Tag Archives: obesity

Lancet confirms fat is bad

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Earlier this week, the prestigious medical journal The Lancet published an article about the health effects of obesity [1].

Spoiler alert – obesity kills you.

That sounds a lot like old news.  Why is a leading medical journal wasting space printing studies that tell us what we already know?  Well, up until now, the answer wasn’t as settled as people might have thought.

From the earliest writings of the ancient Greeks, fat people were always considered weak-willed or morally lacking.  Obese people either over-indulged or were lazy sods that deserved the indignation of the clearly morally superior skinny people.  Medical science initially seemed to back up that notion with hard data.  Body Mass Index (or BMI, your weight in kilograms divided by your height in metres squared) between 20 and 25 was the ultimate goal, and if you were above that, you were set to live a shorter and unhappier life.

Then a few years ago, a few studies came out showing that being overweight wasn’t as dire as people thought, and in fact, some studies showed that being overweight and mildly obese offered a small survival advantage over a weight in the “normal” range [2].  This was known as the obesity paradox.

So questions hung in the air like the sickly sweet smell of freshly baked donuts – Did the medical community get obesity wrong?  Were we meant to be cuddly instead of bony?  Were the lard nazi’s tricking us into lifestyles of kale and sit ups under false pretences?

The study by the objectively named Global BMI Mortality Collaboration seems to have definitively answered those questions.  The Global BMI Mortality Collaboration was a collective effort of more than 500 researchers from more than 32 countries, who pooled the resources of 239 different studies involving more than 10 million adults.  The collaborators weeded out more than 6 million people to form a group of 3,951,455 people who had never smoked and had not been diagnosed with a chronic disease before being recruited, and who had survived for more than 5 years after being recruited.  This made their group of participants in this study as statistically robust as possible.  These participants were followed for about 14 years.  Overall, 385,879 of them died.  To see whether obesity had an impact on mortality, they adjusted the raw numbers for age and gender, and calculated the likelihood of a participant dying depending in their BMI.

It isn’t good news for those of us who are of ample proportion.  Compared to those in the healthiest weight range, the most obese had a two-and-half times greater risk of dying from any cause.  Those who were overweight but not obese, which the previous studies suggested may have been ok, had an increased risk of dying too, but only by about 7%.  Obese males had a higher risk of dying than obese females, and obesity was worse for you if you were obese and young rather than obese and old.  Though before all the skinny people start skiting, those with a BMI of under 20 also had a higher mortality.  The best place to be was with a BMI of 20-25.

 

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Statistically speaking, this is a really strong study, so the conclusions it draws are hard to argue with.  It confirms that the BMI of 20-25 is the ideal weight, and that either extreme of body weight is certainly undesirable.

There are a couple of things to note.  Firstly, being overweight still isn’t that bad.  Sure, it’s not ideal like the older studies may have said, but a 7% increase in all-cause mortality isn’t going to particularly cut your life short.  So don’t panic about your love handles just yet.

Secondly, despite the statistical power of this study, it really only answers the single question: Is obesity related to mortality?  It answers it, and it answers it conclusively, but it doesn’t tell us how or why obesity and mortality are related, which are more important questions overall.

Because while it’s necessary to know that obesity, illness and death are related, knowing how they are related can then help us understand the why of obesity, which will then help doctors give patients real information that they can use.

For example, the Lancet study didn’t look at causation.  Is it that obesity causes chronic diseases which then cause early mortality like is the case with smoking?  Or is it that there’s another cause underlying both obesity and chronic disease, with obesity being unfairly framed in a guilt-by-association way?

Obesity Guilty Framed

What about mitigating factors?  If you’re fat but you’re also very fit, what’s your mortality then?  If you have a gastric bypass or a gastric sleeve and you shed a hundred pounds, does your mortality improve?  I’ll try and answer some of these question in future blogs.

Like all good research, this study in The Lancet seems to have generated more questions than answers.  What’s certain is that more research needs to be done.

If you are obese and you are concerned about your health, then talk to your GP or dietician.  Be sensible with your health.  Sure, obesity isn’t great, but you can sometimes do as much damage to yourself through poorly designed weight loss programs than you can with a dozen donuts.

