Olive Leaf Extract – A potential treatment, but not for what you think

Here in Australia, it’s winter. It’s currently warmer in the fridge than it is outside. We’ve just been blasted by a wall of frigid air straight from Antarctica, and much of the south-eastern corner of our continent has snow drifts over parts that not so long ago were baking under the hot Autumn sun. It’s not something we’re used to in Australia.

Of course, now that winter is firmly entrenched, more people are coming to see me with their viral upper respiratory tract infections, better known as ‘colds’. Yes, ’tis the season to be sneezin’!  Over my years of practice, I’ve seen enough people with a cold to last me a thousand winters.

What always fascinates me are the things that people try to use to cure their cold. I think I’ve heard everything over the last decade: garlic, ginger, peppermint, chicken soup, honey, tea, honey mixed with lemon mixed with tea, or honey mixed with lemon mixed cayenne pepper mixed with tea.   Some people rub Vicks on their feet. Other people douse their pillows in eucalyptus oil.

Another common recommendation that gets around the grape vine and social media is olive leaf extract, used in traditional ‘medicine’ for thousands of years, and those witch-doctors and shamans can’t all be wrong.

One published review described the ‘science’ of olive leaf extract: “Constituents of the olive tree, Olea europaea, have been studied and utilized in folk medicine for centuries. Olive leaf extract, derived from the leaves of the olive tree, contains phenolic compounds, specifically oleuropein, that have demonstrated potent antimicrobial, antioxidant, and anti-inflammatory activity. Oleuropein and derivatives such as elenolic acid have been shown to be effective in in vitro and animal studies against numerous microorganisms, including retroviruses, coxsackie viruses, influenza, and parainfluenza as well as some bacteria. Research suggests that olive leaf constituents interact with the protein of virus particles and reduce the infectivity and inhibit replication of viruses known to cause colds, influenza, and lower respiratory infection. Olive leaf extract has also been shown to stimulate phagocytosis, thereby enhancing the immune response to viral infection. Anecdotal reports indicate olive leaf extract taken at the onset of cold or flu symptoms prevents or shortens the duration of the disease. For viral sore throats, gargling with olive leaf tea may alleviate symptoms, possibly by decreasing inflammation and viral infectivity.” [1]

It’s always a concern when a supposedly peer reviewed journal allows an article to get through which seriously discusses anecdotal evidence as something worthy of attention. Anecdotal evidence is the weakest level of evidence possible. Anecdotal evidence is essentially just stories and opinion [2]. There’s anecdotal evidence for the Tooth Fairy. The other ‘evidence’ that this review describes is from in vitro studies, which are trials in test tubes not in people. In vitro evidence is only helpful in a general sense. Just because a reaction happens in a test tube or petri dish doesn’t mean that it will happen in a real life human being.

So then, do the claims for olive leaf extract stand up to the rigors of modern scientific enquiry or is it like every other cold and flu ‘remedy’ – just another individualised mythology?

Being sceptical, I wanted to find out. So I searched through the published medical literature for quality clinical trials that studied olive leaf extract in humans, and I found only six trials. Interestingly, all of the trials studying olive leaf extract weren’t looking at its effect on immune function but on cholesterol and blood sugar control, blood pressure, and oxidative stress.

In 2009, Kendall et al published a single-centre, randomized, single-blinded, prospective pilot comparison of the effect of dietary supplementation with olive leaf extract on the markers of oxidative stress in 45 healthy young adult volunteers. They found that olive leaf extract had no effect on oxidative stress compared to the control group [3].

Susalit et al (2011) published a double-blind, randomized, parallel and active-controlled clinical study looking at the tolerability, cholesterol-lowering and anti-hypertensive effect of Olive leaf extract in comparison with Captopril (a common blood pressure medication) in patients with early hypertension. After 8 weeks of treatment, there were similar reductions in blood pressure in both the olive leaf extract and the blood pressure pill groups. There was a significant drop in triglyceride levels in the olive leaf extract group, but not in Captopril group [4].

