Gluten mad!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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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 and dualism revisited

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Are we a body with a mind, or a mind with a body?

This may sound like a chicken-and-egg type of conundrum, but it’s a deep philosophical question. The concept of the separation of the mind from the body is known as dualism, and has been debated for centuries because the answer to that question then guides a lot of other philosophies and theories.

Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist. She believes that the body and brain are separate from the mind, which significantly influences her teaching. Take, for example, her social media meme-of-the-day today. She posted that, “The brain does not change itself… our MIND changes the brain”. If one assumes that the mind is separate from our brain, then its plausible that the mind influences the brain.

Except that it doesn’t. Our mind is a product of our brain, not a separate entity. Neurological damage from injuries or tumours, electrical stimulation of the brain in the lab, the effect of illicit drugs on the brain like LSD or marijuana, and everyday examples like the changes to our thinking under the influence of caffeine or alcohol, all prove that changes to the structure and function of the brain change thought patterns. It isn’t the other way around. Every brain changes itself too – the brain of an embryo or foetus undergoes massive changes but foetuses don’t have streams of conscious thought. Dr Leaf’s meme is scientifically misguided.

Perhaps what is more worrying is Dr Leaf’s use of scripture to try and justify her view that the mind and the brain are separate. To introduce her meme, Dr Leaf wrote, “Read Luke 16:19-31 to see that the mind is separate from the brain – this is God’s divine design.”

There are a number of scriptures that theologians use to discuss the biblical basis for the separation of the body and soul, but Luke 16:19-31 isn’t one of them. That passage is the parable of Lazarus and the rich man.

It says:

‘There was a rich man who was dressed in purple and fine linen and lived in luxury every day. At his gate was laid a beggar named Lazarus, covered with sores and longing to eat what fell from the rich man’s table. Even the dogs came and licked his sores.
‘The time came when the beggar died and the angels carried him to Abraham’s side. The rich man also died and was buried. In Hades, where he was in torment, he looked up and saw Abraham far away, with Lazarus by his side. So he called to him, “Father Abraham, have pity on me and send Lazarus to dip the tip of his finger in water and cool my tongue, because I am in agony in this fire.”
‘But Abraham replied, “Son, remember that in your lifetime you received your good things, while Lazarus received bad things, but now he is comforted here and you are in agony. And besides all this, between us and you a great chasm has been set in place, so that those who want to go from here to you cannot, nor can anyone cross over from there to us.”
‘He answered, “Then I beg you, father, send Lazarus to my family, for I have five brothers. Let him warn them, so that they will not also come to this place of torment.”
‘Abraham replied, “They have Moses and the Prophets; let them listen to them.”
‘“No, father Abraham,” he said, “but if someone from the dead goes to them, they will repent.”
‘He said to him, “If they do not listen to Moses and the Prophets, they will not be convinced even if someone rises from the dead.”’ (Luke 16:19-31, NIV)

I’m not sure exactly where the convincing proof of the separation of our mind and our body is found in this passage. This is a description of the afterlife, and in this parable, the rich man was very specific about memories (“I have five brothers …”) as well as physical sensations (“I am in agony in this fire”) and even parts of the body (Lazarus’s finger, his tongue). Jesus isn’t telling a story of how the mind is separate to the body, but of a different dimension in which the body and the mind are still together. This passage isn’t proof for the concept of dualism, but against it.

Dualism also has a number of fatal scientific and philosophical flaws, in particular that dualism is conceptually fuzzy, experimentally irrefutable, considers only the adult mind, and violates physics, in particular the law of conservation of energy.

So Dr Leaf bases her teaching on a scientifically and philosophically untenable concept and then attempts to use a scripture which refutes dualism in her attempt to support it. That’s audacious, but then to claim that it’s God’s divine design is, at best, a little brazen.

Dualism may be one of her fundamental philosophies, but I think Dr Leaf should review the basis for it, and possibly reconsider her reliance on it.

For a more in-depth discussion on Dr Leaf and dualism, please see my essay: Dr Caroline Leaf, Dualism, and the Triune Being Hypothesis

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.

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

Runners-Wine-Club

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

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

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

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

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

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

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

Cheers!

References

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

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

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

Dr 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.