References
[1]        Global BMI Mortality Collaboration. Body-mass index and all-cause mortality: individual participant data meta-analysis of 239 prospective studies in four continents. Lancet 2016 13 july 2016.
[2]        Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA : the journal of the American Medical Association 2013 Jan 2;309(1):71-82.

Can an aspirin a day keep the psychiatrist away?

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Floating across my Facebook feed this morning was an article on the possible link between depression and inflammation.  Its premise was that depression, the joyless soul-sucking disease affecting millions of people around the world, is related to inflammation.  If that were true, might mean that we could cure depression with medications that stop inflammation.  Maybe we should be consuming an aspirin a day to keep the doctor away, and not the proverbial apple?

Inflammation is a hot topic right now.  Inflammation in the medical sense refers to a normal body process to promote healing and recovery from sickness or injury.  It’s a complex dance of chemical signals which is triggered by damage to tissue.  Inflammation is essential to life. Without it, we would be unable to repair our tissues if they were damaged.

When tissues are damaged, a number of local cells in the damaged area release pro-inflammatory cytokines which then trigger a cascade of responses; increase in the size of the local blood vessels to allow greater blood flow to the area, attracting pus-cells (neutrophils) to the area, and increasing the ‘leakiness’ of the blood vessels to allow the pus cells into the area. This response is governed by a number of chemical mediators throughout the body, including histamine, serotonin, complement system, kinins, substance P, prostaglandins and leukotrienes, cytokines and nitric oxide. Anti-inflammatory cytokines balance out the process, keeping the pro-inflammatory cytokines in check so that the process doesn’t spiral out of control.

Despite the literal plethora of chemical reactions going on simultaneously, most of the time the reaction eventually runs out of noxious agents, the anti-inflammatory cytokines dampen down the reaction, and the tissue returns to either normal, or at least functional.  Though inflammation isn’t just limited to repairing damage but also preparing for damage –psychological stress prepares the inflammation system for potential damage.  Physical stress triggers the inflammation system to repair any damage.

Chronic inflammation occurs when the acute illness or injury does not fully resolve and continues to smoulder, the natural healing pathway is obstructed, or the body remains in a psychological state in which it is always expecting a fight.  In chronic inflammation, the processes of active inflammation, tissue destruction and attempts at healing occur simultaneously. In terms of cytokines, the anti-inflammatory cytokines can’t balance out the excess pro-inflammatory cytokines.

There’s a theory about depression which is gaining momentum within the scientific community, that depression and a number of other psychiatric and neurodegenerative conditions are the result of chronic inflammation which occurs because of chronic stress.

Remember when I said before that psychological stress readies the inflammatory system for potential damage?  Well, what if that damage never comes?  If there’s chronic psychological stress, the system is constantly being worn down, and never getting a chance to recover.  This seems to make sense – chronic stress reduces new nerve cell production and growth, and may interfere with the action of nerve growth factors like BDNF and neurotransmitters like serotonin.  Hence why this article by Feelguide seems to ring true.

But is it true?  Is depression fundamentally an inflammatory disease, and if so, can we treat it with medications that decrease inflammation, like aspirin?

Let’s go through the various statements made in the Feelguide article and see what the medical evidence says.

First, a necessary correction to avoid confusion.  The Feelguide article says that, “New research is revealing that many cases of depression are caused by an allergic reaction to inflammation.”  Depression is not an allergic reaction.  A true allergy is an antibody response which releases a chemical called histamine from cells called mast cells.  If the current theory about depression and inflammation is true, then depression is related to cytokines, chemicals that are entirely different to histamine.  It may be really annoying to sneeze like you’re demon possessed if a cat’s been in the same room a week ago, but it’s not going to make you depressed.

Is inflammation caused by obesity, high sugar diets, high quantities of trans fats, unhealthy diets in general?  There’s limited evidence that the foods you eat result in inflammation.  Most of the positive data comes from observational studies which are relatively weak.  Better, stronger studies generally give conflicting information [1].  For example, if high fat, sugary foods were really the cause of low grade inflammation, then diets like the Palaeolithic diet, which replace sugary, fatty processed foods with a bucket load of vegetables should improve inflammation.  Yet there have been no statistically significant changes in inflammatory markers recorded in subjects following the Palaeolithic diet [2].

