The soul, stress, sugar and spin

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Stress and sugar.  In our post-modern society’s orthorexic narrative, these are two of the biggest villains.  So combining them into a diabolical duo reinforces their evil even more.

Dr Caroline Leaf is a communication pathologist, self-titled cognitive neuroscientist and Christian life coach.  In her latest newsletter to her adoring fans, Dr Leaf has accused sugar and stress of mass murder, with our soul’s approach to stress as their accomplice.

I’m sure Dr Leaf means well, but just because she’s not trying to frighten sales out of the gullible and vulnerable doesn’t mean she gets a free pass on the accuracy of her information.

To boil it down, Dr Leaf’s argument goes something like this:

Our choices turn good stress into bad stress
Bad stress releases excess cortisol which leads to disease and death
Therefore our choices to stress causes disease and death

We control our choices through our minds
Therefore, our mind is the key to stress illness
(oh, and sugar …)

The arguments seem plausible on the surface.  Most people have heard enough about stress to know about ‘good’ stress and ‘bad’ stress.  It doesn’t seem too much of a stretch to say that ‘bad’ stress is a significant cause of disease and death.  In the middle of her essay, Dr Leaf jumps from stress to sugar with no preceding link, but again, most people have heard that sugar is unhealthy, so they would probably just accept that statement too.

Unfortunately for Dr Leaf, her article has several critical errors which turn her well-meaning educational essay into a science-fiction short story.

To start with, her essay is built on the dysfunctional premise that the mind controls the brain, so each higher argument or premise is fundamentally skewed from the outset, and in doing so, Dr Leaf simply creates a circular argument of distorted factoids.

For example, her opening sentence: “The hypothalamus is a central player in how the mind (soul) controls the body’s reaction to stress and foods.”  The hypothalamus is a part of the limbic system deep in the brain.  It’s the main pathway from the brain to the endocrine system as Dr Leaf goes on to correctly assert, but essentially it runs on auto-pilot, responding automatically to information already being processed at a level beyond the reach of our conscious awareness and control.  For example, the hypothalamus regulates our body temperature, but it does so without our conscious control.  We can not consciously will our body temperature up or down just with our minds.

It’s the same with the stress response – there are many times where people have a subconscious stress response, where their mind feels like there’s nothing to be afraid of, but their hypothalamus is still priming their system for fight or flight.  White coat hypertension is a prime example.  White coat hypertension, or “White Coat Syndrome” is the phenomenon of people having high blood pressure in their doctor’s office but not at home.  Patients will say to me all the time, “I don’t know why my blood pressure is so high in here.  I feel fine.  I know there’s nothing to be afraid of here.”  But while their conscious mind is relaxed, their deeper subconscious brain remembers those injections that hurt, or that one time a doctor stuck the tongue depressor too far down their throat and they felt like they choked on it, and their hypothalamus is preparing them for whatever nastiness the doctor has for them this time.

Dr Leaf’s statement fails because she wrongly equates our brain with our mind, a subtle perversion which doesn’t just invalidate her premise, but significantly skews the essay as a whole.

As a quick aside, Dr Leaf also says that the hypothalamus “integrates signals from the mind and body, sending them throughout our bodies so that we can react in an appropriate and functional manner, ‘so that the whole body is healthy and growing and full of love’ (Eph. 4:16 NLT)”.  Ephesians 4:16 isn’t talking about the physical body, but about the body of Christ.  You don’t need to be a Biblical scholar to know this, you just have to be able to read.  Here is what the Bible says, “And He Himself gave some to be apostles, some prophets, some evangelists, and some pastors and teachers, for the equipping of the saints for the work of ministry, for the edifying of the body of Christ, till we all come to the unity of the faith and of the knowledge of the Son of God, to a perfect man, to the measure of the stature of the fullness of Christ; that we should no longer be children, tossed to and fro and carried about with every wind of doctrine, by the trickery of men, in the cunning craftiness of deceitful plotting, but, speaking the truth in love, may grow up in all things into Him who is the head — Christ — from whom the whole body, joined and knit together by what every joint supplies, according to the effective working by which every part does its share, causes growth of the body for the edifying of itself in love.” (Ephesians 4:11-16, emphasis added).

