’t do. Gene expression is simply DNA being read. Our genetic makeup, the DNA code, is stable. It does not fluctuate. There is no part of Dr Leaf’s statement that is scientifically accurate.

Ultimately, Dr Leaf continues on her pursuit of pseudoscience, an affront to the people who trust her to tell them the truth, and the God of all truth that she purportedly represents.

References

  1. Xue, Y., et al., Human Y chromosome base-substitution mutation rate measured by direct sequencing in a deep-rooting pedigree. Curr Biol, 2009. 19(17): 1453-7 doi: 10.1016/j.cub.2009.07.032
  2. Oxford Dictionary of English – 3rd Edition, 2010, Oxford University Press: Oxford, UK.

Dr Caroline Leaf and the genetic remodelling myth

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We are all slowly mutating!

Yep, it’s true. Not to the same extent as you might see in shows like X-Files or Dr Who, but still, our DNA is slowly accumulating permanent changes to the pattern of the genes that it contains. Thankfully, it’s only in science fiction that the mutations result in zombie apocalypse scenarios.

Dr Caroline Leaf is a Communication Pathologist and a self-titled cognitive neuroscientist. Still glowing from the unquestioning adulation of her faithful followers at the Switch On Your Brain conference last week, Dr Leaf has hit social media again. Most of her posts have been innocuous quotes that look borrowed from Pinterest, but today, Dr Leaf has ventured into the pseudoscientific again by claiming that, “Our genes are constantly being remodeled by our response to life’s experiences.”

Unless your response to life’s experiences is to stand next to an industrial microwave generator or live in a nuclear waste dump, Dr Leaf’s statement is pure fiction. Dr Leaf confuses the mutation of our genes with the expression of our genes.

The only way our genes actually change is through mutation. A mutation is a permanent change in the sequence of the DNA molecule. A genetic mutation is a permanent change in the DNA sequence that encodes a gene. DNA is constantly mutating, because of environmental damage, chemical degradation, genome instability and errors in DNA copying or repair [1: p97]. Still, the actual rate of DNA mutation is about 1 in 30 million base pairs [2]. So DNA is very stable, and changes for a number of reasons, only some of which are related to our external environment. And as I alluded to just before, slightly tongue-in-cheek, our responses are not the main contributor to these environmental influences, unless we deliberately expose ourselves to ionizing radiation or smoke cigarettes. Our DNA does not change because of our thought processes as Dr Leaf advocates [3].

What does change more readily is the expression of those genes. Gene expression is the cell machinery reading the genes and making the proteins that the genes encode. The genes are expressed to make the proteins needed for the cell to maintain its function. Which genes are expressed is dependant on the cell’s stage of development and the environment it finds itself in. For example, when the body encounters a high level of dietary iron, a series of steps activates a gene to promote the production of ferritin, a protein that helps to carry iron in the blood stream [1: p375-6]. Gene expression isn’t solely dependent on our environment though, because an embryo is expressing genes like crazy in order to make the proteins to build a human being, but the gene expression in an embryo is largely following a pre-determined time course, not the environment [4] (and certainly not because of responses to life’s experiences).

In summary, our genes are controlled by a myriad of different factors, nearly all of which have nothing to do with our responses or choices. Our genes are not changed by our choices or our responses. Our genes may be mutating, but God designed our cells with mechanisms to repair them. Our genes are not being remodelled by our responses. That’s the realm of science fiction.

