Saturation be damned

Night time reading

I love interacting with this informed and educated community of ours who take responsibility for own health, read and interpret scientific articles, ask intelligent and incredibly tricky questions and look at the world through a prism of human evolution. It’s really really cool. I also don’t own a television or read newspapers. I know, I am missing out on the vital information on the recent exciting advances in the field of laundry detergents, easily foldable exercise equipment and female hygiene products. But I’ll take my chances.

So when I was approached recently by an Australian reporter to comment on why saturated fat might not be as bad as everyone thinks, I was temporarily stunned. Everyone still thinks that? An hour-long lunch outside in the company of co-workers brought me back to reality. Listening to the less-than-lithe lady lecturing a younger employee that “pasta is perfectly healthy as long as you avoid creamy sauces and stick with tomato-based ones and add psyllium husks to increase fibre” plunged me back to earth from the AHS12-induced heights.

Oh boy. On this planet, margarine is still a health food.

So I thought I’d write down some thoughts on fats, why we still need to talk about them, the strength of evidence and where we go from here. The article ended up being published at The Age and I was amused to see our hour-long phone conversation and the exchange of several emails with attached studies reduced to one sentence quoted from me, but I am not complaining since I think the article was quite well-balanced and hopefully gives people some food for thought. Here is the link.

If you are totally new to all this, I recommend that you read my post on fat basics and the slightly more complicated polyunsaturated fat primer.

Don’t all scientists and doctors agree that saturated fat is bad?

My main gripe with conventional advice to reduce saturated fat in the diet is that it makes it sound that everyone in science and medicine agrees that it is the right thing to do. They say “scientists” and you imagine a group of nerdy-looking men and women in lab coats and glasses with clipboards, all nodding in unison: “Saturated fat will kill you”.

Bad cow, bad!

Sorry, no. Far from it. In the year 2012 we still run trials on dietary fat and its effect on mortality, cardiovascular disease and weight. In fact, a Pubmed search on “dietary fat” yields close to 700 article from 2010 to present date.

If “saturated fat will kill you” is a done deal why do all these folks get research grants and waste years of their life on the pointless pursuit of the truth that has long been discovered and incorporated into every government-led nutrition advice?

And yet, the consensus is farther away than ever. Nutrition and Metabolism Society publishes critiques of the American Dietary Guidelines, as well as scores of papers on the subject. Then there is THINCS, The International Network of Cholesterol Skeptics, which really sounds like an evil mad scientist organisation from a Bond movie, but in fact has respected members like a biochemist Dr Mary Enig and a scientific researcher Dr Uffe Ravnskov.

Not to mention a fine gathering of clinicians, scientists, nutritionists, researchers, physiotherapists, bloggers at Harvard Law School this year for 2012 Ancestral Health Symposium, most of whom seemed to think that bacon is rad and margarine is bad.

Can you refute XYZ study and the rest of the body of evidence on saturated fat?

Yawn. I have no intention on memorising every study conducted in the last 50 years, no matter how bad or good they are. We have been eating fat, lard, meat, eggs, butter, ghee, coconut oil for thousands of years. I think the burden of proof lies on those who say that these traditional foods have been our silent killer all along. All I can do is to politely present the vast body of scientific evidence that does not support the lipid hypothesis (YES! IT IS STILL A HYPOTHESIS!)

Sarcasm alert. Lipid Hypothesis 2.0 = we have come to realise that total fat intake has no bearing on heart disease or weight (sorry! Our bad!) But it’s all about the type of fat. There are only 2 types of fat: saturated (=evil, comes from animals, eating animals is bad, you immoral cruel self-serving glutton) and unsaturated (=pure good, comes from vegetables, like cottonseed, soybean, canola and sunflower, botany be damned). Substituting unsaturated for saturated fat is the real reason why we are healthier, thinner and fitter than thousands of generations of traditional cultures because they couldn’t work out how to get 10% of their daily calories from PUFA, suckers.


He needs to be told how unhealthy he is from his 40% SAFA intake. Those coconuts will kill you, buddy! (Source:

Several studies have shown improvement in CV markers and mortality when saturated fats were replaced with PUFA. Regardless of how good/bad sat fats are, shouldn’t we make the substitution just in case anyway?

This is a very common reasoning from many educated doctors and academics. They are now aware that sat fats are not much of a problem. Great. But what’s the harm in tinkering our diets if all we have is improvement, right?


I have a real problem with a blanket advice to increase PUFA in general as if they are all the same. PUFA are not all created equal, they have different physiological functions and effects on the body! (go back to basics). At the very least they should be differentiated into omega-3 and omega-6. However, even that’s too simplistic.

If you are planning on dividing fats on the basis of the biochemical structure and biological function, you have just only scratched the surface. Behold! All saturated fats are actually not the same either. Lauric fatty acid is metabolised differently and has different effects on serum lipid profiles than stearic. Even omega-3 are not a homogenous group (gasp!). The intake of the shorter-chained ALA (alpha-linolenic acid) does not come close to providing the same benefit as the long-chained DHA due to inefficient conversion.

Jacobsen’s analysis of 11 cohort studies, quoted in the article as the final proof of the miracle qualities of PUFA,  showed that substituting PUFA for SAFA seemed to reduce CV events and mortality. However, simplification, as usual, can only take you this far. The analysis lumped omega-3 and omega-6 PUFA together and did not take into account the deleterious effect of trans fatty acids separately from SAFA.

“Linoleic acid selective PUFA interventions produced no indication of benefit but rather a fairly consistent, but non-significant, signal toward increased risk of coronary heart disease and death. ” (Kuipers ER al, 2011, hyperlinked above)

That’s what happens when you simplify a complex concept. Why? Because the public are so dumb they won’t get it? Because 2 types of fat is quite enough to remember? And to make things even more visually and conceptually appealing let’s represent them as ying and yang, bad and good, dark and light?

So you have some studies, “they” have some studies. How do lay people know who to trust?

As much as I respect Evidence Based Medicine, I am well aware of its limitations. You can pull apart every study, point out the confounders, small sample size, confirmation bias, lack of double-blinding, the grant approved by a completely impartial third party with key investments in related area. Let’s not reduce the process to “Mine is bigger than yours.”

Nothing in biology makes sense except in the light of evolution“. Repeat this 5 times before going to bed every night.

How much omega-6 was available in our diet as Homo sapiens for 2 million years up to the advent of industrial processing? How much oil can you get out of a soybean without the benefit of extraction chemicals?

Aaaaaaah! Would you just tell me how much PUFA/SAFA/Carbs I should be eating?

Talking about macronutrients (fatty acids, carbs, etc) is useless unless it applies to food. If the advice to increase PUFA translates into “eat more fish” I will be the first one to shout it from the rooftops! But what if it translates into “eat more peanut butter”? Still PUFA! But are you going to get the same benefits? You don’t need to read an insightful review by Christopher Ramsden on omega-3 vs omega-6 to know that peanut butter ain’t gonna make you healthier than salmon. But sometimes we really really want to believe it. And deluding ourselves is oh so easy when somebody in a position of authority gives you the green light.


Focusing too much on macronutrients is what allowed abominations like “low fat banana bread” to become a healthy morning tea snack. The “reductionism” approach has successfully indicted natural foods such as eggs, coconut, avocado, butter. At the same time we have low fat sausage rolls, sugary cereal, margarine and other foods devoid of any nutrition, riding on the coat tails of the lipid hypothesis 2.0.

One of the benefits of using the evolutionary approach is that it allows you to make rational decisions about your life choices without having to double-check them with Pubmed. And it doesn’t involve re-enactment of Paleolithic times, although heaven knows, I find some modern social conventions really tedious (like people requesting to know how I am going on a Monday morning prior to my first cup of coffee). As the opponents of the Paleo approach correctly point out, we don’t really know what our ancestors ate. But I sure as hell know what they DIDN’T eat: excessive amounts of sugar, grains, seed oils and other industrially produced food-like substances. Not even almond flour cupcakes. Sorry.

Regulating your fat intake is easy: eat fish, seafood, meat (preferably grass-fed), eggs, some nuts, seasonal fruit and veggies.

Go back to eating food, not labels.

What the @#$! do I feed my child?

A blackboard used by Albert Einstein in a 1931 lecture in Oxford. Source: Creative Commons

I find maths and science quite soothing. There is something beautiful about straight numbers and clear cut conclusions. You must have already picked up on my love of graphs and diagrams. They got me through med school.

However, once you finish a beautifully straightforward equation or reach a perfectly logical conclusion using an algorithm you hit a little snag. How do you translate all these numbers to real life?