There’s no subtlety about this misuse of scripture.  Even non-Christians would be able to figure out that this verse has nothing to do with the physical body.  Dr Leaf has demonstrated that she either doesn’t read the Bible or doesn’t understand it.  Either way, this is a shameful indictment on Dr Leaf’s claim that she’s a “Biblical expert”, and should be ringing alarm bells for every pastor that is considering letting her get behind the pulpit of their church.

Dr Leaf rolls on with her list of medical misinformation.  Some of it is subtle (the “stages of stress”, also termed the General Adaptation Model, is an outdated model of the stress response [1], and CRF and ACTH are released during all stages of stress, not just stage 1).  Some of it is outlandish, like her claim that high levels of stress leads to Cushing’s Syndrome (see http://emedicine.medscape.com/article/2233083-overview#a4 for a list of the causes of Cushing’s Syndrome and note that stress isn’t on the list).

Dr Leaf’s also suggested that it was solely our perception of stress that was the key factor in the outcome of stress, making reference to “a study” showing a 43% increase in mortality if you thought stress was bad.  This is an example of cherry-picking at it’s finest, where one study’s findings are misrepresented to try and support one’s pre-existing position.  Dr Leaf didn’t bother to list her references at the end of the article, instead expecting people to find it for themselves, but I’ve previously seen the study she’s referring to.  Keller and colleagues published the study in 2012 [2].  Their survey suggested a correlation between overall mortality and the combination of lots of stress and the belief that stress is bad.  But remember, correlation does not equal causation, a golden rule which Dr Leaf is quick to ignore when the correlation suits her argument.  The Keller study, while interesting, did not control for the impact of neuroticism, the “negative” personality type which is largely genetically determined and is independently associated with a higher mortality [3-9].  It does not prove that thinking about your stress in a better way makes you live longer.

Dr Leaf went on to claim that “the researchers estimated that the 18,200 people who died, died from the belief that stress is bad for you—that is more than two thousand deaths a year.”  Even here, Dr Leaf manages to get her facts wrong.  The authors actually wrote, “Using these cumulative hazards at the end of the study follow-up period under the assumption of causality, it was estimated that the excess deaths attributable to this combination of stress measures over the study period was 182,079 (controlling for all other covariates), or about 20,231 deaths per year (over 9 years).”

Dr Leaf can’t even get her vexatious arguments right.  Not that the number really matters, because notice how the authors described the magic number as an “assumption of causality”.  Basically the authors said, ‘Well, IF this was the cause of death, then these would be the numbers of deaths attributable.’  They NEVER said that anyone actually died because of their beliefs about stress.  Indeed, the results showed that just believing that stress was bad didn’t make any difference to the mortality rate as Dr Leaf suggested – it was the interaction of high stress AND the belief it was bad that was associated with a higher mortality.  But why let pesky issues like methodological rigour get in the way of sensationalist hyperbole.

Then in the penultimate paragraph, Dr Leaf suddenly decides to throw sugar into the mix.  Somehow without justification, stress is bad and therefore sugar is also bad, and they both throw the hypothalamus and the rest of the body into toxicity.

Dr Caroline Leaf is promoted, by herself and by many in the Christian church, as a Biblical and scientific expert, but in one short promotional essay, Dr Leaf makes multiple critical scientific and exegetical errors.  In other words, her errors in discussing scientific findings and basic Biblical text are so massive that they are incongruent with her claim to be an expert.

Something needs to change – either Dr Leaf revises her knowledge and improves her accuracy, or she needs to stop misleading people from pulpits, both virtual and real.