References

  1. Strachan, T. and Read, A., Human Molecular Genetics. 4th ed. 2011, Garland Science, New York, USA:
  2. Xue, Y., et al., Human Y chromosome base-substitution mutation rate measured by direct sequencing in a deep-rooting pedigree. Curr Biol, 2009. 19(17): 1453-7 doi: 10.1016/j.cub.2009.07.032
  3. Leaf, C.M., Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health. 2013, Baker Books, Grand Rapids, Michigan:
  4. Ralston, A. and Shaw, K. Gene Expression Regulates Cell Differentiation. Nature Education, 2008. 1(1): 127; http://www.nature.com/scitable/topicpage/gene-expression-regulates-cell-differentiation-931

Like to read more about Dr Leaf’s teaching and how it compares to current science? Download the free eBook HOLD THAT THOUGHT, Reappraising The Work Of Dr Caroline Leaf

Dr Caroline Leaf – Contradicted by the latest research

This is my most popular post by far.  I truly appreciate the support and interest in this post, but I’ve discovered and documented a lot more about Dr Leaf’s ministry in the last two years.  I welcome you to read this post, but if you’d like a more current review of the ministry of Dr Caroline Leaf, a new and improved version is here:
Dr Caroline Leaf – Still Contradicted by the Latest Evidence, Scripture & Herself

* * * * *

Mr Mac Leaf, the husband of Dr Caroline Leaf, kindly took the time to respond to my series of posts on the teachings of Dr Leaf at Kings Christian Centre, on the Gold Coast, Australia, earlier this month. As I had intended, and as Mr Leaf requested, I published his  reply, complete and unabridged (here).

This blog is my reply.  It is heavily researched and thoroughly referenced.  I think it’s fair to say that while Dr Leaf draws her conclusions from some scientific documents, there is more than enough research that contradicts her statements and opinions.  I have only listed a small fraction, and only on some of the points she raised.

In fairness, the fields of neurology and neuroscience are vast and rapidly expanding, and it is impossible for one person to cover all of the literature on every subject.  This applies to myself and Dr Leaf.  However, I believe that the information I have read, and referenced from the latest peer-reviewed scholarly works, do not support Dr Leaf’s fundamental premises.  If I am correct, then the strength and validity of Dr Leaf’s published works should be called into question.

As before, I welcome any reply or rebuttal that Dr Leaf wishes to make, which I will publish in full if she requests.  In the interests of healthy public debate, and encouraging people to make their own informed decisions on the teachings of Dr Leaf, any comments regarding the response of Mr Leaf, Dr Leaf or myself, are welcome provided they are constructive.

This is a bit of a lengthy read, but I hope it is worthwhile.

Dear Mr Leaf,

Thank you very much for taking the time out to reply to some of the points raised in my blog.  I am more than happy to publish your response, and to publish any response you wish to make public.

ON INFORMED DECISIONS

I published my blog posts to open up discussion on the statements made by Dr Leaf at the two meetings that I attended at Kings Christian Centre on the Gold Coast.  As you rightly point out, people should be able to make informed decisions.  A robust discussion provides the information required for people to make an informed choice.  Any contributions to this discussion from either yourself or Dr Leaf would be most welcome.

I apologise if you interpreted my blogs as judgemental, or if you believe there are any misunderstandings.  You may or may not have read my final two paragraphs from the third post, in which I acknowledged that I may have misunderstood where she was coming from, but that I would welcome her response.  If there were any misunderstandings, it is likely because Dr Leaf did not make any attempt to reference any of the statements she made on the day.  You may argue that she was speaking to a lay audience, and referencing is therefore not necessary.  However, I have been to many workshops for the lay public by university professors, who have extensively referenced their information during their presentations.  A lay audience does not preclude providing references.  Rather, it augments the speakers authority and demonstrates the depth of their knowledge on the subject at hand.

YOUR DEFENCE

It’s interesting that you feel the need to resort to defence by association, and Ad Hominem dismissal as your primary counter to the points I raised.

Can you clarify how attending the same university as Dr Christaan Barnard, or a Nobel laureate, endorses her arguments or precludes her from criticism?  I attended the University of Queensland where Professor Ian Frazer was based.  He developed the Human Papilloma Virus vaccine and was the 2006 Australian of the Year.  Does that association enhance my argument?

Can you also clarify why a reference from a colleague was preferred to letting Dr Leaf’s statements and conclusions speak for themselves?  Dr Amua-Quarshie’s CV is certainly very impressive, no doubt about that, although he doesn’t list the papers he’s published.  (I’m assuming that to hold the title of Adjunct Professor, he’s published peer-reviewed articles.  Is he willing to list them, for the record?)