In the last few weeks I have read somewhere around 30+ journal articles on child metabolism alone. The numbers are simple, the graphs are straightforward but as we very well know the applications to child nutrition can be vastly different. For all the parents out there the only biochemical pathway they are likely to be interested in is the one between the fridge and the pantry.

Here is a short summary of my last few slightly dry posts on child metabolism (on conventional advice, BMRmalnutrition and catch up growth) and MY conclusions.

1. Children grow. Therefore children are not in “energy balance” in simple terms. The energy cost of growth is high including both the energy density plus quality nutrients to ensure lean body mass increase.

2. Energy quantity (calories) is important but ultimately you cannot build muscle and bone with broccoli or worse, orange cordial. The quality of nutrients needs to be concentrated to provide more bang for your buck: high nutrient density in a small volume fit for a small stomach.

3. Children regulate their energy needs with their appetite. No calorie calculators required. When the nutrient quality has been addressed the appetite will take care of the rest. If they are hungry they will eat.

4.  Babies, infants and children have less reserves to cope with malnutrition. Even a minor infection may potentially result in muscle loss.

5. Point 4 makes it obvious that it’s not a good idea to put children (=growing bodies) on calorie restricted diets for weight loss.

6. A decrease in activity is a pretty good marker for malnutrition especially for small children. This should give some worried-well parents some confidence, especially where breastfed babies are concerned. If you baby is happy and active it is likely that they are getting enough energy.

7. When children recover from even a minor infection their energy requirements are 4-5 times what they were before. They are going to be very hungry. Feed them. A lot.

8.The period of catch up growth during recovery puts children in a slightly vulnerable metabolic state. They seem more likely to develop insulin resistance (in skeletal muscle), sensitivity to glucose and store abdominal fat.

9. Point 8 makes you think that the post-recovery window is crucial for providing good nutrition for longer term gains. Maybe it is not a good time to provide sweet treats or let children laze around. My thoughts go towards fatty chewable chunks of meat and providing plenty of opportunities for spontaneous activity.

10. My personal way of identifying junk food: if a child is willing to have it after a steak dinner it’s junk. Nobody makes room for more meat or pumpkin when they are stuffed. But there is always stomach space to be found when lollies, cakes, milkshakes and ice-cream are on offer.

The diet recommended by our health authorities always confuses me. I assume (perhaps naively) that they read the same studies and they study the same physiology books. I’m stumped at how they arrive at their conclusions. Today Cancer Council NSW, backed by the Obesity Policy Coalition and the Parent’s Jury, announced the latest villains in the child obesity epidemic: Toucan Sam

and the Paddle Pop lion:

The research by Cancer Council NSW and the University of Sydney found  that 74% of supermarket products adorned with bright cartoon packaging are not up to our healthy nutritional standards. The specific complaints were high-sugar, high-salt and high fat. Apparently the adorable visages of cartoon characters and chiseled jaws of our sporting heroes are just too much for the little kiddies (and their parents) to resist.

“Although stopping short of calling for plain packaging (???) Cancer Council nutritionist Kathy Chapman said regulations around the marketing of foods to children were urgently needed.”

Deep breath. I am not defending sugary cereals. (Not entirely sure how the high-fat monster has slipped into the discussion since the foods in question are mostly low in fat to the point of deficiency. But that’s another matter). In fact, I’m happy to wear a t-shirt: “Friends don’t let friends eat cereal”.  I am more concerned about the whiff of a new scare campaign and propaganda. Plus, when it comes to my own child, I’m the one with a wallet, sorry kiddo.

The second issue is that we rely on these guys for their interpretation of science to tell us which foods are healthy and which are not. I hope we all agree that Froot-Loops are not exactly health food. Nobody buys those because they think that the multiple colours are indicative of the high antioxidant and phytonutrient content. On the other hand Kathy Chapman “welcomes cricketers fronting Weet-Bix” presumably because she thinks that this brand of bland cardboard-like blocks of processed wheat is a healthy alternative. Never mind that most children cover it with malt, sugar, fruit and honey just to make it palatable.

And because the University of Sydney (the home of GI) is involved in this story I’ll throw in a GI reference:

Froot-Loops 69
Weet-Bix 69


P.S. I have a very special guest post coming up for you next time. The guest is currently in the middle of the creative process and I am not sure how long before we see the final result. But I know it is going to be something.

Catch me if you can

Before my foray into the world of celebrities I was talking about babies, children and the effect that illness can have on their metabolism. I have also alluded to something called catch up growth and the fact that it might be important for the overall risk of obesity and chronic disease.

What is catch up growth? The medical dictionary defines it as:

“…an acceleration of the growth rate following a period of growth retardation caused by a secondary deficiency, such as acute malnutrition or severe illness…”

The easiest way to track catch up growth in visual form (and you know that I like my visuals) is on growth charts. Children tend to follow an individual growth curve, predetermined largely by genetics, and this phenomenon is called “the canalisation of growth”. As we have established in the previous post, an illness or or a period of malnutrition may result in falling off the curve. Catch up growth is the body’s attempt to get back onto the original curve.

Growth curve flattening and fall (example only)

Accelerated growth during recovery phase

It has been known for quite a long time from observational studies that babies and children who undergo a period of catch up growth seem to be at higher risk for obesity and diabetes later in life. This was also observed in children born small for gestational age (SGA),  which is an indirect indicator of fetal malnutrition. Similar phenomenon was noted in children growing up in famines (the Dutch famine study) and the survivors of the Leningrad blockade in the WW2.

Studies conducted in the 60′s and 70′s looked further into the energy metabolism of catch up growth. They showed that the rate of growth in these children is astonishingly up to 15-20 times the rate of normal pattern. Moreover, this period was accompanied by both increase in appetite and increase in BMR in the order of 4-5 times the controls. It seems that when children were fed ad libitum they spontaneously increased their food intake to ensure their bodies get back on the curve. As their weight approached the expected measure for height their appetite would decrease back to normal levels.

Another interesting observation made around 1980 was that children do not regain lean body mass at the same rate as they lose it. Muscle recovery lags behind the recovery of fat tissue even when children regain their weight and get back on their growth curve. As one of the studies frames it:

“The impressive gains in weight made by recovering malnourished infants are largely fat; reconstitution of lean tissue does not occur equally well at all rates of weight gain.”

Let’s go back to some visuals or rather my illustration of the above.

Body composition changes during illness and recovery

The greater degree of the initial weight loss, the more unbalanced the pattern of catch up growth.

Later research started to elucidate the mechanism by how this imbalance occurs. Several studies have identified that the phenomenon of catch up fat is accompanied by hyperinsulinaemia, relative insulin resistance in skeletal muscles and hyperresponsiveness to insulin in adipose tissue.

Basically, when the child is recovering from a period of malnutrition their bodies produce more insulin for the same amount of glucose. Their muscles “shut down” the insulin gates and their fat tissue opens the gates wide so that glucose is shuttled away from the muscles and into fat.

Some of the more recent studies have tried to explain this phenomenon using terms like “thrifty gene”. Since no such gene has yet been identified to my knowledge I’m a little unconvinced. What interests me however is whether this slightly worrying pattern is diet-dependent. In other words, what do you feed a sick malnourished child to prevent this from happening? Is there a single dietary cause? What did all these children in observational studies eat?

Looking for causes in cohort data is always a fruitless exercise and a reminder that we should use it to generate hypotheses only. Randomised controlled studies on actual babies are obviously out of the question, I doubt there is an ethics committee on earth which would agree to withholding food from children and then watch them lose and then regain weight on various dietary regimens. There are always rats but they have an obvious disadvantage of being…well, rats.

One zealous study examined the rats undergoing catch up growth after semi-starvation. Those re-fed a high-fat diet were found to have more hypinsulinaemia, higher fat deposition and lower metabolic rate than the rats fed a low-fat diet. Both re-fed groups had worse metabolic derangement compared to controls. A closer attention to the high-fat diet tells you that the rats were fed 1:1 corn oil:lard mixture as 50% of their diet. What does it tell you? That it’s not a good idea to feed rats 25% of their diet as corn oil. Not much else really. It also makes it clear that both re-feeding diets resulted in higher insulin response to the same glucose load, higher adiposity, lower thermogenesis and other markers of disordered metabolism.

So we are back to generating hypotheses.