References

[1]        McEwen BS. Stressed or stressed out: what is the difference? Journal of psychiatry & neuroscience : JPN 2005 Sep;30(5):315-8.
[2]        Keller A, Litzelman K, Wisk LE, et al. Does the perception that stress affects health matter? The association with health and mortality. Health Psychol 2012 Sep;31(5):677-84
[3]        Okbay A, Baselmans BM, De Neve JE, et al. Genetic variants associated with subjective well-being, depressive symptoms, and neuroticism identified through genome-wide analyses. Nature genetics 2016 Apr 18.
[4]        Servaas MN, Riese H, Renken RJ, et al. The effect of criticism on functional brain connectivity and associations with neuroticism. PloS one 2013;8(7):e69606.
[5]        Hansell NK, Wright MJ, Medland SE, et al. Genetic co-morbidity between neuroticism, anxiety/depression and somatic distress in a population sample of adolescent and young adult twins. Psychological medicine 2012 Jun;42(6):1249-60.
[6]        Koelsch S, Enge J, Jentschke S. Cardiac signatures of personality. PloS one 2012;7(2):e31441.
[7]        Vinkhuyzen AA, Pedersen NL, Yang J, et al. Common SNPs explain some of the variation in the personality dimensions of neuroticism and extraversion. Translational psychiatry 2012;2:e102.
[8]        Gonda X, Fountoulakis KN, Juhasz G, et al. Association of the s allele of the 5-HTTLPR with neuroticism-related traits and temperaments in a psychiatrically healthy population. Eur Arch Psychiatry Clin Neurosci 2009 Mar;259(2):106-13.
[9]        Lahey BB. Public health significance of neuroticism. Am Psychol 2009 May-Jun;64(4):241-56.

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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.

Book review: “Think and Eat Yourself Smart” by Dr Caroline Leaf

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Think and Eat Yourself Smart
Dr Caroline Leaf
328 pages, Published by Baker Books USA

My rating: 2 / 10

As a society, we are obsessed with food.  With copious food blogs, celebrity chefs and reality cooking shows, food has become more about our social status and self-identity than about nourishment.

Food has always been intimately connected to our health and well-being, and the modern food obsession has taken that to extreme levels as well.   Organic, paleo, sugarless, raw food, cleansing and other popular diets have morphed into ‘movements’, the polite shorthand way of describing popular obsessions that are borderline cults.

Trying to cash in on this wave of cultural orthorexia is Dr Caroline Leaf with her latest book, “Think and Eat Yourself Smart”, published in early April by Baker Books.

Dr Leaf describes the book as “an attempt to reintroduce a culture of thinking and effort back into eating, one based on diligently stewarding the body and world God entrusted to us.  In the spirit of renewing the mind, it is a lifestyle book that seeks to reimagine what we eat within an integrated spirit, mind and body framework.”

And that would be fine in theory, though in practice, Dr Leaf uses the book more as a vehicle for divulging her personal food preferences and her socio-political ideology while recycling most of her dubious brain science.

But before we go any further, let me issue a disclaimer: There’ll be some who will look this review and assume I’m being critical of Dr Leaf’s book for the sake of being critical.  I recognise that I’m not Dr Leaf’s number one fan, however, I want to say from the outset of this review that I have approached this as dispassionately and objectively as I can.

“Think and Eat Yourself Smart” is certainly not all bad.  Dr Leaf raises some legitimate issues.  For example, she’s critical of the vitamin and supplement industry and the staggering cost of supplements compared to their very limited benefits.  She discusses the previous dietary advice regarding low-fat foods, and how the misguided attempt to reduce our dietary fat intake lead to a compensatory increase in starch and sugars.  She also discussed the current concerns about too much sugar and refined carbohydrates, and raises the very real problem of food waste and food security.  The recipes at the back of the book contain the usual over-rated hipster foodie ingredients like dandelion, kale, quinoa and chia seeds to maintain Dr Leaf’s foodie creds, although some of the recipes themselves sound alright.

