Sunday, May 25, 2014


Fatty Acids

There are four main types of fatty acids, which are classified by the number and structure of carbon-carbon double bonds:

·         Saturated fatty acids (SFA) (no double bonds)
·         Monounsaturated fatty acids (MUFA) (1 double bond)
·         Polyunsaturated fatty acids (PUFA) (>1 double bond)
PUFAs can be further broken down into omega 3s (n-3) and omega 6s (n-6) which refers to the
·         Trans fatty acids (TFA) (≥ 1 double bond in the trans position, mentioned later) 

There are many types of fats, below is a table of some of the common fats categorised by the number of carbons* and double bonds and those in bold tend to be the most commonly mentioned

Foods contain a number of different fatty acids in different proportions, so it’s wrong to say ‘X is a saturated fat’

·         Animal fats have fairly equal proportions of SFA and MUFA, with ruminants and dairyhaving low PUFA and poultry,eggs, pork andfish/seafood having more PUFA
·         Fish/seafood is the best source of long chain omega 3s (LCO3s) such as EPA and DHA but grass-fed/pastured meat, dairy and eggs also contains some (algae also contains DHA)
·         Olive oil is very high in oleic acid (hence the name)
·         Nuts, seeds and seed oils (sunflower, safflower, soybean, cottonseed, canola, etc) are generally high in PUFA from linoleic acid, except canola which is high in MUFA and flax which is high in alpha-linolenic acid
·         Coconut oil is the major source of lauric acid

A notable fat that’s missing from this list is butyric acid (4:0), which is produced by bacterial fermentation of fibre in the large intestine and is also found in dairy.

* Short chain fatty acids (SCFA) are those with < 6 carbons, medium chain with 6-12, and long chain with > 12

PUFAs and Eicosanoids

Of the fats, only linoleic acid and alpha-linolenic acid are essential (because they can’t be synthesised) and so are considered the essential fatty acids, but this misses the point.  The omega 6 and omega 3 families of PUFA have a number of biological functions when DGLA/AA and EPA/DHA are converted to eicosanoids (or docosanoids for DHA) by the cyclooxygenase enzyme family (COX).  In their present form, LA and ALA fulfil no essential functions and need to be converted to DGLA/AA and EPA/DHA (respectively) by desaturation and elongation enzymes (see below).  The conversion of ALA to DHA is so low (~0.5%) that DHA has been suggested to be an essential fatty acid as well [1]

There are a number eicosanoids produced from long chain PUFAs, and each in turn has several biological functions.  As a general rule, those produced from AA are pro-inflammatory, while those produced from DGLA, EPA and DHA are anti-inflammatory.  However, increasing dietary AA, at least in the short term doesn’t seem to increase inflammation [2], while increasing EPA+DHA reduces markers of inflammation [3] [4]

Trans Fats

One of the properties of PUFAs is that the presence of multiple double bonds makes them vulnerable to oxidation (causing them to become rancid more quickly (shorter shelf life)). This was a problem for those promoting PUFA rich vegetable (seed) oils in the early 20th century as being both cheaper and healthier than animal fats.  Fats/oils can be partially hydrogenated to improve shelf life.  Partial hydrogenation is a process that adds hydrogens to the fats, thereby reducing the number of double bonds.  However, partial hydrogenation results in double bonds where the hydrogen atoms are at different sides of the double bond (trans), whereas the hydrogens are at the same side in the double bonds of other fats the (see below).

The trans fats (TFA) produced by this process certainly have a longer shelf life and are more solid at room temperature (mimicking animal fats), but increase inflammation and have a number of deleterious effects, particularly related to cardiovascular disease [5]. A common TFA produced by partial hydrogenation is elaidic acid (18:1 n-9) (an isomer of oleic acid) and these TFA are commonly found in partially hydrogenated oils and certain processed foods.