Recent developments implicate a group of messengers called IGFs, insulin-like growth factors. A series of experiments on none other than zebrafish showed that low cell oxygen level as would occur in malnutrition or disease can disrupt IGF signalling which activated the MAP kinase pathway, necessary for growth. Restoring oxygen to the tissues did not always result in full system reboot. Pathways other than MAP kinase may be activated which could explain the different growth pattern. Sigh… let’s wait for the zebrafish to give us the answer.

While you are digesting all of this info I will put together my take on some of these fascinating issues. Of course, I could be the only one who actually finds this stuff so intriguing and you might be going about your day without giving the concept of catch up growth a second thought. But I reckon some of this might still apply to you whether you are a determined bachelor or a mother of four. What if you were the one who had a prolonged illness at some point in your childhood? What if this pattern of metabolic disregulation also applies to the yo-yo dieters amongst us? Aha, now you are thinking about this.

Look out for my summary post on child metabolism in the next couple of days.

More reading:

Ashworth A, Milward DJ, Catch up growth in children (1986) Nutrition Reviews 44(5):157-163

Jackson AA, Wootton SA, The energy requirement of growth and catch up growth, Proceedings of an I/D/E/C/G Workshop held in Cambridge, USA 1989

Dulloo AG et al, Pathways from weight fluctuations to metabolic diseases: focus on maladaptive thermogenesis during catch-up fat (2002) International Journal of Obesity 26(S2): S46-S57

Ong KKL et al, Association between postnatal catch-up growth and obesity in childhood: prospective cohort study (2000) BMJ 320:7240



Down the slippery slide we go!

J.Waterhouse "A sick child brought into the Temple of Aesculapius" 1877

Continuing from my last post about metabolism in babies and children, today I will address what happens when a child goes through a period of inadequate food intake.

Viral or bacterial infections, prolonged hospital stay and chronic disease are some of the common causes of temporary malnourishment in Western children. Frank underfeeding is fairly rare though it still happens in certain extreme dietary lifestyles. While there are definitely differences between chronic malnutrition (the kind we associate with “the starving children in Africa”) and a week-long diarrhoeal illness in a typical Australian child, there are many similarities.

A few older studies (they weren’t too hampered by ethical considerations in those days) examined underfeeding in babies and children in some detail trying to establish how the body copes with the lack of energy and nutrients.

If you remember from the previous post, energy intake in children accounts for their BMR (basal metabolic rate), activity and growth.

Intake = BMR + Activity + Growth

As it turns out, the body puts a different priority on each of these components. Survival (BMR) comes first followed by Growth and then Activity. As a consequence, a malnourished child will first decrease activity levels.

If reducing energy expenditure does not compensate for inadequate intake then growth becomes affected. Within growth 2 parameters are easily measured: height (length in infants) and weight, both can be tracked along growth centiles on standard growth charts. A prolonged illness might result in the slowing of weight gain which will be reflected in drop down a centile. Weight loss comes both from fat loss and muscle loss. While the organs are relatively protected in minor illness, the muscle mass is not.  Catabolism (breakdown) of muscle tissues has been reported even after measles immunisations and asymptomatic Q fever.

A profoundly malnourished child will also slow their height velocity possibly resulting in stunted growth.  All of the above will happen way before the metabolic rate of individual organs is affected.

Sequence of metabolic events in malnutrition in childhood

Reduction in activity in a malnourished infant may be subtle to the outside observer. The child does not necessarily lie motionless and exhausted in her cot but they might be less vigorous and inquisitive. An interesting study was conducted back in 1979 in a Mexican village. The investigators followed two groups of children: one was given supplementation of vitamins, minerals, strained foods and milk (in fact the diets of their mothers were supplemented in pregnancy as well), the other group was not. Supplemented babies were more active, cried less, spent more time out of their cribs. In one of the experiments 2 year olds were taken out onto a 3 x 3 quadrangle and their movements recorded for 10 minutes. Investigators recorded the movements of well-fed and malnourished infants. Some toys were placed in one end, their caregiver and two observers at opposite ends.

This is a tracing of the movements of a control child (no supplementation):

Source: Chavez and Martinez 1979

This is a tracing made by a supplemented child:

Whoa, somebody went a little crazy! Obviously the results could be related to both quality and quantity of the food given, better development in better fed infants, an uncertain deficiency in controls or some other factor. Nevertheless it is clear that malnutrition can affect the physical activity of children. One of the first questions a parent is asked by a pediatrician or a general practitioner is: “Is your baby happy and active?” This graph makes it clear why.

Anorexia, or loss of appetite, is something that most parents witness in a sick child. Spontaneous decrease in food intake is well described in scientific literature. What can be simpler: a sick child doesn’t feel like eating and loses weight as a result? However, while anorexia accounts for some of the weight loss, it does not explain all of it.

As I have mentioned before, children tend to lose muscle mass in addition to fat loss during illness. Muscle wasting, the two words that terrify any self-respected gym junkie, is a costly exercise in a child. Body composition is notoriously hard to measure in infants but we know that adipose tissue in 2 year olds can measure between 20-25%. So why don’t the children use their soft cushioning for energy when sick? As it turns out being ill makes it harder for the body to access fat stores. The signals from body’s own hormones and the activation of the immune system causes a switch to protein catabolism and utilisation of amino acids stored in the muscle for gluconeogenesis (creating glucose in the liver for release into the bloodstream).

Another mechanism by which acute disease contributes to the loss of muscle mass is the paradoxical increase in BMR, or hypermetabolism. Mechanisms of this are not entirely clear but it has been recorded across many studies. One of the main suspects is fever. The often quoted figure is the 13% raise in BMR for every 1 degree Celsius above 37° (It comes from an old study by Dubois, 1938, unfortunately I do not have a full text). However, these mechanisms cannot compensate for muscle wasting and decreased organ metabolic rate in chronic active disease and profound malnutrition. Protein can also be lost directly from the gastrointestinal tract via the process called protein-losing enteropathy  due to a variety of infectious, inflammatory or congenital causes.

It may be helpful to think of energy status in malnutrition and disease as a balance between energy conservation and energy loss. The adaptive mechanisms that the body tries to use fail in the face of a serious and/or prolonged illness resulting in negative energy balance.

Energy balance in response to illness

So let’s apply some of these factors to a hypothetical situation: an otherwise healthy 18 month old catches a nasty gastrointestinal bug, like Campylobacter, at his playgroup.

The first sign that something is wrong might be a slight decrease in activity. Vomiting and diarrhoea, energy-draining processes by themselves, prevent nutrient absorption.  Appetite decreases and the actual food intake may stop altogether. Negative energy balance kicks off a conservation response and the child’s activity reduces even more. If the episode is complicated by high fever you can expect BMR to rise slightly. Reduced activity will only be able to compensate the energy deficit up to a point. Laying down new tissues for growth has already come to a halt. By this stage the body may start to break down muscle for glucose and fat stores for energy. The longer this infection hangs around the more muscle is wasted. BMR starts to reduce due to the loss of fat free mass. After a week or two of being unwell you have on your hands a lethargic possibly dehydrated child, with reduced fat and muscle mass and a reduced appetite.

If the adverse stimulus (=infection in this case) is not removed the road to chronic malnutrition with subsequent growth stunting and reduced organ metabolic rate continues. The resolution of infection sends a powerful recovery signal and catch up growth begins.

However, catch up growth pattern is not the same as the normal growth. After taking a step back, the body has to leap 2 steps forward to get back on track. And it seems to have some trouble doing that. In my next post I’ll discuss the catch up growth and how it’s linked to obesity.

If you have children of your own I apologise if this post was a little unsettling. When your baby is unwell the last thing you want is a little paranoid voice in your head whispering about the inevitable lean body mass loss etc. I will discuss my ideas about the optimal nutritional strategies for recovery a little later, I promise.

More reading:

Scrimshaw NS, Energy cost of communicable diseases in infancy and childhoodProceedings of an I/D/E/C/G Workshop held in Cambridge, USA November 14 to 17, 1989

Wiskin AE et al Energy expenditure, nutrition and growth Arch Dis Child 2011;96:567-572

Veldhuis JD et al Endocrine Control of Body Composition in Infancy, Childhood, and Puberty Endocrine Reviews 2005;26(1):114-146

Beisel WR Magnitude of the host nutritional responses to infection, American Journal of Clinical Nutrition 1977;30(8):1236-1247

Fat, glorious fat. Part II

If you have read the first post in this series and still came back for more I’m impressed. From the comments and messages that I have received (thank you all very very much) many of you appreciated going back to basic biochemistry. I don’t believe that science is an abstract concept, quite the opposite. Its applicability to everyday life is very underestimated by medical professionals and scientists alike. Either that or they believe that the public is really stupid and can’t possibly understand it. So instead they will just tell you what to do. No need to think. Baaaa.

