Does sadness make you sick?

LeafMeme20160107

We’ve all heard of being “homesick”, or “heartsick”, or “lovesick”.   Sometimes when we’re extremely sad, we feel the knot in our stomachs, the pressure in our chests, or the confusion and distraction in our minds as the waves of sadness wash over and discombobulate us.

But can being sad really make you physically ill as well as emotionally distraught?

Dr Caroline Leaf declared today on her social media platforms that “Feeling sad can alter levels of stress-related opioids in the brain and increase levels of inflammatory proteins in the blood that are linked to increased risk of comorbid diseases including heart disease, stroke and metabolic syndrome.”

Dr Caroline Leaf is a communication pathologist and a self-titled cognitive neuroscientist.  She believes that our cognitive stream of thought determines our physical and mental health, and can even influence physical matter through the power of our minds.

She also added some further interpretation to her meme: “So this is more evidence that our thoughts do count: they have major epigenetic effects on the brain and body! We need to apply the principles in the Bible and listen to the Holy Spirit – no excuses this year!”

With all due respect to Dr Leaf, the study she quotes doesn’t prove anything of the sort.

Dr Leaf’s meme is a copy and paste of the opening paragraph of a news report published by the university’s PR people to promote their faculty.  This isn’t a scientific summary, it’s a hook to draw attention to an article which amounts to a PR puff piece.  If Dr Leaf had read further into the article, I don’t think she would have been quite so bold in claiming what she did.

The article discussed a study by Prossin and colleagues, published in Molecular Psychiatry [1].  You can read the original study here.  The study specifically measured the change in the level of the activity of the opioid neurotransmitter system and the amount of a pro-inflammatory cytokine IL-18 across two experimental mood states, and in two different groups of volunteers, people with depression, and those without.

For a start, it’s important to note that the study isn’t referring to normal day-to-day sadness.  This was an experimentally induced condition in which a sad memory was rehearsed so that the same feeling could be reproduced in a scanner, and the study was looking at the effect of this sad “mood” on people who were pathologically sad, that is, people diagnosed with major depression.

It’s well known that people with depression are at a higher risk of major illnesses, such as heart attacks, strokes and diabetes [2] The current study by Prossin et al looked experimentally at one possible link in the chain, a link between a neurotransmitter system that’s thought to change with emotional states, and one of the chemical mediators of inflammation.

They found that:

> Depressed people were much sadder to start with, and remained so throughout the different conditions.  The depressed people stayed sadder in the ‘neutral’ phase, and the healthy cohort couldn’t catch them in the ‘sad’ phase.
> Depressed people had a much higher level of the inflammatory marker to start with, and interestingly, this level dropped significantly with the induction of the neutral phase and the sad phase.  What was also interesting was that the level of the inflammatory marker was about the same in the baseline and the sad phase for the healthy volunteers.
> A completely different pattern of neurotransmitter release was seen in the two different groups.  People with depression had an increase in the neurotransmitter release over a large number of areas of the brain, whereas in the healthy controls with normal mood, the sad state actually resulted in a decreased amount of neurotransmitter release, and in a much smaller area within the brain.  This suggests that the opioid neurotransmitter system in the brains of depressed people is dysfunctional.

Affect/Sadness Scores - Prossin et al Molecular psychiatry 2015 Aug 18.

Affect/Sadness Scores – Prossin et al Molecular psychiatry 2015 Aug 18.

IL18 v Mood state/diagnosis - Prossin et al Molecular psychiatry 2015 Aug 18.

IL18 v Mood state/diagnosis – Prossin et al Molecular psychiatry 2015 Aug 18.

Effectively, the results of the study reflect what’s already known – the emotional dysregulation seen in people with depression is because of an underlying problem with the brain, not the other way around.  And, sadness in normal people is not associated with a significant change in the evil pro-inflammatory cytokine.

So, according to Prossin’s article,

  1. normal sadness in normal people is not associated with physical illnesses.
  2. sadness is abnormally processed in people who are depressed, which maybe related to an abnormal inflammatory response, which might explain the known link between depression and increased risk of illness

The article is not “more evidence that our thoughts do count.”  If anything, it shows that underlying biological processes are responsible for our thoughts and emotions and their downstream effects, not the thoughts and emotions themselves.

And unfortunately, it appears that Dr Leaf hasn’t got past the opening paragraph of a puff piece article before jumping to a conclusion which only fits her worldview, not the actual science.

References

[1]        Prossin AR, Koch AE, Campbell PL, Barichello T, Zalcman SS, Zubieta JK. Acute experimental changes in mood state regulate immune function in relation to central opioid neurotransmission: a model of human CNS-peripheral inflammatory interaction. Molecular psychiatry 2015 Aug 18.
[2]        Clarke DM, Currie KC. Depression, anxiety and their relationship with chronic diseases: a review of the epidemiology, risk and treatment evidence. Med J Aust 2009 Apr 6;190(7 Suppl):S54-60.

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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

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/#

Fat checking … sorry, fact checking

Screen Shot 2014-11-13 at 5.11.18 pm

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

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

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

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

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

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

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

References

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