Whatever his credentials, his endorsement means very little, since both Dr Leaf and Dr Amua-Quarshie would know from their experience in research that expert opinion is one of the lowest forms of evidence, second worst only to testimonials [1].  Further, both he and Dr Leaf are obviously close friends which introduces possible bias.  His endorsement is noteworthy, but it can not validate every statement made by Dr Leaf.  Her statements should stand up on their own through the rigors of critical analysis.

On the subject of evidence, disparaging your critics is not a substitute for answering their criticism.  Your statement, “By your comments it is obvious that you have not kept up to date with the latest Scientific research” is an assumption that is somewhat arrogant, and ironic since Dr Leaf is content to use superseded references dating back to 1979 to justify her current hypotheses.

DR LEAF’S EVIDENCE

In the blog to which you referred, Dr Leaf makes a number of statements that are intended to support her case.  These include the following.

“A study by the American Medical Association found that stress is a factor in 75% of all illnesses and diseases that people suffer from today.”  She fails to reference this study.

“The association between stress and disease is a colossal 85% (Dr Brian Luke Seaward).”   But again, she fails to reference the quote.

“The International Agency for Research on Cancer and the World Health Organization has concluded that 80% of cancers are due to lifestyles and are not genetic, and they say this is a conservative number (Cancer statistics and views of causes Science News Vol.115, No 2 (Jan.13 1979), p.23).”  It’s good that she provides a reference to her statement.  However, referencing a journal on genetics from 1979 is the equivalent of attempting to use the land-speed record from 1979 to justify your current preference of car.  The technology has advanced significantly, and genetic discoveries are lightyears ahead of where they were more than three decades ago.

“According to Dr Bruce Lipton (The Biology of Belief, 2008), gene disorders like Huntington’s chorea, beta thalassemia, cystic fibrosis, to name just a few, affect less than 2% of the population. This means the vast majority of the worlds population come into this world with genes that should enable the to live a happy and healthy life. He says a staggering 98% of diseases are lifestyle choices and therefore, thinking.”  Even if it’s true that Huntingtons, CF etc account for 2% of all illnesses, they account for only a tiny fraction of genetic disease.  And concluding that the remaining 98% must therefore be lifestyle related is overly simplistic.  It ignores the genetic influence on all other diseases, other congenital, and environmental causes of disease.  I will fully outline this point soon.

Similarly, “According to W.C Willett (balancing lifestyle and genomics research for disease prevention Science (296) p 695-698, 2002) only 5% of cancer and cardiovascular patients can attribute their disease to hereditary factors.”  Science is clear that genes play a significant role in the development of cardiovascular disease and most cancers, certainly greater than 5%.  Again, I will discuss this further soon.

“According to the American Institute of health, it has been estimated that 75 – 90% of all visits to primary care physicians are for stress related problems (http://www.stress.org/americas.htm). Some of the latest stress statistics causing illness as a result of toxic thinking can be found at: http://www.naturalwellnesscare.com/stress-statistics.html”  These websites not peer-reviewed, and both suffer from a blatant pro-stress bias.

You’ll also have to forgive my confusion, but Dr Leaf also wrote, “Dr H.F. Nijhout (Metaphors and the Role of Genes and Development, 1990) genes control biology and not the other way around.”  So is she saying that genes DO control development?

EVIDENCE CONTRADICTING DR LEAF

Influence Of Thought On Health

Dr Leaf has categorically stated that “75 to 98% of all illnesses are the result of our thought life” on a number of occasions.  She repeated the same statement in her most recent book so it is something she is confident in.  However, in order to be true, this fact must be consistent across the whole of humanity.