So this particular discussion is going to be a little more in depth. I have really struggled to put together something which would be understandable but not simplistic. Please do not feel compelled to read it all at once if your eyes start glazing over. And yes, I had to skip over things and I’m hoping to get to those later.  I have about 5000 words sitting in my drafts.

To refresh your memory this is where we got to in the last post.

Let’s zoom in on PUFA. As I have mentioned before there are 3 families of PUFA: omega-3, omega-6 and some omega-9. I will leave that last group for now as these fatty acids are made in our body and seem to be less clinically relevant.

The other two families are often represented in the media and health circles as ying and yang. I don’t quite agree with that as you will see. Not a days goes by that you don’t hear of another miracle PUFA perform: from curing heart disease and diabetes to depression, weight loss and sexual performance. How biologically plausible are these claims? In other words, step 1 of the Framework of Common Sense requires us to ask a question: is it supported by what we know about human metabolism?

We know that PUFA are not the body’s preferred fuel. Instead they are an important component of cellular membranes, they initiate and control inflammation, they also participate in brain and retina formation in babies and are necessary for the synthesis of cellular messengers called endocannabinoids. Phew.

Sounds pretty important, right? However, PUFA are also involved in two of the most critical processes in our body: oxidation and inflammation. Both are essential to life, both are dangerous when they get out of control, both deserve a separate post so for now just keep them in the back of your mind

From general lets move to specifics. While the resident nutritionist on the Today show might believe that all omega fatty acids in their respective family are the same it is far from the truth.

I’m sure that all of you have heard of essential fatty acids. “Essentiality” in biochemical terms means that our body cannot synthesise these by itself and has to receive them via food. It also implies that without these essential fatty acids our health and maybe even life are seriously impaired. Two of the fatty acids in the PUFA family have been found to be “essential”: omega-3 alpha-linolenic acid (ALA from here) and omega-6 linoleic acid (LA). In the  beginning of the 20th century the studies by the Burr husband-wife team found that a lack of certain fats on a very restrictive diet makes some unfortunate rats very sick. Prior to this fats were considered important only as a source of energy and a delivery vehicle for vitamins A, D, E, K. It turned out that some fatty acids are much more than that.

Omega-3: parents, apple pies and essentiality

Let’s start with ALA. Its major function in the body is to be a parent, or the precursor, to the long chain omega-3 acids. When it is taken up from the diet it is converted to EPA and DHA, the two omega-3 siblings which cause much excitement in medical circles. EPA concentration in our body is very low as it seems to be converted immediately to its brother: DHA. However important EPA and DHA are, they are not “essential” in a biochemical sense, because we can synthesize them from ALA.

The problem is that this synthesis is not very efficient: the rate of conversion for ALA to EPA is around 8%. That is out of 1mg of ALA from flaxseed oil you will only make 0.08mg of EPA. DHA conversion rate is even poorer. It ranges from 0.5% in normal adults to 4% in young women (I’ll touch on that later).

Imagine you have decided to bake an apple pie on a Saturday afternoon. Maybe you are one of the millions of people who is still blissfully unaware that apple pie is not a health food. Maybe you will try to mitigate the damage by using margarine instead of butter. Maybe you had a rough week and you just don’t care. Back to the pie. There is no question that apples are “essential” to an apple pie. Most of us do not grow apples in our backyard or synthesise them in our bodies. You have to go and get apples from the outside source. But let’s say that the efficiency of apple:pie conversion is 8%. To get 800g of pure apple flesh after core removal, peeling, etc. you will need 10kg (Please note: demonstration purposes only. I did not actually measure apple:pie conversion so do not write saying you only needed 3 kg). To improve the efficiency of this process you can get an intermediate product like diced apples. You can even go and buy a whole apple pie, saving yourself all this headache.

In a similar way we don’t have to get our EPA/DHA from ALA (this is starting to sound like a children’s puzzle!). You can get your long chain omega-3 fatty acids directly from the diet. This way you will avoid the inefficient conversion and bypass the parent altogether. And as you know from the above, you don’t want to have to much of unnecessary oxidation-prone PUFA hanging around your body. Let’s focus on getting more bang for our nutritional buck.

And here are the long-awaited visuals.

Note: intermediate fatty acids have been omitted

This is something you need to know because the current nutritional recommendations push for more omega-3 in our diets. I will discuss the clinical evidence later but here we have the same problem as we had with every other advice: for the sake of “simplicity” all omega-3 are lumped together. Flaxseed oil, walnuts, canola oil – all contain high level of ALA, the parent molecule. They are also promoted as equally good sources of omega-3 as fish and other marine products, which are rich in EPA/DHA, the happy offspring. Meat, dairy and eggs, the way they are supposed to be (grassfed and pastured), never even get a mention.

Perfect example of opportunistic advertising

The implications are particularly important for vegetarians and vegans. And also everyone who heeds the Government advice (hello, Meatless Mondays!) and drastically reduces their meat consumption. This well-meaning study supplemented lactating women with flaxseed for 4 weeks in an attempt to increases DHA in their breast milk for the baby’s brain and retina development. The results saw a substantial rise in plasma ALA and every other intermediate fatty acid BUT the one they were actually aiming for: DHA. While it is possible that in vegetarians and vegans this process is amplified out of necessity to survive these results are still pretty poor.

Omega-6 is also “essential” but which one?

The biochemically “essential” parent FA in the omega-6 family is LA, linoleic acid. Just like in the case of omega-3 its essentiality is very relative. True, you can induce omega-6 deficiency in rats by feeding them nothing but purified sucrose, casein and some vitamins. Omega-6 deficiency was also found in very sick patients who received their nutrition via intravenous solution (TPN) with no omega-6 fats added. Needless to say that awkward oversight has seen been rectified and modern TPN solutions do not pose such issues. In reality you literally cannot take a step without tripping over LA nowadays. Ever since the happy days of Ancel Keys, McGovern committee, farming subsidies and industrialisation of food everything that is processed, packaged, patented and promoted (wow this was 4 p’s) contains this omega-6 FA.

In the body LA follows a series of reactions the result of which is a long chain omega-6 AA, Arachidonic Acid (I promise this is the last acronym). AA is a central player in the cascade of reactions which promote inflammation. Just like in my apple pie story you can also get AA directly from the diet, namely meat and poultry, eggs and organ meats. Inflammation is not all bad, it’s an essential part of our response to injury or infection and the first step of the healing process. But like all good things it has to come to an end. This is where the complexity and the innate wisdom of our bodies really hits you: AA itself promotes the synthesis of compounds which resolve the inflammation.

Note: intermediate fatty acids have been omitted

To help AA with this task we also have DHA and EPA from the omega-3 family. Therefore it is vital that we have a good balance between the key players of omega-3 and omega-6 family. I will cover inflammation and its main mediators, eicosanoids, in a later post.

One more thing to add to our little diagram is the enzymes which actually perform the conversion of short chain PUFA to long chain PUFA. Both families, omega-3 and omega-6, use the same enzymes and therefore they are in competition for them. Too much of the members of one family will interfere with the functioning of the other family. This is where the concept of a healthy 3:6 ratio comes from. High concentration of LA suppresses the conversion of ALA to EPA and DHA. On the other hand too much EPA can cause AA deficiency.

Let’s apply these new facts to a common diet and see where it leads us.

Warning: box food. Not for human consumption.

Most of the processed pre-packaged food come with a surprise addition of LA in form of soybean oil, sunflower oil, cottonseed oil, other unspecified vegetable oil. This is the source of LA which did not even exist a 100 years ago. Because you have heard about essential fatty acids and how important they are, you also go out of your way to buy health products which contain them like nuts and nut butters, seed trail mix, nut bars etc. You know all about the important omega-3 FAs so you buy flaxseed oil, walnuts and omega-3 fortified box food. The problem is that the overwhelming load of LA, inflammatory in its own right, is effectively shutting down the already-poor conversion of omega-3. And since you are getting most of your omega-3 from plant sources in the from of ALA you need that conversion!

So where does this all leave us? “Essentiality” is a biochemical concept which can be misleading if applied to the actual food. In reality the essential (=very important) fatty acids seem to be DHA and AA, possibly EPA. Even the most important PUFA are only needed in small quantities which is reflected in the composition of breast milk and animal tissues. The conventional wisdom tells us that just because they are essential more must be better. We can argue about the actual requirements (I bet you have noticed that I haven’t offered “the perfect ratio” or the required percentage of PUFA in the diet) however it is probably not very useful. Evolutionary clues should tell you that eating meat, some fish, eggs, pastured dairy and some plants will give you all the PUFA you need. Supplementing with artificial sources may just be akin to playing with fire.