The Feelguide article claims that, “By treating the inflammatory symptoms of depression – rather than the neurological ones – researchers and doctors are opening up an exciting new dimension in the fight against what has become a global epidemic”, but let’s not get too excited.  Again, there’s precious little evidence that medications or supplements reported to reduce inflammation make any difference to depression.  For example, the article mentions omega-3 and curcumin as having some benefit in the treatment of depression, which is half-right.  There’s some evidentiary support that EPA-predominant omega-3 supplements may have some effect on depression, but none at all for DHA omega-3’s [3] or curcumin [4].

When it comes to other medications with an anti-inflammatory effect, the results are similarly mixed.  The issue seems to be the specific cellular action of the medication on a particular immune cell in the brain called the microglial cell.  For example, normal anti-inflammatory medications like aspirin and other Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) increased the activity of these special microglial cells which resulted in an increase in depressive symptoms in otherwise healthy individuals, whereas a medication called minocycline has been noted to decrease the activity of these microglia, and reduced the risk of depressive symptoms (in animal studies at least) [5].

So we really can’t say whether medications believed to have an anti-inflammatory effect really have any significant benefit.  As neuroscientists, Dr Dora Brites and Dr Adelaide Fernandes wrote,

“Nevertheless, we should be cautious in believing that depression can be treated by therapies targeting inflammation. Further studies are required to evaluate whether a combined therapy with anti-inflammatory compounds and antidepressants will result in additional clinical benefits.” [5]

That’s really because we don’t know whether inflammation causes depression, or if depression causes inflammation.  The article by Feelguide seem pretty confident, but the science is still a long way from being settled.

The final word is this:
1. Depression is complicated and still poorly understood.
2. It may be related to inflammation, but please don’t rely on herbs or medications that claim to have anti-inflammatory or “immune boosting” properties.
3. If you really want to try and treat your depression without pharmaceutical medications, take some EPA Omega 3 supplements by all means, although I’d encourage you to exercise and engage with a good psychologist too, both of which have more evidence of benefit overall.

References

[1]        Minihane AM, Vinoy S, Russell WR, et al. Low-grade inflammation, diet composition and health: current research evidence and its translation. The British journal of nutrition 2015 Oct 14;114(7):999-1012.
[2]        Pitt CE. Cutting through the Paleo hype: The evidence for the Palaeolithic diet. Aust Fam Physician 2016 Jan-Feb;45(1):35-8.
[3]        Hallahan B, Ryan T, Hibbeln JR, et al. Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression. The British journal of psychiatry : the journal of mental science 2016 Apr 21.
[4]        Andrade C. A critical examination of studies on curcumin for depression. J Clin Psychiatry 2014 Oct;75(10):e1110-2.
[5]        Brites D, Fernandes A. Neuroinflammation and Depression: Microglia Activation, Extracellular Microvesicles and microRNA Dysregulation. Front Cell Neurosci 2015;9:476.

Cutting through the Paleo hype

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Paleo-Diet-Meal-Plan1

Fad diets come and go. One of the most popular fad diets of recent times is Paleo.

The Palaeolithic diet, also called the ‘Stone Age diet’, or simply ‘Paleo’, is as controversial as it is popular. It’s been increasing in popularity over the last few years, and has had some amazing claims made of it by wellness bloggers and celebrity chefs. Advocates like ‘Paleo’ Pete Evans of MKR fame, claim that the Palaeolithic diet could prevent or cure poly-cystic ovarian syndrome, autism, mental illness, dementia and obesity [1].

So what does the published medical literature say? Is there really good research evidence to support the vast and extravagant claims of Paleo?

About 10 months ago, I started reviewing the medical research to try and answer that very question. My review of the medical literature turned up some interesting results, and so rather than post it just as a blog, I thought I would submit it to a peer-reviewed medical journal for publication. After a very nervous 9-month gestation of submission, review, and resubmission, my article was published today in Australian Family Physician [2].