And yet, in a recent peer-reviewed publication, Mara et al state, “At any given time close to half of the urban populations of Africa, Asia, and Latin America have a disease associated with poor sanitation, hygiene, and water.” [2]  Bartram and Cairncross write that “While rarely discussed alongside the ‘big three’ attention-seekers of the international public health community—HIV/AIDS, tuberculosis, and malaria—one disease alone kills more young children each year than all three combined. It is diarrhoea, and the key to its control is hygiene, sanitation, and water.” [3]  Hunter et al state that, “diarrhoeal disease is the second most common contributor to the disease burden in developing countries (as measured by disability-adjusted life years [DALYs]), and poor-quality drinking water is an important risk factor for diarrhoea.” [4]

Toilets and clean running water have nothing to do with stress or thought.  We live in a society that essentially prevents more than half of our illnesses because of internal plumbing, with additional benefits from vaccination and population screening.  If thoughts have any effect on our health, they are artificially magnified by our clean water and sewerage systems.  Remove those factors and any effects of thought on our health disappear from significance.  Dr Leaf’s assertion that 75 to 98% of human illness is thought-related is a clear exaggeration.

Let me be clear – I understand the significance of stress on health and the economy, but it is not the cause of 75-98% of all illnesses.  I’m not sure if there is a similar study in the US, but the latest Australian data suggests that all psychological illness only counts for 8% of visits to Australian primary care physicians [5].

In terms of cancer, I don’t have time to exhaustively list every cancer but of the top four listed in the review “Cancer Statistics 2013” [6] , here are the articles that list the gene x environment interactions:

  1. PROSTATE – There are only two risk factors for prostate cancer, familial aggregation and ethnic origin. No dietary or environmental cause has yet been identified [7].  It is most likely caused by multiple genes at various loci [8].
  2. BREAST – Genes make up 25% of the risk factors for breast cancer, and significantly interacted with parity (number of children born) [9].
  3. LUNG/BRONCHUS – Lung cancer is almost exclusively linked to smoking, but nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
  4. COLORECTUM – Approximately one third of colorectal cancer is genetically linked [11].

So the most common cancer is not linked to any environmental factors at all, and the others have genetic influences of 25% to more than 50%.  This is far from being 2% or 5% as Dr Leaf’s sources state.

Also in terms of heart disease, the INTERHEART trial [12] lists the following as significant risk factors, and I have listed the available gene x environment interaction studies that have been done on these too:

  1. HIGH CHOLESTEROL – Genetic susceptibility accounts for 40-60% of the risk for high cholesterol [13].
  2. DIABETES – Genetic factors account for 88% of the risk for type 1 diabetes [14].  There is a strong genetic component of the risk of type 2 diabetes with 62-70% being attributable to genetics [15, 16].
  3. SMOKING – nicotine addiction has a strong hereditary link (50-75% genetic susceptibility) [10].
  4. HYPERTENSION – While part of a much greater mix of variables, genetics are still thought to contribute between 30% and 50% to the risk of developing high blood pressure [17].

So again, while genes are a part of a complex system, it is clear from the most recent evidence that genetics account for about 50% of the risk for cardiovascular disease, which again is a marked difference between the figures that Dr Leaf is using to base her assertions on.

Atrial Natriuretic Peptide

I am aware of research that’s studied the anxiolytic properties of Atrial Natriuretic Peptide.  For example, Wiedemann et al [18] did a trial using ANP to truncate panic attacks.  However, these experiments were done on only nine subjects, and the panic attacks were induced by cholecystokinin.  As such, the numbers are too small to have any real meaning.  And the settling is completely artificial.  Just as CCK excretion does not cause us all to have panic attacks every time we eat, ANP does not provide anxiolysis in normal day to day situations.  Besides, if ANP were really effective at reducing anxiety, then why do people suffering from congestive cardiac failure, who have supraphysiological levels of circulating ANP [19] , also suffer from a higher rate of anxiety and panic disorders than the general population? [20]

The Heart As A Mini-Brain

As for Heartmath, they advance the notion of the heart being a mini-brain to give themselves credibility.  It’s really no different to an article that I read the other day from a group of gut researchers [21] – “‘The gut is really your second brain,’ Greenblatt said. ‘There are more neurons in the GI tract than anywhere else except the brain.’”  The heart as a mini-brain and the gut as a mini-brain are both figurative expressions.  Neither are meant to be taken literally.  I welcome Dr Leaf to tender any further evidence in support of her claim.

