Dr Caroline Leaf – Scientific heresy

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Imagine that this Easter, the guest speaker at your church stands up from the pulpit and calmly mentions during the sermon that Jesus wasn’t really buried in a tomb, but was kept by his disciples in a house until he recovered enough from his wounds to go on his merry way.

What would you think of that speaker? Would you smile and nod, or even shout an ‘amen!’, buy their book, and encourage your pastor that they should be invited back again?

One would hope that there would be a polite but resounding outcry. Even if the rest of the message was perfect, you wouldn’t want someone to come back to your pulpit if they couldn’t get the basics of their subject right, even if they were considered a popular speaker or self-declared expert.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. Dr Leaf preaches every day from both physical pulpits all over the globe, and a virtual pulpit through the power of Instagram and Facebook.

Dr Leaf used her position of social media prominence today to share this little jewel, “The brain cannot change itself; you, with your love power and sound mind, change your brain.”

Um … that’s not true … at all … in any way.

For a start, the most prolific period for brain development is actually pre-birth, and then the first year of life. But foetal brains don’t have their own thoughts. It’s not like the movie “Look Who’s Talking” inside the average uterus. The brain of an unborn baby is growing and changing at an exponential rate without any thoughts to guide them [1].

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Number of synapses per constant volume of tissue as a function of pre- and postnatal age. (Stiles, J. and Jernigan, T.L., The basics of brain development. Neuropsychol Rev, 2010. 20(4): 327-48 doi: 10.1007/s11065-010-9148-4)

 

In our adult years, our brain still continues to develop. But that development isn’t dependant on our thought life. Significant consolidation of our brain’s neural pathways occur when we’re asleep [2], but our thought life isn’t active during sleep.

Model of sleep stage-specific potentiation and homeostatic scaling. Gronli, J., et al., Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress. Front Behav Neurosci, 2013. 7: 224 doi: 10.3389/fnbeh.2013.00224

Model of sleep stage-specific potentiation and homeostatic scaling. (Gronli, J., et al., Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress. Front Behav Neurosci, 2013. 7: 224 doi: 10.3389/fnbeh.2013.00224)

Indeed, real cognitive neuroscientists have shown that our stream of thought is simply a tiny fraction of our overall neural activity, a conscious glimpse of the brains overall function [3-5]. So you don’t change your brain at all. “You” can’t, because it’s your brain’s directed activity which causes the growth of new synaptic branches to support it, all of which is subconscious.

Therefore, suggesting that our brain can only change with our conscious control is patently false, and so clearly against the most fundamental principles of neuroscience that such a claim is the neuroscientific equivalent of saying that Jesus didn’t die on the cross, he just swooned.

Dr Leaf has committed scientific heresy.

At this point, supporters of Dr Leaf often suggest that she wasn’t speaking literally, but metaphorically. She didn’t really mean that the brain can’t change itself, just that our choices are really important.

Somehow I doubt that. Dr Leaf wasn’t being metaphorical when she claimed that her patients in her research projects grew their intelligence when they “applied their minds”:
“Now with a traumatic brain injury, basically IQ generally goes down around twenty points because of the kind of damage with traumatic brain injury. Well her IQ was 100 before the accident, it was 120 after the accident. So here with holes in her brain, and brain damage, she changed … she actually increased her intelligence. Now I’m pretty convinced at this stage, cause I’ve been working … besides her I’ve been working with lots and lots of other patients, seeing the same thing, when these students applied their mind, their brain was changing, their academic results were changing.” [6]

Dr Leaf believes that your mind can literally change your brain. It was the subject of her entire TEDx talk in February.

It sounds innocent enough until you consider the broader implications of this way of thinking – those with brain damage haven’t recovered fully because they just haven’t applied their minds enough. The same for those with learning disabilities or autism, ADHD, Downs syndrome, cerebral palsy, dyslexia, or any other neurological disorder … because you only need to “apply your minds” to change your brain. “You have a powerful mind. You have a sound mind. You have a mind that is able to … to achieve what you’re dreams are. You are as intelligent as you want to be.” [6]

Or, in other words, don’t blame it on your brain if you’re intellectually disabled, mentally ill, or vacuous. You simply haven’t applied your brain well enough. Stop sitting around and think better.