Good sources of further basic information:

1. Weston A Price Foundation: Know your Fats by Mary Enig

2. IUPAC (International Union of Pure and Applied Chemistry) Lexicon of lipid nutrition  

3. DHA-EPA Omega 3 Institute (good for food sources)

4. SciTopics: Lipid Peroxidation

5. The medical biochemistry page: Omega-3, and -6 PUFAs

6. Julianne’s Paleo and Zone Nutrition: omega-3 and omega-6 post

And of course there are loads of posts from people much smarter than me like Peter from Hyperlipid, Stephan from WholeHealthSource, Dr Harris from Archevore and others addressing more intricate issues around PUFA.

Edit: a few typos and broken links, my bad.

Fat, glorious fat. Part I

I address this subject with a certain trepidation, as there is a thin line between making science accessible and on the other hand unforgivingly oversimplifying difficult concepts.

In this first post of my Fat series I’d like to go back to the basics of fat biochemistry. If you have spent enough time in lecture theatres scribbling down the chemical formulae for beta-oxidation of fats, feel free to take a nap. If you don’t know your linoleic from your myristic, here is your chance!

Fats have received a pretty bad rep over the years. One of the most common misconceptions comes from the word itself: fat! Fat is bad! Fat makes you fat! We see these images in the media: an obese person gorging themselves on something that is considered unhealthy. You can see the glistening cheeks and mouth, thick fingers dripping oil, fat from the stomach traveling directly to their thighs. Your inner Puritan is horrified, judgement is formed in your mind even before you have consciously acknowledged it to yourself.

The media do a great job perpetuating the myth of “saturated fat clogging your arteries”. Here is a recent addition to the shock and awe campaign on fat, courtesy of the British government. As much as you want to imagine your blood vessels as pipes where you are pouring soft sticky fat mass every time you eat a burger, it bears absolutely no resemblance to what actually happens.

Fats, or better put fatty acids (FAs), are a diverse family with its own overachievers and black sheep. We mostly think of fats as something that provides calories: 9 calories per each gram of fat, the highest value out of all other macronutrients. They tell us that’s what makes us fat. But the caloric value of fats is only important if they are actually “burned” for energy. Dietary fats are used for much more than just providing calories: they are a vital component of the cellular membranes for each of the 50 trillion cells in the body. When you don’t receive enough cholesterol in your diet, your liver makes some by using the saturated fats from your food (why would it do that? Doesn’t it know that cholesterol causes heart disease?). Your brain is 60-80% fat and every neuron in your body has a fatty insulating myelin shield.
Most of us though think of fat as this stubborn orange-peel substance on our thighs, sticky soft sludge pouring through our arteries or the thick yellow deposit packing our tired liver.

So how can something so good be so very bad?

Let’s start with deciphering the common terms surrounding fats.

Triglyceride is the term commonly interchanged with fat, it consists of 3 fatty acids on glycerol backbone. Most dietary fats come into the body in form of triglycerides. Just like other animal fat, our own fat is also stored in triglycerides.

In biochemistry fatty acids are classified on the basis of saturation. The fatty acid is called saturated if carbons in its chain have a hydrogen atom at each one of the 4 available bonds. This arrangement makes for a chain which is straight and stable like a string of pearls. And because these can be easily packed together, they are solid at room temperature (think a block of butter).

An unsaturated fatty acid has at least one carbon which is missing a hydrogen. This makes the carbon form a double bond with its neighbour. Monounsaturated FAs have only 1 double bond in their chain. Polyunsaturated have obviously more than one. The double bonds in the chain give the fatty acid some interesting properties. Firstly, they are more vulnerable to the free radical attack, or oxidation, which can make them rancid. Secondly, double bonds change the shape of the fatty acid molecule: instead of a string of pearls you get a chain with a kink or two. This lowers the melting point of unsaturated fats, making them liquid at room temperature.

Here is what we are up to at the moment.

Fatty acids can be further classified by their length. Most of the saturated fat coming from animal sources is in the form of long chain saturated fatty acids: LCSFA, with >12 carbons each, for example palmitic, myristic and stearic. The carbon-carbon bond has the potential to release energy, which makes these FAs a very effective source of fuel. This is also the way your body stores them in your fat (adipose) tissue.

I think it’s important to understand the storage issue. We are so used to seeing stored fat as an inconvenience or an indicator of disease that we have forgotten why it is there in the first place. It is there to be burned. Think of it as fuel for your fireplace. You don’t collect dry timber and then get annoyed that it takes up too much room in your backyard. It is their for one reason only: to use it for energy (warm up your house) when there is a dire need. Humans have evolved to have extra energy stored away for further use.

Next question: when you stock firefuel for winter, do you use timber or rubber tyres? Both will burn, both will give off heat. But you will still choose something which is more benign and will not poison your entire family with fumes. If saturated fatty acids are so very dangerous, does it make sense that our body will carry a toxic load which will “clog your arteries” the moment it is released into the bloodstream. The fact that we have evolved to store saturated fats should be the first clue that they are the preferred source of energy and that the body considers them harmless.

If you are still with me, congratulations, you have high tolerance for dry science. Let’s plow along. Next we have MCSFAs, or the medium chain saturated fatty acids (the more common abbreviation is MCTs for medium chain triglycerides). They have between 8-12 carbons in their chains and the major dietary sources of those are breast milk (estimates range from 10-25%) and tropical oils (coconut oil and red palm). Lauric acid is a common example of a medium chain fatty acid. Unlike LCSFA, which are transported via lymphatic system in little vehicles called “chylomicrons”, MCTs travel via the portal vein from the intestine directly into the liver where they are preferentially used to form ketones. This is interesting because the conventional wisdom tells us that ketosis is always bad. So it’s kind of strange that a newborn baby would naturally receive a load of fat which encourages ketone production. Add to that the fact that your brain functions just as well (or maybe even better) on ketones and that your heart likes them as well, and there is another myth busted.

Finally, the SCSFA are obviously the short chains. Butyric acid is predictably enough in butter. But overall the dietary sources of these are very few. However, your intestinal bacteria happily produce them through fermenting fibre. Like MCSFAs they go straight to the liver.

If you are a male and therefore likely a visual learner, here is an updated pic :

Monounsaturated fatty acids, MUFA, (like oleic acid) are considered healthy by conventional standards. I, for once, agree with their assessment but for a completely different reason. The lipid hypothesis proponents support oleic acid because of their love affair with olive oil. I find it hard to believe that olive oil must be an essential part of our diet, mainly because there are plenty of regions in the world that do not naturally grow olives and somehow are still doing ok. However, monounsaturated fatty acids make up a big portion of animal fat, as much as 44% in pork lard, so it makes sense that we have evolved to process them. So if you want to increase monounsaturated FAs in your diet, fatty chunks of meat will get you much further than a tablespoon of olive oil on your salad.

Finally we come to polyunsaturated fatty acids, PUFA. They are subdivided into omega-3, omega-6 and omega-9 by the position of their first double bond if you count from the methyl (or omega) end of the chain. The FA with the first double bond in position 3 is therefore omega-3 PUFA and so on.

Animals do not tend to store large amounts of polyunsaturated fatty acids, mainly because they are not a very good source of energy. Therefore traditional animal fats are quite low in PUFA. Fish products are widely promoted for their PUFA content but while the relative PUFA composition are high compared to SFA, it is still a minuscule number in absolute terms. “Vegetable” oils (if you believe that seeds are from the same family as, let’s say, carrots) come on the top of that list. You have to eat 900 grams of smoked salmon to get the same amount of PUFA as in 1 tablespoon on sunflower oil kindly provided by the industrial processing technology. All PUFA tend to be lumped together in one big “healthy” basket but there are significant differences in their effect on the body.

To finish off just a quick summary of fat composition of common foods. Click on the table for better resolution.

Source: Wikipedia

And here is an updated diagram for you to memorise before the next post. Consider this your homework.

In the next post I will go a little deeper and talk about the “essentiality” of omega-3 vs omega-6. I will also address some clinical implications, health claims and health myths. Now go and have some fat!