Hard-Wired For Optimism

As for being wired for optimism, the brain is likely pre-wired with a template for all actions and emotions, which is the theory of protoconsciousness [22].  Indeed, neonatal reflexes often reflect common motor patterns.  If this is true, then the brain is pre-wired for both optimism and love, but also fear.  This explains the broad role of the amygdala in emotional learning [23] including fear learning.  It also means that a neonate needs to develop both love and fear.

A recent paper showed that the corticosterone response required to learn fear is suppressed in the neonate to facilitate attachment, but with enough stress, the corticosterone levels build to the point where amygdala fear learning can commence [24].  The fear circuits are already present, only their development is suppressed.  Analysis of the cohort of children in the Bucharest Early Intervention Project showed that negative affect was the same for both groups.  However positive affect and emotional reactivity was significantly reduced in the institutionalised children [25].  If the brain is truly wired for optimism and only fear is learned, then positive emotional reactivity should be the same in both groups and the negative affect should be enhanced in the institutionalised cohort.  That the result is reversed confirms that neonates and infants require adequate stimulation of both fear and love pathways to grow into an emotionally robust child, because the brain is pre-wired for both but requires further stimulation for adequate development.

The Mind-Brain Link

If the mind controls the brain and not the other way around as Dr Leaf suggests, why do anti-depressant medications correct depression or anxiety disorders?  There is high-level evidence to show this to be true [26-28].  The same can be said for recent research to show that medications which enhance NDMA receptors have been shown to improve the extinction of fear in anxiety disorders such as panic disorder, OCD, Social Anxiety Disorder, and PTSD [29].

If the mind controls the brain and not the other way around as Dr Leaf suggests, why do some people with acquired brain injuries or brain tumours develop acute personality changes or thought disorders?  Dr Leaf has done PhD research on patients with closed head injuries and treated them in clinical settings according to her CV.  She must be familiar with this effect.

One can only conclude that there is a bi-directional effect between the brain and the stream of thought, which is at odds with Dr Leaf’s statement that the mind controls the brain and not the other way around.

FURTHER CLARIFICATION

One further thing.  Can you clarify which of Dr Leaf’s peer-reviewed articles have definitively shown the academic improvement in the cohort of 100,000 students, as you and your referee have stated?  And can you provide a list of articles which have cited Dr Leaf’s Geodesic Information Processing Model?  Google Scholar did not display any articles that had cited it, which must be an error on Google’s part.  If her theory is widely used as you say, it must have been extensively cited.

I understand that you are both busy, but I believe that I have documented a number of observations, backed by recent peer-reviewed scientific literature, which directly contradict Dr Leaf’s teaching.  I have not had a chance to touch on many, many other points of disagreement.

For the benefit of Dr Leaf’s followers, and for the scientific and Christian community at large, I would appreciate your response.

I would be grateful if you could respond to the points raised and the literature which supports it, rather than an Ad Hominem dismissal or further defense by association.

Dr C. Edward Pitt

REFERENCES

1. Fowler, G., Evidence-based practice: Tools and techniques. Systems, settings, people: Workforce development challenges for the alcohol and other drugs field, 2001: 93-107.

2. Mara, D., et al., Sanitation and health. PLoS Med, 2010. 7(11): e1000363.

3. Bartram, J. and Cairncross, S., Hygiene, sanitation, and water: forgotten foundations of health. PLoS Med, 2010. 7(11): e1000367.

4. Hunter, P.R., et al., Water supply and health. PLoS Med, 2010. 7(11): e1000361.

5. FMRC. Public BEACH data. 2010  16JUL13]; Available from: <http://sydney.edu.au/medicine/fmrc/beach/data-reports/public&gt;.