Wainstein et al (2012) performed a randomized controlled trial on 79 adults with non-insulin dependent diabetes, comparing a single 500mg dose of olive leaf extract with placebo over 14 weeks. They measured the HbA1c (a surrogate measurement of the average blood sugar over a three month period) and plasma insulin levels. They also did studies in rats to study the mechanism of action of the olive leaf extract. In the human trials, the subjects treated with olive leaf extract exhibited significantly lower HbA1c and fasting plasma insulin levels. This effect was thought to be reflected in the rat study which suggested that olive leaf extract reduced the digestion and absorption of starch from the intestines [5].

de Bock et al (2013) did a randomized, double-blinded, placebo-controlled, crossover trial on 46 patients in New Zealand, over a 30 week period. The participants were middle aged and overweight. The researchers were primarily studying insulin sensitivity but they also looked at glucose and insulin profiles, cytokines, lipid profile, body composition, 24-hour ambulatory blood pressure, and carotid intima-media thickness. The olive leaf extract group had a statistically significant improvement in insulin sensitivity and responsiveness of the pancreatic β-cell. Interestingly, the olive leaf extract supplementation improved some inflammatory markers, but not others, and made no difference to the patients lipid profile, blood pressure, body composition (their body fatness), carotid intima-media thickness (a risk predictor of cardiovascular disease), or liver function [6].

For completeness, de Bock lead another trial, also published in 2013, although this trial was more a study of the absorption of the compounds in olive leaf extract than a study of their effects [7]. There was a 1996 Belgian study which was written in French. I’m not very good with French, but according to the English abstract, there was no difference between the olive leaf extract and placebo in terms of blood pressure and blood sugar levels [8].

Reconciling the research on olive leaf extract makes for an interesting narrative. There are a couple of really strong, methodologically robust trials on olive leaf extract, and with positive results in favour of it. However, I can count them on one hand, and while the results are encouraging for proponents of olive leaf extract, there needs to be a lot more research before those claims can be made with certainty. And in contrast to its usual selling points, those positive effects for olive leaf extract were for blood sugar control, not the prevention or treatment of viral illnesses.

The bottom line – olive leaf extract may one day prove to be a useful herbal supplement, but there’s not enough clinical evidence to support it at the present moment. And there’s certainly no evidence that olive leaf extract will do anything for your viral upper respiratory tract infections.

So next time you get a cold, don’t bother spending money on olive leaf extract. Have a couple of paracetamol, a long hot shower and a good rest.

And if symptoms persist, don’t forget to see your GP.


[1]        Roxas M, Jurenka J. Colds and influenza: a review of diagnosis and conventional, botanical, and nutritional considerations. Alternative medicine review : a journal of clinical therapeutic 2007 Mar;12(1):25-48.
[2]        Fowler G. Evidence-based practice: Tools and techniques. Systems, settings, people: Workforce development challenges for the alcohol and other drugs field 2001:93-107.
[3]        Kendall M, Batterham M, Obied H, Prenzler PD, Ryan D, Robards K. Zero effect of multiple dosage of olive leaf supplements on urinary biomarkers of oxidative stress in healthy humans. Nutrition 2009 Mar;25(3):270-80.
[4]        Susalit E, Agus N, Effendi I, et al. Olive (Olea europaea) leaf extract effective in patients with stage-1 hypertension: comparison with Captopril. Phytomedicine : international journal of phytotherapy and phytopharmacology 2011 Feb 15;18(4):251-8.
[5]        Wainstein J, Ganz T, Boaz M, et al. Olive leaf extract as a hypoglycemic agent in both human diabetic subjects and in rats. Journal of medicinal food 2012 Jul;15(7):605-10.
[6]        de Bock M, Derraik JG, Brennan CM, et al. Olive (Olea europaea L.) leaf polyphenols improve insulin sensitivity in middle-aged overweight men: a randomized, placebo-controlled, crossover trial. PloS one 2013;8(3):e57622.
[7]        de Bock M, Thorstensen EB, Derraik JG, Henderson HV, Hofman PL, Cutfield WS. Human absorption and metabolism of oleuropein and hydroxytyrosol ingested as olive (Olea europaea L.) leaf extract. Molecular nutrition & food research 2013 Nov;57(11):2079-85.
[8]        Cherif S, Rahal N, Haouala M, et al. [A clinical trial of a titrated Olea extract in the treatment of essential arterial hypertension]. Journal de pharmacie de Belgique 1996 Mar-Apr;51(2):69-71.

Dr Caroline Leaf and the obesity overstatement

Screen Shot 2015-01-16 at 1.36.01 am

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.

Screen Shot 2015-01-16 at 1.24.17 am

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.


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.

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.


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.


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.


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?


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.


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


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.