So, why Paleo, and what’s the evidence?

Why Paleo?

The rationale for the Palaeolithic diet stems from the Evolutionary Discordance hypothesis – that human evolution ceased 10,000 years ago, and our stone-age genetics are unequipped to cope with our modern diet and lifestyle, leading to “diseases of civilization” [3-9]. Thus, only foods that were available to hunter-gatherer groups are optimal for human health – “could I eat this if I were naked with a sharp stick on the savanna?” [10] Therefore meat, fruits and vegetables are acceptable, but grains and dairy products are not [11].

Such views have drawn criticism from anthropologists, who argue that that there is no blanket prescription of an evolutionarily appropriate diet, but rather that human eating habits are primarily learned through behavioural, social and physiological mechanisms [12]. Other commentators have noted that the claims of the Palaeolithic diet are unsupported by scientific and historical evidence [13].

So the Palaeolithic diet is probably nothing like the actual palaeolithic diet. But pragmatically speaking, is a diet sans dairy and refined carbohydrates beneficial, even if it’s not historically accurate?

Published evidence on the Palaeolithic Diet

While the proponents of the Palaeolithic diet claim that it’s evidence based, there are only a limited number of controlled clinical trials comparing the Palaeolithic diet to accepted diets such as the Diabetic diet or the Mediterranean diet.

Looking at the studies as a whole, the Palaeolithic diet was often associated with increased satiety independent of caloric or macronutrient composition. In other words, gram for gram, or calorie for calorie, the Paleo diets tended to make people fuller, and therefore tend to eat less. Of course, that may have also been because the Paleo diet was considered less palatable and more difficult to adhere to [14]. A number of studies also showed improvements in body weight, waist circumference, blood pressure and blood lipids. Some studies showed improvements in blood sugar control, and some did not.

The main draw back of clinical studies of Paleo is that the studies were short, with different designs and without enough subjects to give the studies any statistical strength. The strongest of the studies, by Mellburg et al, showed no long-term differences between the Palaeolithic diet and a control diet after two years [15].

The other thing to note is that, in the studies that measured them, there was no significant difference in inflammatory markers as a result of consuming a Palaeolithic diet. So supporters of Paleo don’t have any grounds to claim that Paleo can treat autoimmune or inflammatory diseases. No clinical study on Paleo has looked at mental illness or complex developmental disorders such as autism.

Other factors also need to be considered when thinking about Paleo. Modelling of the cost of the Palaeolithic diet suggests that it is approximately 10% more expensive than an essential diet of similar nutritional value, which may limit Paleo’s usefulness for those on a low income [16]. Calcium deficiency also remains a significant issue with the Palaeolithic diet, with the study by Osterdahl et al (2008) demonstrating a calcium intake about 50% of the recommended dietary intake [17]. Uncorrected, this could increase a patients risk of osteoporosis [18].

To Paleo or not to Paleo?

The bottom line is the Paleo diet is currently over-hyped and under-researched. There are some positive findings, but these positive findings should be tempered by the lack of power of these studies, which were limited by their small numbers, heterogeneity, and short duration.

If Paleo is to be taken seriously, larger independent trials with consistent methodology and longer duration are required to confirm the initial promise in these early studies. But for now, claims that the Palaeolithic diet could treat or prevent conditions such as autism, dementia and mental illness are not supported by clinical research.

If you’re considering going on the Palaeolithic diet, I would encourage you to talk with an accredited dietician or your GP first, and make sure that it’s right for you. Or you could just eat more vegetables and drink more water, which is probably just as healthy in the long run, but without the weight of celebrity expectations.