Unfortunately, every truth is outweighed by a multiplex of factoids and misrepresentations.  Dr Leaf clearly favours organic food, which despite her claims, have not been shown to be better tasting, more nutritious, less toxic, and better for the environment.  She’s clearly against genetically modified organisms (or GMO’s), a stance which is more populist than scientific.

Dr Leaf’s underlying premises are also deeply flawed.  It’s clear that she’s been heavily influenced by the work of Michael Pollan and other post-modern food gurus of the same ilk.  She’s critical of modern food systems including all food processing, food transportation, and supermarkets, claiming that modern agriculture and food processing destroys all nutrients and taste.  Dr Leaf claims that “Real food is food grown the way God intended: fresh and nutritious, predominantly local, seasonal, grass-fed, as wild as possible, free of synthetic chemicals, whole or minimally processed, and ecologically diverse.” (p29)

Dr Leaf’s definition of “real food” is nothing more than a romanticised post-modern social construct, and claiming it’s God’s idea doesn’t make it any less misleading.  Of course we want our food to be fresh, and we also want it to be nutritious.  But fresh and nutritious are not dependent on being local, seasonal, ecologically diverse (whatever that means), grass-fed and wild.  In fact, how something can be grass-fed and wild seems contradictory.  Processing food makes it safer, and in most cases, more nutritious that the unprocessed farm gate versions.  There’s virtually no pesticide residues left on conventional produce either, so that’s a moot point.

In fact, modern food is actually easier to eat and digest, more nutritious, tastier, safer, and longer lasting than ever before in human history. Today’s canned and frozen foods are infinitely healthier than in the past, and in some cases, more nutritious than the vegetables straight off the farm (canned tomatoes, for example, because nutrients are more easily absorbed from cooked tomatoes).  Dr Leaf’s idealised view of our agrarian past is false, and the notion that we should return to it is inane.

Dr Leaf also spends a great deal of time trying relate our nutritional health to our thinking.  I discussed this in the pre-review of the book, here.  She claims that “Research shows that 75 to 98% of current mental, physical, emotional and behavioural illnesses and issues come from our thought life; only 2 to 25% come from a combination of genetics and what enters our bodies through food, Medication, pollution, chemicals, and so on.  These statistics show that the mindset behind the meal – the thinking behind the meal – plays a dominant role in the process of human food related health issues, approximately 80 percent.” (p84)

Again, this is a false premise based on bogus science.  75 to 98% of current mental, physical, emotional and behavioural illnesses and issues do not come from our thought life.  What you think and how you feel makes no difference to how your body processes the nutrients you put into it.

This excessive focus on the power of thought is a segue back to her previous teaching, a justification as to why she as a self-titled cognitive neuroscientist should be writing about food.  Unfortunately, the information contained in the second part of the book makes it obvious that she’s not an expert on either.

Sure, Dr Leaf discusses responsibility and choices which are important to what we put in our mouths, but there are so many other variables that are more intrinsic to our individual diets than just personal responsibility.  Like, poverty, income, education, cooking skills or geographic location for example.

Dr Leaf claims that how you think changes how you eat, and how you eat changes how you think.  Except the last part of that statement is mutually exclusive to her premise that the mind is separate to the brain and controls the brain.  What you put in your mouth might change the function of your brain, but how can that change the way you think if the mind is separate to the brain?

This paradox is the death-knell to her books credibility and usefulness.  Not that it makes any difference to Dr Leaf, who conveniently forgets this central tenet of her teaching whenever it suits her.

The advice she provides is also off-track.  The answer to processed food isn’t to plant your own garden, or raise your own chickens, or join a local agro-economic food co-op.  That sort of advice is impractical for the vast majority of her audience.  It excludes everyone who lives in a modern city, or who, like me, has an uncanny ability to kill all but the hardiest of plants.  Even her exhortation to eat “real food” is unnecessarily complicated.