As a church, we can, and should, be doing a lot better for those amongst us who suffer from neurological and mental disorders. It starts by being more judicious with who is allowed at that privileged position of the pulpit. We need to be eliminating scientific heresy from the pulpit, not clapping and shouting ‘amen!’

References

  1. Stiles, J. and Jernigan, T.L., The basics of brain development. Neuropsychol Rev, 2010. 20(4): 327-48 doi: 10.1007/s11065-010-9148-4
  2. Gronli, J., et al., Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress. Front Behav Neurosci, 2013. 7: 224 doi: 10.3389/fnbeh.2013.00224
  3. Baars, B.J., Global workspace theory of consciousness: toward a cognitive neuroscience of human experience. Progress in brain research, 2005. 150: 45-53
  4. Baars, B.J. and Franklin, S., An architectural model of conscious and unconscious brain functions: Global Workspace Theory and IDA. Neural Netw, 2007. 20(9): 955-61 doi: 10.1016/j.neunet.2007.09.013
  5. Franklin, S., et al., Conceptual Commitments of the LIDA Model of Cognition. Journal of Artificial General Intelligence, 2013. 4(2): 1-22
  6. Leaf, C.M., Ridiculous | TEDx Oaks Christian School | 4 Feb 2015, 2015 TEDx, 20:03. https://http://www.youtube.com/watch?v=yjhANyrKpv8

Dr Caroline Leaf – It’s no joke

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So, stop me if you’ve heard this one … This guy walks into a bar, and says, “Owww, that bar is really hard.”

Ok, that was a bad joke. Hey, I’m no Robin Williams. Some people have the knack of being able to make people laugh in almost any situation. I can get a few laughs, but I’m not a naturally gifted comic.

Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist. She isn’t a comedian either.

Her post today was a light-hearted dig at giant lizards with a taste for organic free-range humans, or perhaps the fact that most people know being “all organic, gluten free” should be left to the sanctimonious foodies of San Francisco.

The other part of her post wasn’t meant to be funny, but certainly contained a healthy dose of irony. In trying to justify her bit of light comic relief, she posted another of her subtly erroneous factoids, this time claiming that, “Laughing 100-200 times a day is equal to 10 minutes of rowing or jogging!”

Not according to real scientists, who have worked out that laughing is actually the metabolic equivalent to sitting still at rest, while jogging or rowing burns between 6 to 23 times as much energy, depending on how fast you run or row [1].

That would mean that I would have to laugh for at least a whole hour a day (or about 700 times based on the average chortle) to be even close to the energy burnt by a light jog.

On the grand scale of things, this meme probably doesn’t really matter. These sort of factoids are thrown around on social media all the time, and it won’t make a big difference to the health and wellbeing of most people. But it does help establish a pattern. Dr Leaf habitually publishes memes and factoids that clearly deviate from the scientific truth, proving that Dr Leaf has become a cross between a science fiction author and life coach, not a credible scientific expert. From her social media memes to her TV shows, all of her teaching becomes tainted as untrustworthy.

While today’s meme may not be so serious, if Dr Leaf can’t get her facts straight, pretty soon the joke will be on her.

References

  1. Ainsworth, B.E., et al., 2011 Compendium of Physical Activities: a second update of codes and MET values. Med Sci Sports Exerc, 2011. 43(8): 1575-81 doi: 10.1249/MSS.0b013e31821ece12

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

Fats and Figures cover 1400

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

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

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

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

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

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

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

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

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

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

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

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

2. Is sugar bad for you?

That depends.

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

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

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

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

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

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

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

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

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

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

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

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

3. Is obesity bad for you?

Again, that depends.

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

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

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

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

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

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

In a word, no.

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

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

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

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

5. Is alcohol good for you?

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

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

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

6. Is exercise good for you?

In a word, yes!

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Dr Caroline Leaf: All scare and no science?

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On her social media feed today, Dr Leaf posted a meme implying that conventionally farmed food was toxic.

Dr Caroline Leaf is a communication pathologist and self-titled cognitive neuroscientist. Anyone who’s been following Dr Leaf will know from her frequent food selfies that she is an organic convert.

Dr Leaf is welcome to eat whatever she chooses, though not content to simply push her personal belief in organic foods, Dr Leaf is now actively criticising conventional food, publishing memes on her social media posts which imply that conventional produce is poisonous.