Edit: a few errors which I blame on the brain fog commonly experienced after a hospital shift…

Q&A on fructose, soy and meal frequency

I was in the middle of writing an overview on polyunsaturated fats when I received a comment from a reader Doug with some interesting questions. I started my answer in Comments but it quickly blew out of proportions so I have decided to post it. One of the main reasons being is that I get these questions very often and I would like to answer them fully once and for all.

Question 1: Why is fructose a “neolithic” agent of disease? Ancient man had fruit and I have seen intelligent speculation that it was just as sugary as modern fruit (especially in tropical regions). Wouldn’t it be more precise to say “refined sugar” instead of “fructose”? And isn’t the real culprit here high-fructose-corn-syrup?

Fructose is a hepatotoxin, its major damage site being the liver. Like other toxins its action can be plotted on a dose-response curve: the more you have the greater the damage. Alcohol is another example of hepatotoxin: may be even beneficial in moderation (possibly via polyphenols and action on blood vessels) but deadly in large quantities.

The other issue with any toxins is their idiosyncratic nature: some people can take a lot, some people will develop problems with small amount. If your liver is already damaged via alcohol, hepatitis viruses, autoimmune process, fatty liver disease, then the safe level of fructose is probably zero.

Ancient man definitely ate fruit, however the quantities of fructose were probably incomparable to modern standards. Unlike today, when fruit is available in the supermarket all year around, fruit was mostly seasonal and fruit trees were not cultivated in orchards. Subtropical climates probably favoured higher fruit consumption, Northern Europeans – hardly any.

HFCS is not used in all Western countries: Australia we only use sugar but we are still on track to overtake the US in the obesity race.

So the bottom line is the dose maketh the poison. If you wouldn’t eat 6 oranges in one sitting why drink it? The quantity of fructose in 1 apple is about 4g, the standard soda is around 30g.

I also addressed some of these issues in my previous fructose post.

Question 2: Do the Japanese eat fermented soy? I know that soy comprises a large part of their diet and yet they are very healthy as a group; the healthiest in the industrial world? What type of soy are they eating and how does it differ from the soy eaten in the West?

It has been shown (Dietary Intake and Sources of Isoflavones Among Japanese, Kenji Wakai, Isuzu Egami, Kumiko Kato, Takashi Kawamura, Akiko Tamakoshi, Yingsong Lin, Toshiko Nakayama, Masaya Wada, Yoshiyuki Ohno, Nutrition and Cancer,Vol. 33, Iss. 2, 2009) that 90% of soy intake in Japan comes from fermented/precipitated sources: tofu, miso, natto and fried tofu. It is mostly used as a condiment, not a staple food. Some estimate  that the average daily soy intake is around 10g, the equivalent of 2 teaspoons. And while the overall cardiovascular mortality of the Japanese is much better than in the US, the differences in the diet are too great to draw any conclusions from 1 ingredient. 30.3% of Japanese are daily smokers vs 17.5% Americans, it doesn’t mean that we should start smoking to match their health status.

Question 3: I have read good arguments for frequent meals and infrequent meals. It seems that there is science to support either lifestyle. What is your argument against frequent meals and how do you answer the objections that there are many studies that show that people who ate more frequent meals had BETTER insulin sensitivity?

Most of the studies favouring high meal frequency were performed with SID (standard industrial diet). Eating cornflakes for breakfast makes most people mighty hungry by mid-morning and more likely to binge out on sugary and unhealthy food. In this context higher meal frequency would indeed lead to better glucose control. However, the story changes when you introduce protein and/or fat into the meal. In this study obese men fed higher protein meal reported better satiety on larger LESS frequent meals.

Also do not forget that most studies comparing meal frequency do not  take HUNGER into account. The meals are spread out in a pre-determined fashion, making the study subjects eat “by the clock”. Resetting your metabolism on better nutrition will actually allow you to follow your hunger/satiety signals, not the traditional morning tea time.

Anybody who follows primal nutrition will tell you, snacks become obsolete after a while. Meal frequency decreases spontaneously when your body is fully replete with nutrients. Low meal frequency is not something to force your body into, it just happens under the right conditions.

For more info I recommend Martin Berkhan, the intermittent fasting king. His website contains links to many research studies supporting this hypothesis.

I hope this answers some of Doug’s and possibly others’ questions. Now back to my fats!

Making sense of lactose intolerance in babies

From Nestlè Infant Formula Guide:
“Lactose-free or soy-based formulas are important for babies with a clinically proven allergy or food intolerance…”

My previous article on breastfeeding addressed the attitudes surrounding the breast vs bottle debate. As I have mentioned before, even though there is still room for improvement, breastfeeding initiation rates are not bad in most Western countries. However, the rates drop sharply by 6 months with mothers quoting different reasons for early weaning, lactose intolerance being one of the major ones.

This post is going to be quite “sciency” so I’m going to get serious and attempt to keep sarcasm to a minimum.

Self-diagnosis of lactose intolerance in both adults and babies is very common. Before drawing any conclusions let’s look at some science involved. Lactose is a disaccharide which means it is made up of two single sugar molecules: glucose and galactose. Only these  monosaccharides  can be absorbed through our intestine which is why mammals possess an enzyme lactase which does the job.

Lactase is one of the brush border enzymes located on the surface of our small intestine where the digestion of lactose takes place.

Microvilli house enzymes on their surface

Several types of lactase deficiency have been described.

1. Congenital lactase deficiency - this is an extremely rare genetic condition where the body makes no lactase at all. This condition is normally diagnosed in the first week of life, often even before the baby leaves the hospital due to extreme failure to thrive. These babies require intensive follow up by paediatric gastroenterologists.

2. Late onset lactose intolerance - lactase levels gradually diminish from the age of 2-7. In Asian and African populations almost 90% of people show lactose intolerance due to very low levels of this enzyme. On the other hand Northern Europeans continue to have higher levels through adulthood with only 5% considered lactose intolerant. Other populations seem to be somewhere in between with differences between individuals depending on the genetic makeup. However, even in adults, the ability to tolerate dairy also depends on the overall health of your gut. Viruses, unhealthy gut bacteria and chronic inflammation from some foods can all cause the symptoms of lactose intolerance which can be reversed. More on that later.

3. Acquired lactose intolerance in infancy – this is what I will be talking about here. I find that the lack of understanding and the myths surrounding this condition are far and wide and should concern every parent. Two major mechanisms for acquired lactose intolerance are fast intestinal transit and mucosal inflammation.

First thing you have to know is that lactose is the sugar unique to mammalian milk. Every baby needs lactose for a very specific reason. Apart from providing about 40% of energy, lactose contains galactose, a monosaccharide essential to brain development. Galactose is incorporated into glycolipids (galactolipids) and glycoproteins in the cells throughout the body and especially in the central nervous system. We are still learning the exact mechanisms and the role of galactolipids but it is obvious that depriving a growing brain of some of its building blocks might not be a good idea. Human breast milk contains the highest concentration of lactose among all mammals. This is the main reason why evolution gave us lactase.

The problem with lactase (if you can call it a problem) is that it has a slow release time in the small intestine, regardless of total quantity of lactose in a meal. This means that anything that increases the intestinal transit time also compromises the digestion of lactose. So when it comes to the digestion of milk, the slow and steady tortoise literally wins the race. If the bolus of food moves too fast there isn’t enough lactase to break down the lactose in the meal and it swooshes past into the colon. There is no lactase in the colon but there is plenty of bacteria. Happy to receive an unexpected source of energy, bacteria use fermentation to process lactose with by-products like acids and gases. The results of this lethal cocktail are quite unpleasant, whether you are a baby or an adult: bloating, diarrhoea, acidic stool causing “nappy rash” and abdominal pain.

So what causes the fast transit of the food through the intestines? Lower fat and higher carbohydrate concentration of the meal are the common culprits. If you are an adult, it’s simple enough: skim latte will send you running to the loo faster than a full-fat one. If you are a breastfed baby though your milk supply depends on the mother. Breast milk is higher is carbohydrates at the beginning of the feed with fat content gradually increasing by the end of the feed. Taking a baby off the breast too soon will result in a lower-fat feed. Therefore breastfeeding women are recommended to empty one breast completely  before offering the other.

Another reason for lower-fat breast milk is the mother’s own diet. High carbohydrate low-fat diet during lactation changes the composition of the breast  milk to similarly higher-carb lower-fat. Our ancestors knew this and nursing mothers in traditional societies were encouraged to eat plenty of high quality animal fats to support the growth of the infant. However, in our times ancient wisdom gives way to the cult of thin. So first they tell you that you need to  lose all that pregnancy blubber pronto. Then they inform you that the best way  to lose weight and stay healthy is to reduce saturated fat in your diet. Skim  milk and reduced fat yoghurt are conveniently provided. And by the way, did you  know that Gwyneth Paltrow follows a macrobiotic diet (and doesn’t she look like  one sexy lollipop?) so why don’t you reduce your consumption of animal products  as well? What’s that? Your baby has colic? She must be lactose intolerant: here  is a tin of soy formula.