Ultimately, Dr Leaf’s advice isn’t dangerous, but just old and confusing.  Most of the useful information she gives is obscured by the plethora of unnecessary and irrelevant opinions and factoids.  It’s also nothing new.  There have been countless books and blogs written by real nutritionists and dieticians that say the same essential things in much simpler ways.  Even John Oliver did a better job of explaining problems associated with sugar and our modern food systems (* Warning * – Strong language and adult themes).  He’s an agnostic satirical comedian who doesn’t pretend to be a scientific expert, and he still get’s the message across more effectively than Dr Leaf.

To conclude, if you want sound nutritional advice, I’d suggest you head for books by actual dieticians. Professor Rosemary Stanton is one author I would recommend. She’s a Professor of Nutritional Science and Visiting Fellow of the School of Medicinal Sciences at the University of New South Wales.  She’s published hundreds of academic and consumer articles including 33 books on good nutrition.  She’s been lecturing and writing about good food for longer than I’ve been alive.

In contrast, Dr Leaf’s book “Think and Eat Yourself Smart” is a repackaging of stale opinion and dubious science by an author who isn’t a nutritionist, or even a cognitive neuroscientist for that matter.  There might be some helpful advice in there, but it would be difficult for an average reader to pick out what’s beneficial and what’s bogus.

To that end, “Think and Eat Yourself Smart” is a lot like a frozen microwave dinner.  It looks good on the packaging, but what you get on the inside isn’t the same.  There’s a few nutritional morsels, to be sure, but most of it is just offal and gristle that’s been homogenised to an unrecognisable mush and then reassembled.

If you’re a Dr Leaf devotee, or you’re interested in her socio-political views, then by all means, buy this book.  If you want sound nutritional advice, look elsewhere.

 

Let boys be non-stigmatised boys

Boys will be boys ...

“When I was a boy …”

Many a stirring yarn has been started with those exact words, as aging men relive their childhood adventures with sentimental grandiosity increasingly taking over from detail as each passing year blends in with the blur of distant memories.

Ps Greg Gibson wrote an article that caught my attention as it floated across my Facebook feed last night.  Gibson is a pastor in Knoxville, Tennessee.  His “when I was a boy” story recalled his happy times as an energetic child, a serene innocence punctuated by two years of Ritalin-induced misery.

His point: “I think we should let boys be boys, and non-medicated ones at that. Therefore, parents, if at all possible, don’t medicate your boys.”

I think I understand what he’s trying to say, that it’s ok to be an energetic child and to see the extra energy as a strength to harness, not a weakness to control.

That would be fine, except that in trying to normalise energetic behaviour, he also winds up demonising Ritalin.  It may not have been his intention, but whenever someone respected in the community says something negative about stimulant medication or ADHD, it reinforces the oppressive stigma attached to those who suffer from it.

Ps Gibson’s fundamental assumption, that normal but energetic children are being misdiagnosed as ADHD and therefore unnecessarily medicated, happens far less often than the opposite – children with ADHD are misdiagnosed as energetic children that just need to be taught how to control themselves.

Personally, I don’t know of any parent who ever wanted to medicate their child with Ritalin.  If anything, it’s the opposite, because if your child’s on Ritalin, then you must be a lazy parent, or given them too much sugar, or too much screen time, or not hugged them enough as babies, or didn’t practice vaginal seeding, or whatever other form of parent-guilt is being perpetrated by the media at the time. Parents will do everything they can in their power to avoid using Ritalin, because of a culture that blames and shames.

Unfortunately, this means that children who could be helped by Ritalin or other stimulant medication are left behind, because ADHD isn’t the mislabeling of normal energetic children who just need better structure, or better posture, or who learn differently.  ADHD is a real disability, a dysfunctional lack of planning and control that’s abnormal compared to other children, affecting their entire lives.

For example, these children find it hard to play with other kids because they can’t follow basic social rules like the rules of games, or waiting their turn.  These children find school difficult, because they can’t concentrate for long enough to focus on completing a multi-step task, or have a long enough attention span to make new memories for words or facts.