As I’ve written before, despite Dr Leaf’s blinding passion and quasi-religious zeal for organic foods, there is no evidence that organic food is any more beneficial than conventional food (Dangour et al, 2009; Bradbury et al, 2014). Indeed, there’s no magic to a healthy food lifestyle. Eat more vegetables. Drink more water. Conventional veggies and conventional water do just fine. Sage advice, even if it doesn’t lend itself to food selfies.

While organic zealots believe they have the high ground on the topic of food safety, the published science cuts through the hype. As noted by Smith-Spangler et al (2012), there is some evidence that there may be less pesticide residue on organically grown foods, but there is no significant difference in the risk of each group exceeding the overcautious Maximum Residue Limit.

Two points on the Maximum Residue Limit that are particularly important:

  1. The Maximum Residue Limit is extremely cautious, and most food tested is well below this already overcautious limit. The Maximum Residue Limit is set to about 1% of the amount of the pesticide that has no effect on test animals.   According to a recent survey of grapes done by Choice Australia, the amount of residue was well below the Maximum Residue Limit (about 1% of the Maximum Residue Limit on average) (Choice Australia, 2014). So on the average bunch of grapes in Australia, the pesticide residue is about one ten thousandth of the level that is safe in animals, and this pattern is the same across all conventional produce. Thinking in more practical terms, “a 68 kg man would have to eat 3,000 heads of lettuce every day of his life to exceed the level of a residue that has been proven to have no effect on laboratory animals … an 18 kg boy would have to eat 534 apples every day of his life to exceed a residue level that is not dangerous to laboratory animals. And an 18 kg girl would have to eat 13,636 kg of carrots every day of her life to exceed such a level.” (ecpa.eu, 2014)

    2. Organic foods have pesticides too. Granted, this is at lower levels than their conventional counterparts, but it’s there all the same (Smith-Spangler et al, 2012). I once had a lively discussion with an organic food zealot about the pesticides in organic farming. Her argument was that organic pesticides are safe because they’re “natural” poisons. So are arsenic, cyanide, belladonna and digitalis (foxglove), but why let the truth get in the way of ones opinion. Poisons are poisons whether they’re “natural” or not. The Maximum Residue Limit applies to organic foods just the same as conventionally farmed produce for that reason.

Another interesting thing … in the Choice survey, the organic grapes had no detectable pesticides, but so did conventionally farmed grapes bought at a local green grocer. So organic food zealots can’t claim that they have a monopoly on low pesticides in their foods.

Not that having lower pesticide residues means that organic foods are necessarily safer. Organically farmed produce has a higher risk of contamination from E. coli and other potentially toxic bacteria, depending on the farming method used (Mukherjee et al, 2007; Sample, 2011).

So to bring it all together, conventional produce has levels of pesticide residues so low that it would take an extra-ordinary feat of vegetarian gluttony to exceed a level that was still found to be non-toxic in animals. The risk to human health from conventional farming with pesticides is nanoscopic. Organic foods may have less pesticide, but they have a higher risk from enterotoxigenic bacteria.

Since there is nothing to fear from conventional foods, it seems irresponsible for Dr Leaf to promote the unscientific idea that conventional foods are poisonous. One wonders why Dr Leaf would engage in a campaign of fear against healthy, nutritious foods? Personal bias perhaps, although that doesn’t bode well for her credibility as an objective scientist. Another plausible reason could be marketing. Fear sells things, that’s Marketing 101. Gardner (2008) wrote, “Fear sells. Fear makes money. The countless companies and consultants in the business of protecting the fearful from whatever they may fear know it only too well. The more fear, the better the sales.”

Posts like today’s make Dr Leaf seem like all scare and no science. Publishing images with the skull and cross bones and the word “POISON” is certainly not attempting to allay anyone’s anxiety, and that fact that it‘s directly tied to a reminder of her upcoming book on food only makes shameless promotion all the more likely. I’m sure that a Godly woman of Dr Leaf’s standing wouldn’t stoop so low as to use fear and mistruth just to make better sales, but posts like today’s open her up to legitimate questions from others regarding her credibility and her motivation.

For her sake, I hope that she tightens up her future posts, and reconsiders her stance on the science of organic and conventional foods.