Let’s move on to the second common reason of transient lactose intolerance:  mucosal inflammation. The inside (mucosal) surface of the small intestine is very fragile, especially in babies, and can be easily damaged. Minor viral infections affecting the gut (viral gastroenteritis) can temporarily reduce  lactase concentration and cause the typical symptoms of lactose intolerance. Luckily, intestinal mucosa heals very rapidly and the damage will be completely  repaired in a few weeks. In the meantime, it is recommended that the mother keeps breastfeeding,  as it will speed up the healing time and prevent “nipple  confusion”.

A more serious cause of mucosal damage is chronic inflammation due to a  food allergy/intolerance. In addition to the typical symptoms of lactose intolerance, the baby might also show the signs and symptoms of inappropriate immune system activation (atopy): eczema/other skin complaints and asthma (rarely diagnosed in babies under 12 months old). In the context of exclusive breastfeeding, casein (one of milk proteins) is often seen as the main offender. However, the levels of casein in human breast milk are actually quite low, compared to cow’s milk, and casein allergy is a lot more common in formula-fed babies. In addition, babies that do develop casein allergy also tend to get allergic to soy protein as well. Therefore switching to soy formula rarely solves the problem. And brings a host of its own issues: phytoestrogens and aluminum toxicity among others.

The baby may also develop an intolerance to the food consumed by the mother, typically wheat, soy, milk proteins and others. If mucosal damage due to protein intolerance is suspected, the only way to  treat it is to remove the offending agent from the mother’s diet, not to remove breast milk. If the symptoms appear after the introduction of solids, then every opportunity should be taken to remove wheat and soy proteins from baby’s food. If there is a history of allergies, atopy, eczema or asthma in the family it is the strongest argument yet to breastfeed and continue to do for as long as possible. Numerous studies show that breastfeeding provides strong protection against atopy in childhood and later in adulthood.

OK, I know that was a lot to take in. For the parents out there: I hope this has made some sense and dispelled some of the myths surrounding lactose intolerance. For the adults: same principles of lactose intolerance apply. Both fast intestinal transit time and intestinal damage reduce your tolerance to dairy. Only we have less enzyme to play with.

Important points:
 1. Lactose is vital for baby’s nervous system development
2. Every baby is born with enough lactase enzyme to adequately process breast milk (congenital lactase deficiency excepted)
  3. Lactose intolerance is a transient phenomenon in infants and breastfeeding should not be interrupted except in the most severe cases.
  4. Both intestinal transit time and mucosal damage are the main factors in individual dairy tolerance in all age groups.
5. The mother’s diet can cause LI: inadequate dietary fat (especially from animal products), consumption of wheat, soybean and occasionally milk proteins.
6. Breastfeeding provides the best protection against developing allergies in infancy and later in life.

ABA article, Lactose Intolerance and the Breastfed Baby
Johns Hopkins Medical Institutions (2011, May 1). Formula-fed preemies at higher risk for dangerous GI condition than babies who get donor milk. ScienceDaily. Retrieved June 26, 2011, from­ /releases/2011/04/110430171122.htm
Noble R, Bovey A, Resolution of lactose intolerance and colic in breastfed babies,
presented at the ALCA Vic (Melbourne) Conference on the 1st November, 1997
Concerns for the use of soy-based formula in infant nutrition. Paediatr Child Helath 2009 Feb 14(2): 109-113
Osborn DA, Sinn JKH. Formulas containing hydrolysed protein for prevention of allergy and food intolerance in infants. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD003664. DOI: 10.1002/14651858.CD003664.pub3

The Framework of Common Sense

For something as mundane as fuel for our bodies, food and our relationship with it are extremely complicated. Our nutritional knowledge is molded from birth. First, from our parents: Eat your greens! Drink milk for strong bones! No dessert until you clean your plate! In the tempestuous years of teenage rebellion, we do a 180 and discard the well-meaning advice of our elders and embrace the “coolness” of junk food and alcohol. At least I did. Some “Peter Pans” remain in the grips of the party food (pizza, sausage rolls, lemonade) beyond adolescence. Others make a transition to responsible adulthood by becoming your typical health conscious consumer. But most still continue to seek some authority to take on a parent role: government guidelines, scientists (as a vague joint body supposedly united by a common purpose and understanding), doctors, newspapers, weight loss shows, personal trainers, Sharon from next door because she has lost 7 kilos on the Lemon Detox diet. Once the authority figure is established, everything they say equals gospel and every decision you make is referred to their wisdom.

Here is a radical concept. You have a brain. So do I. I propose a framework. I will call it The Framework of Common Sense. Every time you hear of a new diet, new pill, new exercise regime, new wonder berry from Tibet, you apply the FCS and voila! Your rusty neurons spring into action. A word of warning though. FCS requires applying critical thinking to every new concept. Always. You can never turn your brain off and just go with the flow. If your attention is already starting to drift I suggest you go back to this.

Good, you are still here. Let’s get started.

STEP 1: The laws of metabolism

This is where you ask yourself: does it make sense from physiological point of view? This one has a caveat: you have to know the basics of human biochemistry. Sorry.
Important things to know here:
A. Availability of mechanisms for digestion and absorption: is human body actually designed to process this food?
B. Nutrient density: does the diet in question provide enough vital nutrients for health without the need for supplementation?
C. Hormonal response: does the diet produce the hormonal environment necessary for everyday functioning and for special circumstances like growth, pregnancy, menopause, old age?
D. Inherent harm: can the diet cause damage to the body as suggested by biochemical mechanisms ?(note: do not confuse with Implied harm which is suggested by scientific evidence. It is further down the list)

STEP 2: Evolutionary environment

Is there evidence that people have consumed this food for a sizable chunk of human history? If yes, is there evidence that humans thrived on it?

Do not make your step 2 more important than step 1. Just because the food is ancient, it doesn’t mean it is automatically “good”. Australian Aborigines have been eating grubs and insects for thousands of years. I’m pretty sure that even if it turns out that cockroaches can cure cancer, they would never become a delicacy in the Western world. On the other hand, just because the food is modern doesn’t make it “bad”. Cheese is a modern food (and therefore off limits for the hardcore Paleo crowd). But step 1 tells you that cheese is A. Easily digested (unless people have specific issues with casein) B. High in essential fats, vitamin K, calcium etc. C. Has little effect on hormone levels D. Doesn’t cause inherent harm.

STEP 3. Scientific evidence

A. Implied harm: is there scientific evidence that the food or diet results in long term harm?
B. Implied benefit: is there scientific evidence that it is beneficial for health and longevity?

In science, the top level of evidence is a double-blinded multi-centre long term Randomised Controlled Trial (RCT). Two groups of people, similar in major demographics (age, gender, race, health status). The intervention allocated (in this case, a diet) is identical but for one variable. Neither investigators nor participants know the group allocation of an individual participant. Participants are followed up regularly and for a long time to assess risk and efficacy. You tell me if it is possible to test a diet using this principles.

The second tier in scientific evidence is observational studies. You select a group of people and observe their eating habits for some years and then record how many heart attacks, cancer, strokes etc. they get over the years. Or you ask heart disease patients about their dietary habits and then compare to healthy people. Or you do a national dietary survey and compare it to national disease statistics. Lots of loopholes in all of the above. Therefore…

Do not give step 3 higher priority than steps 1 and 2. Recognise limitations of scientific studies. For those who only trust scientific evidence, here is a nice review of the available evidence that the use of parachutes improves the outcomes of jumping off an airplane. Enjoy.