One of my patients, a little boy about seven years old, was brought in by his mother because a chiropractor wanted me to arrange a blood test on his behalf.  When I asked why, the mother said the little boy had dyslexia which the chiropractor was ‘treating’ (actually, this chiropractor was blaming a disease that didn’t exist, and wanted me to arrange a test that was resigned to the pages of history, but that’s another story).  When I talked to the mother about the child’s symptoms, it was pretty obvious that he had ADHD, amongst other things.  After seeing a developmental paediatrician to confirm the diagnosis, and taking Ritalin for just one week, his reading improved three whole reading levels, and after a month, he had not only caught up, but had passed a number of his class-mates.

This is a real life example of how ADHD can hold children back, and how stimulant medication can help.  While there are always exceptions to the rule, stimulant medications help more often than they hinder.  They’re sometimes the difference between a child meeting his full learning potential, or being unnecessarily held back, languishing at the bottom of his class as his peers go further ahead in leaps and bounds.

Our culture needs to move on.  We need to stop our social prejudices making life more difficult than it already is for children and their families who battle with ADHD.  We need to see that medications for ADHD can be the difference between a life of learning and a life unfairly held back.

Let’s change the tune.  Rather than saying, “Let boys be non-medicated boys”, how about we say, “Let boys be non-stigmatised boys.”  It’s only through the break-down of the stigma surrounding ADHD and stimulant medications, that all boys (and girls) can truly meet their full potential, whether they have ADHD or are just a bit more energetic.

If you want more information on ADHD and its treatments, this is a good place to start: http://www.rch.org.au/kidsinfo/fact_sheets/ADHD_an_overview/

If you are concerned that you or your child might have ADHD, talk to your local GP or paediatrician.

Dr Caroline Leaf – Feed your children manure???

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I was entertained somewhat by Dr Leaf’s latest Facebook post this evening. In it, there was a pairing of water and a pot-plant, and sugary drinks and a child, with the words, “If you give this (water) to your plants? Why give this (sugary beverages) to your children.”

Without looking too closely, one might think that Dr Leaf was making a good point. Water is good, and sugar is bad, right?

With just a little more thinking, one can see that the metaphor is pretty weak. Plants aren’t children. Following the same logic of the metaphor, I should feed my children manure instead of food, since it’s clearly good enough for the pot-plant.

What is worrying about this post is Dr Leaf’s linking of diet with our Christian morals. Dr Leaf tries to link the concept of drinking water to the worship of God, because your body is a temple, and “Whether you eat or drink, or whatever you do, do it all for the glory of God.” (1 Corinthians 10:31). By logical extrapolation, Dr Leaf is therefore saying that drinking Coke is dishonouring God and the temple he gave for you. If you drink Coke, then you’re a bad Christian.

Though that’s really only Dr Leaf’s interpretation, because the scripture that she quotes isn’t talking about the composition of the food you eat but about it’s relationship to the sacrifice to idols. As far as I was aware, Coke isn’t used in any worship of idols before it’s bottled and distributed. So really, I don’t think whether you drink coke or other sodas will have any bearing on your relationship with God.

Perhaps Dr Leaf would have better spent her time outlining the studies that back up her overly dramatic statement “that sugary drinks like soda and processed orange juice can cause neurochemical havoc in your brain” rather than just hoping people will take her at her word.

Lets be real … no one in their right mind is encouraging children to have more sugar, mainly because of the excess calories, and not the hysterical notion of “neurochemical havoc”. Dr Leaf’s trying to get it right, but her poor metaphor, and the linking of ones diet to ones honouring of God probably went a step too far.

It would be nice if Dr Leaf could reexamine her knowledge of nutritional science and the scriptures that she uses so that she doesn’t weaken her credibility with such posts in the future.

The truth about ADHD

ADHD is always a popular topic … and an apoplexic topic. Any mention of ADHD seems to induce everyone within ear-shot to uncontrollably expectorate their half-baked opinion on the subject, like the Tourette’s syndrome of ignorance.