References

Bradbury, K.E., et al., Organic food consumption and the incidence of cancer in a large prospective study of women in the United Kingdom. Br J Cancer, 2014. 110(9): 2321-6 doi: 10.1038/bjc.2014.148

Choice Australia, 2014. <http://www.choice.com.au/reviews-and-tests/food-and-health/food-and-drink/groceries/pesticide-residues-in-fruit-and-vegetables.aspx&gt;

Dangour, A. D., Dodhia, S. K., Hayter, A., Allen, E., Lock, K., & Uauy, R. (2009). Nutritional quality of organic foods: a systematic review. Am J Clin Nutr, 90(3), 680-685. doi: 10.3945/ajcn.2009.28041

European Crop Protection Agency, 2014, <http://www.ecpa.eu/faq/what-maximum-residue-level-mrl-and-how-are-they-set>

Gardner, D., The science of fear: Why we fear the things we shouldn’t – and put ourselves in greater danger; 2008, Dutton / The Penguin Group, New York

Mukherjee, A., et al., Association of farm management practices with risk of Escherichia coli contamination in pre-harvest produce grown in Minnesota and Wisconsin. Int J Food Microbiol, 2007. 120(3): 296-302 doi: 10.1016/j.ijfoodmicro.2007.09.007

Sample, I., E coli outbreak: German organic farm officially identified. The Guardian, London, UK, 11 June 2011 <http://www.theguardian.com/world/2011/jun/10/e-coli-bean-sprouts-blamed>

Smith-Spangler, C., Brandeau, M. L., Hunter, G. E., Bavinger, J. C., Pearson, M., Eschbach, P. J., . . . Stave, C. (2012). Are organic foods safer or healthier than conventional alternatives? A systematic review. Ann Intern Med, 157(5), 348-366.

Dr Caroline Leaf, behaviour and genetic destiny

Screen Shot 2014-12-23 at 10.32.41 pm

Today on her Facebook feed, Caroline Leaf posted a quote which said, “Your behavior can and does dictate your genetic destiny”. Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist. In isolation, it sounds like she has found confirmation of her view that our thoughts and behaviour control the physical properties of our DNA (Leaf, 2013, p35).

However, I wanted to look at the quote in a broader context, because in the broader context, the quote still doesn’t confirm Dr Leaf’s teaching.

The quote comes from an American doctor, Sharon Moalem. Dr Moalem is obviously a smart man. According to Wikipedia, “Dr. Moalem is an expert in the fields of rare diseases, neurogenetics, and biotechnology. He is the author of the New York Times bestselling book ‘Survival of the Sickest’ and ‘How Sex Works’. Moalem has cofounded two biotechnology companies and is the recipient of 19 patents for his inventions in biotechnology and human health.” (http://en.wikipedia.org/wiki/Sharon_Moalem)

It’s not that Dr Moalem’s quote is wrong. In the book from which the quote is taken, Dr Moalem discusses the expression of genes (Moalem, 2014). There is no doubt that our behaviour affects the expression of genes. For example, when the body encounters a high level of dietary iron (ie: we eat a big juicy steak), a series of steps activates a gene to promote the production of ferritin, a protein that helps to carry iron in the blood stream (Strachan and Read, 2011, p375-6). These changes in genetic expression are mostly protective (for example, ferritin is used to keep toxic elemental iron from damaging our tissues). There are some behaviours that will override the body’s protection, for example, excessive exposure to UV radiation will eventually lead to skin cancer. But overall, the changes in genetic expression that our behaviour causes are protective, and do not adversely affect our health.

Unlike Dr Leaf, Dr Moalem does not promote the notion that our behaviour changes the genes themselves. Neither does he promote that our behaviour, in isolation, is the only modifier of our genetic expression. The quote that Dr Leaf used came from the second chapter of Dr Moalem’s book, “Inheritance: How Our Genes Change Our Lives, and Our Lives Change Our Genes”. Really, the title says it all. Our behaviour influences our genetic destiny, but our genes influence our behaviour just as much, if not more.

For example, small variations in the genes that code for our smell sensors or the processing of smells can change our preferences for certain foods just as much as cultural exposure. Our appreciation for music is often changed subtly between individuals because of changes in the structure of our ears or the nerves that we use to process the sounds. The genetic structure of the melanin pigment in our skin changes our interaction with our environment because of the amount of exposure to the sun we can handle. Our genetic destiny is also largely influenced by our environment, most of which is also beyond our choice (Lobo and Shaw, 2008).