Now let’s apply the FCS to the Heart Foundation recommended diet (HFD)

STEP 1 Metabolism
A. Digestion and absorption
Major issue here is the massive content of so-called heart healthy whole grains. Your intestine is not a blocked pipe, it doesn’t appreciate being “scrubbed”. And to put it simply, if it comes out the other end in the same form as it goes into your mouth, it wasn’t meant to be digested.
B. Nutrient density
HFD is based on the concept that you can decrease the nutrient density as long as you have the same food volume. As a result you get skim milk, skinless chicken breasts, steamed watery vegetables and cardboard-tasting biscuits. Let alone a total lack of taste, how about the fact that cereals, breads, skim milk are so obviously devoid of nutrients that they have to be artificially fortified with thiamine, vitamin D, zinc, iron, etc.?
C. Hormonal response
55-65% carbohydrates? I don’t care whether you eat them on the form of sweet potato or Caramello Koalas, that’s a lot of insulin. If you are happy to pound the pavement for 10 kms daily and ruin your joints in the process just to control the fat-storing inclinations of that hormone, be my guest. And, guys, be prepared to do weight training every morning too, since insulin decreases testosterone concentration.
D. Inherent harm
3 words: wheat, fructose, hearthealthyindustrialvegetableoils (by the way, since when did canola and sunflower seeds get reclassified as vegetables?)

According to our algorithm we can stop right here. But let’s humour the zealots of conventional wisdom and work down the list.

STEP 2. Evolutionary evidence
7 million years of hominans. 2 million years of humans. 10 thousand years since some agriculture. 200 years of sugar. 50 years of industrial vegetable oils. Do the math.

STEP 3. Scientific evidence
Let’s face it: it’s very shaky. For a comprehensive analysis i.e. debunking of the lipid hypothesis (saturated fat raises your cholesterol, high cholesterol causes heart disease) please read this and this and this.

This algorithm can be applied to any nutrition plan: low-fat, low-carb, vegetarian, Paleo, vegan (horse-strength doses of vitamin B12 pills, anyone?), Jenny Craig and Raw food. I would love to hear some of you having a go at this algorithm. Or let me take on a diet or a food group of your choice.

The upside of using your own brain to make your own decisions is that you are in control of how you live your life. The downside is that you lose that wonderful sense of certainty that tends to come with ignorance. You will no longer be able just to trust media reports that start with the words “in the latest study the scientists have discovered…”. You will not be able to just accept your doctor’s advice to take the fat, salt and taste out of your food without asking WHY. You will have to know more about basic sciences, metabolism, anthropology, endocrinology, statistics and evidence-based medicine. You will have nagging doubts and constantly question yourself and others.

And if any of this is making you uncomfortable (quite understandable) it is never too late to turn back.

Calorie is a calorie is a calorie. Part I

What is a calorie? In the world of physics, a calorie is the amount of energy required to heat 1 gram of water by 1 degree. In nutritional terms, calories mean food energy, energy in turn signifies how much we burn and how much we store. Somewhere in the equation is the first law of thermodynamics, which is generally interpreted as: calories in must equal calories out. If we apply this law to human metabolism we get the conventional wisdom: to lose weight you need to eat less and exercise more. No-brainer, right?

Let’s explore these concepts in a little more detail. I am no physicist (I can just see my physics lecturer nod fervently to this statement). If I can slowly walk my subtle-as-a-sledgehammer brain through these abstract concepts, so can you.

Food calories

How is the caloric value of common foods determined?

The well-known 4,4,9 calorie values per 1 gram of carbs, protein and fat respectively, were first derived in the early 1900s by Wilbur Olin Atwater. He used a machine of his own invention, the respiration calorimeter, to measure the heat production of foods in the typical diet of the beginning of the 20th century. I would hazard a guess that our foods today are somewhat different to the ones Atwater happily incinerated in his lab. The unit “calorie” was used to measure the amount of heat energy released. Proteins, carbs, fats, alcohols, polyols and fibre were all allocated their average values and the rest is history. Apparently the use of Atwater system “has frequently been the cause of dispute, but no real alternatives have been proposed”.

Today most food manufacturers use the Atwater system to calculate the total calories in their product. Another less commonly used method is calorimetry, similar to Atwater’s experiments. The food in question is combusted with oxygen and the amount of heat energy generated is measured. Here is the first hiccup. Human bodies obviously do not “burn” food or generate that much heat. Getting really hot is a major problem for our brains as they tend to get delirious. Instead our bodies generate ATP, the carrier of energy required for all biochemical reactions in your body. Carbs, protein, fat, alcohol – all have the potential to generate ATP.

Why the potential? Because not every morsel that goes through your mouth is used for ATP production. Protein can be broken down to amino acids which can be used as energy. However, they are preferentially used up for cellular repair or the building of new proteins. So if your body is in the state of growth, illness, recovery from your latest unsuccessful attempt at a pull-up (guilty as charged), you might not be “burning” any of the protein that comes from your steak. In the same way, glucose can be used to replenish your glycogen stores in
the liver and skeletal muscles. So if your glycogen stores are empty after a workout, the glucose will be used preferentially to refill them. Fatty acids are used for building cellular membranes and cholesterol for hormones.

Basically, your body is not a furnace and your metabolism is not a ritual burning of a piece of cake. Biochemists have neatly summarised this process in the diagram below. I call it the WTF diagram.

A bit different from “fat=calorie in – calorie out”, don’t you think?

But can’t we average all these processes and come up with a number of food calories required for everyday function? What about Basal Metabolic Rate, the BMR? Someone somewhere has worked it out. I can google the formula! And once I know it, I can just subtract 500 calories daily and it will result in half a kilo loss per week, right?

The BMR story

A nerd in me is very attracted to this simple idea. Calculating an easily predictable weight loss value is so elegant. And knowing your own special number, your Basal Metabolic Rate, is almost empowering.

Harris-Benedict equation
The easiest way to do it is the Harris-Benedict equation suggested in 1919 (that’s before we knew about DNA). It estimates the strongest predictor of your BMR = your muscle mass, by taking into account your age (because older people always have less muscle), your sex (because women are always the weaker sex) and your weight (because your weight always indicates how muscle you carry).  I don’t know about you but I have a few issues with some of these assumptions.

DEXA scan
The next way to do it is to use the actual lean body mass measurement, either by DEXA scan or by the “fat scales”. I will not go in why the “fat scales” is a complete waste of your time and money. Let’s assume you do a DEXA, an x-ray imaging tool which will tell you your exact body composition. You also receive this charming picture. While it may tell you how much muscle you have (and diagnose osteoporosis, which was the initial application of this test), it won’t be able to tell if you are sick with pneumonia, if you are taking antidepressants, if you have  overactive thyroid, insulin resistance, phaeochromocytoma and a host of other things which will determine your own fuel utilisation rate, a.k.a what your body does with your food.

Because your metabolism is not regulated by your muscle cells.
It is regulated by hormones.

Thankfully, in the research world there are two ways to actually measure the metabolic processes which happen in an individual organism: indirect and direct calorimetry.

Indirect calorimetry
Most energy-generating pathways in the body require oxygen and result in the production of carbon dioxide (CO2) as a by-product. Therefore if I fit you with a special gas mask, make you breathe (this shouldn’t be too hard) and then measure the amount of oxygen in and CO2 out, I can get an estimate of how much ATP you are generating, and also how much fat vs glucose you are using for its production. This “metabolic monitoring” is also used in Intensive Care Units to work out the energy requirements of critically ill patients. It is obviously a very involved process. Nevertheless, here is a study which address the potential pitfalls of interpreting measurements without taking into account the hormonal environment.

Are you serious? I am breathing through a machine and you are still not a 100% sure how many calories I need???

Direct calorimetry
This is the final frontier, the golden standard. The description of this  process can be summarised in just a few words: “secure chamber”, “constant  temperature”, “air seal” and my favorite, “the panic button”. Yes, your whole body has to  be inside, sometimes for several days. A couple of problems: first, it only  measures your metabolic rate at that particular time. I hope we all agree that  metabolism is not a static number, multitude of variables can affect it from day  to day. The second problem is that it is a tad inconvenient.

So what are we left with? Helpful websites offer an easy formula to  calculate your BMR measurement, your TDEE (Total Daily Energy Expenditure)  measurement, your AUN (Another Useless Number) measurement. Then you subtract  500 calories (what a lovely even number) from your total, and that should give  you a 1/2-1 kg loss each week. Conveniently, this rate of weight loss seems to be fairly  similar no matter which diet/exercise regime you choose.

It might sound ridiculous that somebody might rely on a formula developed  in 1919 to estimate the BMR of an average healthy person under normal conditions  to apply in 2011 to an overweight individual. Followed by the advice to reduce their food intake by checking the caloric values, found by incinerating these foods under lab conditions. Finished by the recommendation to expend more energy by  exercise while checking the number of calories supposedly burned on a treadmill machine where you input your weight and sex.

In other words, the absolute number of calories is about as useful as knowing how much the loose change in your wallet weighs in poods. The units are  useless and how is it relevant to how much money is there anyway?

In part II I will discuss the application of ‘calories in = calories out’ to weight loss.