I’ve heard them all over the years …

ADHD is over diagnosed.
ADHD is just a label for bad parenting.
ADHD is caused by sugar.
ADHD is caused by food colouring / preservatives / gluten / (any other fad ‘toxin’)
ADHD is cured by diet / meditation / supplements / swiss balls.
ADHD medication (Ritalin) is overused / irresponsible / lazy parenting / harmful / ungodly.
ADHD doesn’t exist in France.
ADHD doesn’t exist at all.

I could go on, but if I do, I’m just going to get myself in a tizz.

ADHD is the new AIDS. There is so much misinformation and discrimination surrounding ADHD in our modern enlightened society that the stigma is worse than the actual illness, which really says something about how badly ADHD is treated in our communities.

One of the cruellest aspects of the cultural mismanagement of ADHD is the fact that it maligns the sufferers while simultaneously isolating them from much needed support. Saying that children with ADHD should just behave themselves, or parents of children with ADHD should just have better parenting skills is victim blaming at its worst.

In order to counter the prevalent ignorance of ADHD, even just a little, I want to give a crash course on the science so that at least somewhere on the searchable web, there is a counterbalance to the thousands of misinformed arm-chair ‘experts’ whose only experience with ADHD is reading the misguided perspectives of other so-called ‘experts’.

ADHD stands for Attention Deficit Hyperactivity Disorder.

The current formal definition that must be matched to have a diagnosis of ADHD is:

  1. Inattention: Six or more symptoms of inattention for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of inattention have been present for at least 6 months, and they are inappropriate for developmental level:
    * Often fails to give close attention to details or makes careless mistakes in schoolwork, at work, or with other activities.
    * Often has trouble holding attention on tasks or play activities.
    * Often does not seem to listen when spoken to directly.
    * Often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (e.g., loses focus, side-tracked).
    * Often has trouble organizing tasks and activities.
    * Often avoids, dislikes, or is reluctant to do tasks that require mental effort over a long period of time (such as schoolwork or homework).
    * Often loses things necessary for tasks and activities (e.g. school materials, pencils, books, tools, wallets, keys, paperwork, eyeglasses, mobile telephones).
    * Is often easily distracted
    * Is often forgetful in daily activities.
  1. Hyperactivity and Impulsivity: Six or more symptoms of hyperactivity-impulsivity for children up to age 16, or five or more for adolescents 17 and older and adults; symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for the person’s developmental level:
    * Often fidgets with or taps hands or feet, or squirms in seat.
    * Often leaves seat in situations when remaining seated is expected.
    * Often runs about or climbs in situations where it is not appropriate (adolescents or adults may be limited to feeling restless).
    * Often unable to play or take part in leisure activities quietly.
    * Is often “on the go” acting as if “driven by a motor”.
    * Often talks excessively.
    * Often blurts out an answer before a question has been completed.
    * Often has trouble waiting his/her turn.
    * Often interrupts or intrudes on others (e.g., butts into conversations or games)

In addition, the following conditions must be met:
– Several inattentive or hyperactive-impulsive symptoms were present before age 12 years.
– Several symptoms are present in two or more setting, (e.g., at home, school or work; with friends or relatives; in other activities).
– There is clear evidence that the symptoms interfere with, or reduce the quality of, social, school, or work functioning.
– The symptoms do not happen only during the course of schizophrenia or another psychotic disorder.
– The symptoms are not better explained by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder.

(http://www.cdc.gov/ncbddd/adhd/diagnosis.html)

In Australia, ADHD cannot be formally diagnosed by anyone other than a paediatrician or a psychiatrist. So even as an experienced GP, I can’t officially diagnose it. The school counsellor or local naturopath can’t diagnose it. You can’t just pluck it out of the air. The diagnosis can only come from a medical specialist with at least a decade of university level training.

The official prevalence rate of ADHD (the number of people with a current diagnosis) is only 5%. According to some US based community surveys, nearly a half of those children are not on medication for it (http://www.cdc.gov/ncbddd/adhd/data.html). So much for Ritalin being overprescribed.