6. Siegel, R., et al., Cancer statistics, 2013. CA Cancer J Clin, 2013. 63(1): 11-30.

7. Cussenot, O. and Valeri, A., Heterogeneity in genetic susceptibility to prostate cancer. Eur J Intern Med, 2001. 12(1): 11-6.

8. Alberti, C., Hereditary/familial versus sporadic prostate cancer: few indisputable genetic differences and many similar clinicopathological features. Eur Rev Med Pharmacol Sci, 2010. 14(1): 31-41.

9. Nickels, S., et al., Evidence of gene-environment interactions between common breast cancer susceptibility loci and established environmental risk factors. PLoS Genet, 2013. 9(3): e1003284.

10. Berrettini, W.H. and Doyle, G.A., The CHRNA5-A3-B4 gene cluster in nicotine addiction. Mol Psychiatry, 2012. 17(9): 856-66.

11. Hutter, C.M., et al., Characterization of gene-environment interactions for colorectal cancer susceptibility loci. Cancer Res, 2012. 72(8): 2036-44.

12. Yusuf, S., et al., Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet, 2004. 364(9438): 937-52.

13. Asselbergs, F.W., et al., Large-scale gene-centric meta-analysis across 32 studies identifies multiple lipid loci. Am J Hum Genet, 2012. 91(5): 823-38.

14. Wu, Y.L., et al., Risk factors and primary prevention trials for type 1 diabetes. Int J Biol Sci, 2013. 9(7): 666-79.

15. Ali, O., Genetics of type 2 diabetes. World J Diabetes, 2013. 4(4): 114-23.

16. Murea, M., et al., Genetic and environmental factors associated with type 2 diabetes and diabetic vascular complications. Rev Diabet Stud, 2012. 9(1): 6-22.

17. Kunes, J. and Zicha, J., The interaction of genetic and environmental factors in the etiology of hypertension. Physiol Res, 2009. 58 Suppl 2: S33-41.

18. Wiedemann, K., et al., Anxiolyticlike effects of atrial natriuretic peptide on cholecystokinin tetrapeptide-induced panic attacks: preliminary findings. Arch Gen Psychiatry, 2001. 58(4): 371-7.

19. Ronco, C., Fluid overload : diagnosis and management. Contributions to nephrology,. 2010, Basel Switzerland ; New York: Karger. viii, 243 p.

20. Riegel, B., et al., State of the science: promoting self-care in persons with heart failure: a scientific statement from the American Heart Association. Circulation, 2009. 120(12): 1141-63.

21. Arnold, C. Gut feelings: the future of psychiatry may be inside your stomach. 2013  [cited 2013 Aug 22]; Available from: http://www.theverge.com/2013/8/21/4595712/gut-feelings-the-future-of-psychiatry-may-be-inside-your-stomach.

22. Hobson, J.A., REM sleep and dreaming: towards a theory of protoconsciousness. Nat Rev Neurosci, 2009. 10(11): 803-13.

23. Dalgleish, T., The emotional brain. Nat Rev Neurosci, 2004. 5(7): 583-9.

24. Landers, M.S. and Sullivan, R.M., The development and neurobiology of infant attachment and fear. Dev Neurosci, 2012. 34(2-3): 101-14.

25. Bos, K., et al., Psychiatric outcomes in young children with a history of institutionalization. Harv Rev Psychiatry, 2011. 19(1): 15-24.

26. Arroll, B., et al., Antidepressants versus placebo for depression in primary care. Cochrane Database Syst Rev, 2009(3): CD007954.

27. Soomro, G.M., et al., Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). Cochrane Database Syst Rev, 2008(1): CD001765.

28. Kapczinski, F., et al., Antidepressants for generalized anxiety disorder. Cochrane Database Syst Rev, 2003(2): CD003592.

29. Davis, M., NMDA receptors and fear extinction: implications for cognitive behavioral therapy. Dialogues Clin Neurosci, 2011. 13(4): 463-74.