So your behaviour can and does influence your genetic destiny, but your genetic destiny is more influenced by our genes themselves, and the environment that is beyond our control.

Dr Leaf’s quote doesn’t look quite so supportive after all.

References

Leaf, C.M., (2013) Switch On Your Brain : The Key to Peak Happiness, Thinking, and Health, Baker Books, Grand Rapids, Michigan

Lobo, I. & Shaw, K. (2008) Phenotypic range of gene expression: Environmental influence. Nature Education 1(1):12

Moalem, S., (2014) Inheritance: How our genes change our lives and our lives change our genes, Grand Central Publishing, New York.

Strachan, T. and Read, A., (2011) Human Molecular Genetics. 4th ed. Garland Science, New York.

Dr Caroline Leaf: Avoid foods containing cellulose

This is an anonymised screen shot taken from Dr Leaf’s Facebook feed just now, showing the very sensible reply of a Canadian dietician to Dr Leaf’s ill-informed assertion.  It’s possible that Dr Leaf’s Facebook minders could delete the dietician’s comments or the post altogether, so I wanted to ensure it was saved for the public record.

In fairness to Dr Leaf, I will post her correction if she is willing to make one.

Caroline Leaf Toxic Ingredients 2

Going green – why envy is an adaptive process

The Bible says, in Job 5:2, “For wrath kills a foolish man, And envy slays a simple one.”

A German proverb goes, “Envy eats nothing, but its own heart.”

Dr Caroline Leaf, communication pathologist and self-titled cognitive neuroscientist, posted today on her social media feeds, “Jealousy and envy creates damage in the brain … but … celebrating others protects the brain!”

Yes, sometimes envy isn’t good for us. Emotions guide our thought process, and like all emotions that are out of balance, too much envy can cloud our better rational judgement and bias our perception of the world. Thankfully, envy doesn’t literally eat out our hearts or literally cause brain damage.

If anything, envy when experienced in a balanced way can actually improve our brain functioning. According to real cognitive neuroscientists, envy and regret are emotions that help us because they both fulfil the role of effectively evaluating our past actions, which improves our choices in the future. As Coricelli and Rustichini noted, “envy and regret, as well as their positive counterparts, share the common nature that is hypothesized in the functional role explanation: they are affective responses to the counterfactual evaluation of what we could have gotten had we made a different choice. Envy has, like regret, a functional explanation in adaptive learning.” [1]

When it comes to the human psyche, there is no black or white, good vs evil distinction between different feelings or emotions. B-grade life coaches and slick pseudoscience salespeople dumb down our emotions into a false dichotomy because it helps sell their message (and their books). Every emotion can be either helpful or unhelpful depending on their context in each individual.

As Skinner and Zimmer-Gembeck wrote, “Emotion is integral to all phases of the coping process, from vigilance, detection, and appraisals of threat to action readiness and coordinating responses during stressful encounters. However, adaptive coping does not rely exclusively on positive emotions nor on constant dampening of emotional reactions. In fact, emotions like anger have important adaptive functions, such as readying a person to sweep away an obstacle, as well communicating these intentions to others. Adaptive coping profits from flexible access to a range of genuine emotions as well as the ongoing cooperation of emotions with other components of the action system.” [2]

If you find your thoughts and feelings tinged by the greenish hue of envy, don’t worry, it’s not necessarily a bad thing. Your heart isn’t going to consume itself and you won’t sustain any brain damage. Use envy or regret as tools of learning, tools to help you evaluate your choices so that you make a better choice next time. Having balanced emotions is the key to learning and growing, coping with whatever obstacles life throws at us.

References

  1. Coricelli, G. and Rustichini, A., Counterfactual thinking and emotions: regret and envy learning. Philos Trans R Soc Lond B Biol Sci, 2010. 365(1538): 241-7 doi: 10.1098/rstb.2009.0159
  2. Skinner, E.A. and Zimmer-Gembeck, M.J., The development of coping. Annu Rev Psychol, 2007. 58: 119-44 doi: 10.1146/annurev.psych.58.110405.085705