Stimulants vs nothing

ADHD is a predominantly genetic disorder which leads to specific structural deficiencies in the brain. Children with ADHD have a significant global reduction in the volume of grey matter, most prominently in a part of the brain called the right lentiform nucleus. These changes usually improve with age and improve with stimulant medication. There is also evidence of changes to the shape and size of other brain structures such as the amygdala and the thalamus (areas of the brain integral to sensory and emotional processing). Early evidence also exists which suggests changes in the white matter pathways connecting a number of critical brain regions. Studies investigating brain development have estimated that the frontal lobe development of ADHD children lags that of normal children by an average of about three years.

These changes in the brain are not caused by the child’s behaviour, since other studies have shown the same changes in the brains of unaffected first degree relatives (brothers or sisters), just to a milder degree.

Modern functional imaging techniques show that the brains of children with ADHD have abnormally low functioning in most of the brain structures related to attention and planning (numerous areas of the frontal cortex as well as the basal ganglia, thalamus and parietal cortices). At the same time, there is extra activity in portions of the brain related to the Default Mode Network (the day-dreaming part of your brain). So children with ADHD have brains in which the ‘day-dreaming’ network activity persists into, or emerges during, periods of task-related activity. This takes processing power away from the competing task-specific processing causing a deficit in performance. Studies show that Ritalin normalises this dysfunction.

The best evidence suggests that dopamine is the main neurotransmitter involved in ADHD. Other neurotransmitters are likely to be involved but the evidence is still being confirmed. Medications like Ritalin improve ADHD symptoms by increasing the amount of dopamine that the nerve cells have access to, improving the clarity of the signal between them.

Underlying all of these neural changes are genetics. While there have been no specific genes discovered in research thus far, twin studies have demonstrated a heritability of ADHD of up to 76%. The most significant environmental factors that are responsible for the remainder of the influence on ADHD are not nutritional factors such as sugar or food additives, but are low birth weight/prematurity and exposure to smoking during pregnancy.

Are there any better treatments for ADHD other than stimulants like Ritalin? Other non-stimulant medications are available although at this stage, Ritalin and Dexamphetamine still out-perform them. Cognitive therapies may mimic some of the brain changes of Ritalin but it is not clear whether the effectiveness of cognitive therapies are equal to or better than the stimulant medications. What is clear is that Ritalin doesn’t lead to a euphoric state (a “drug high”) when given orally. So children can not get addicted to Ritalin when used responsibly.

In summary, ADHD exists. It’s caused by the interaction of a number of genes and some environmental factors such as those related to prematurity, low birth weight and maternal smoking, which alter the growth and development of the brain, specifically the grey matter of the frontal cortex, the basal ganglia and thalamus, and the pathways which connect them. These structural changes cause the day-dreaming part of the brain to be more active and the attention and planning parts of the brain to be less active.

ADHD is not caused by food additives or sugar. There is no evidence that autoimmunity plays a significant part. Forcing your child to consume bone broth or stop eating gluten will not cure them.

ADHD is not caused by bad parenting. Ritalin is not evil. Medications like Ritalin and Dexamphetamine have been shown to improve the functioning of children with ADHD and improve their underlying neurological deficits.

It’s time to cut the crap. Our culture needs to stop victimising the child with ADHD and their parents, who already suffer enough from the ADHD without ignorant busy-bodies and self-titled experts chiming in and making their suffering even more pronounced. It’s time to stop judging those who choose the best for their child by medicating them, who do so in spite of the unfair and ill-informed criticism of everyone from their mother-in-law to the milkman when they do. It’s time to remove the stigma from one of the most common psychiatric disorders of childhood so that every child has an equal chance of growing into an adult that can realise their full potential.

That’s the truth about ADHD.

Bibliography:

Cortese, S. (2012). The neurobiology and genetics of Attention Deficit/Hyperactivity Disorder (ADHD): what every clinician should know. Eur J Paediatr Neurol, 16(5), 422-433. doi: 10.1016/j.ejpn.2012.01.009

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