Comparison of the current Australian Dietary Guidelines Recommendations [19] to the Palaeolithic diet [17]

Australian Dietary Guidelines The Palaeolithic Diet
Enjoy a wide variety of nutritious foods from these five groups every day:  
Plenty of vegetables, including different types and colours, and legumes/beans Ad libitum fresh vegetables and fruits
Fruit
Grain (cereal) foods, mostly wholegrain and/or high cereal fibre varieties, such as bread, cereals, rice, pasta, noodles, polenta, couscous, oats, quinoa and barley All cereals / grain products prohibited, including maize and rice
Lean meats and poultry, fish, eggs, tofu, nuts and seeds, and legumes/beans Ad libitum lean meats and poultry, fish, eggs, tofu, nuts and seeds, but all legumes prohibited
Milk, yoghurt, cheese and/or their alternatives, mostly reduced fat (reduced fat milks are not suitable for children under 2 years) All dairy products prohibited
And drink plenty of water. Ad libitum water (mineral water allowed if tap water unavailable)

References

[1]        Duck S. Paleo diet: Health experts slam chef Pete Evans for pushing extreme views. Sunday Herald Sun. 2014 December 7.
[2]        Pitt CE. Cutting through the Paleo hype: The evidence for the Palaeolithic diet. Australian Family Physician 2016 Jan/Feb;45(1):35-38.
[3]        Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition 2010 Dec;25(6):594-602.
[4]        Eaton SB, Eaton SB, 3rd, Konner MJ. Paleolithic nutrition revisited: a twelve-year retrospective on its nature and implications. European journal of clinical nutrition 1997 Apr;51(4):207-16.
[5]        Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. The New England journal of medicine 1985 Jan 31;312(5):283-9.
[6]        Kuipers RS, Luxwolda MF, Dijck-Brouwer DA, et al. Estimated macronutrient and fatty acid intakes from an East African Paleolithic diet. The British journal of nutrition 2010 Dec;104(11):1666-87.
[7]        Eaton SB, Konner MJ, Cordain L. Diet-dependent acid load, Paleolithic [corrected] nutrition, and evolutionary health promotion. The American journal of clinical nutrition 2010 Feb;91(2):295-7.
[8]        O’Keefe JH, Jr., Cordain L. Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer. Mayo Clinic proceedings 2004 Jan;79(1):101-08.
[9]        Eaton SB, Eaton SB, 3rd, Sinclair AJ, Cordain L, Mann NJ. Dietary intake of long-chain polyunsaturated fatty acids during the paleolithic. World review of nutrition and dietetics 1998;83:12-23.
[10]      Audette RV, Gilchrist T. Neanderthin : eat like a caveman to achieve a lean, strong, healthy body. 1st St. Martin’s Press ed. New York: St. Martin’s, 1999.
[11]      Lindeberg S. Paleolithic diets as a model for prevention and treatment of Western disease. American journal of human biology : the official journal of the Human Biology Council 2012 Mar-Apr;24(2):110-5.
[12]      Turner BL, Thompson AL. Beyond the Paleolithic prescription: incorporating diversity and flexibility in the study of human diet evolution. Nutrition reviews 2013 Aug;71(8):501-10.
[13]      Knight C. “Most people are simply not designed to eat pasta”: evolutionary explanations for obesity in the low-carbohydrate diet movement. Public understanding of science 2011 Sep;20(5):706-19.
[14]      Jonsson T, Granfeldt Y, Lindeberg S, Hallberg AC. Subjective satiety and other experiences of a Paleolithic diet compared to a diabetes diet in patients with type 2 diabetes. Nutrition journal 2013;12:105.
[15]      Mellberg C, Sandberg S, Ryberg M, et al. Long-term effects of a Palaeolithic-type diet in obese postmenopausal women: a 2-year randomized trial. European journal of clinical nutrition 2014 Mar;68(3):350-7.
[16]      Metzgar M, Rideout TC, Fontes-Villalba M, Kuipers RS. The feasibility of a Paleolithic diet for low-income consumers. Nutrition research 2011 Jun;31(6):444-51.
[17]      Osterdahl M, Kocturk T, Koochek A, Wandell PE. Effects of a short-term intervention with a paleolithic diet in healthy volunteers. European journal of clinical nutrition 2008 May;62(5):682-85.
[18]      Warensjo E, Byberg L, Melhus H, et al. Dietary calcium intake and risk of fracture and osteoporosis: prospective longitudinal cohort study. BMJ 2011;342:d1473.
[19]      National Health and Medical Research Council. Australian Dietary Guidelines. Canberra: National Health and Medical Research Council; 2013.

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

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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 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.