However, there are trans fats that actually promote health such as vaccenic acid (18:1 n-7), which is present in ruminants and dairy [6].  There are also a family of isomers (same molecules, different structure) of linoleic acid called conjugated linoleic acids (CLA), which have both a cis and a trans double bond (a conjugated double bond).  The most common of these is rumenic acid (18:2cis-9, trans-11), which is also found in ruminants and dairy (hence the name) and seems to promote health as well [7].  Unfortunately the health effects of CLA are often tested using a different isomer of CLA (18:2 trans-10,cis-12)

* Full hydrogenation of linoleic acid (for example) would simply convert it to stearic acid

Fats and Cholesterol

One of the things people are most concerned about with fats is how they affect cholesterol levels, so here you go

Relative to carbohydrate:

·         SFA on average increases HDL-C and LDL-C, but doesn’t significantly change the total cholesterol to HDL-C ratio (perhaps the best blood lipid based risk factor for CVD [8])
·         MUFA and PUFA increases HDL-C and decreases LDL-C and the total cholesterol to HDL-C ratio
·         TFA increases LDL-C and the total cholesterol to HDL-C ratio*

And relative to carbohydrate for other CVD risk factors:

·         SFA, MUFA and PUFA reduces triglycerides, particularly long chain omega 3s
·         MUFA and PUFA, but not SFA (no change) decreases apo B (protein of LDL)**
·         SFA and MUFA, but not PUFA(no change) increases apo A-1 (protein of HDL)**

Whether or not this is meaningful is another story.  I have argued that you can’t simply assume how things willaffect CVD based on how they affect blood lipids (here and here) and that replacing SFA with PUFAmost likely doesn’t reduce CVD (here)

* It’s interesting that this study found TFA didn’t affect HDL-C when so many studies mention that TFA reduce HDL-C by increasing CETP

** The number of LDL and HDL particles is a better risk factor than the amount of cholesterol in those particles

*** The effects of different SFAs is shownhere

**** The effects of different fats is shown here.  Notably replacement of all whole food fats lowers the total cholesterol to HDL-C ratio

Sunday, May 18, 2014


Proteins are made up of amino acids (peptides are short chains of amino acids). When we eat foods containing protein, the protein is broken down into amino acids during digestion so they can be absorbed and then used in the synthesis of our own proteins or for other functions (see below).  (Amino acids that can be incorporated into proteins are called proteinogenic amino acids)

There are both essential and non-essential amino acids. In this context ‘essential’ means we can’t synthesise it and so must get it from the diet. Although in practice, the synthesis of the non-essential amino acids is quite limited and dietary sources supply plenty of non-essential amino acids, so it’s largely an academic point.  Below are the essential and non-essential amino acids and some of their main functions (the ‘W’ hyperlink goes to Wikipedia and ‘E’ goes to

Essential AAs
Main Functions
Histidine (W)
Converted to histamine for immune response
Isoleucine (W,E)
Muscle recovery, protein synthesis, increase glucose uptake
Leucine (W,E)
Activate mTOR and sirtuins, muscle recovery, protein synthesis
Lysine (W)
Calcium absorption, tissue repair, carnitine precursor
Methionine (W,E)
Methyl donor, cysteine precursor, carnitine precursor
Phenylalanine (W)
Tyrosine precursor
Threonine (W)
Protein balance, collagen and elastin synthesis, antibody formation
Tryptophan (W,E)
Serotonin, melatonin and niacin (vitamin B3) precursor
Valine (W,E)
Muscle recovery, tissue repair, protein synthesis

Non-Essential AAs
Main Functions
Alanine (W,E)
Modest effect on performance and body composition, carnosine precursor
Arginine (W,E)
Nitric oxide precursor, growth hormone secretion
Asparagine (W)
Nervous system development
Aspartate (W,E)
Weak excitatory neurotransmitter, helps convert glutamine to glutamate (and is converted to asparagine in the process)
Cysteine (W,E)
Glutathione and taurine precursor
Glutamate (W)
Main excitatory neurotransmitter, GABA (main inhibitory neurotransmitter) precursor
Glutamine (W,E)
Refills TCA cycle, an energy source for rapidly dividing cells, may improve intestinal permeability
Glycine (W,E)
Inhibitory neurotransmitter outside cortex and co-agonist on NMDA receptors (excitatory) inside cortex the main amino acid in collagen
Proline (W)
Hydroxyproline is an abundant amino acid in collagen
Serine (W,E)
Similar neural function as glycine, but in glial cells
Tyrosine (W,E)
Dopamine, noradrenaline and adrenaline precursor

Some other things to note: isoleucine, leucine and valine are the branched chain amino acids (BCAAs) and methionine and cysteine are the only amino acids that contain sulphur.

You don’t really need to worry about content of those tables much because simply eating protein will simply all the amino acids, but there are some exceptions

·         Many plant proteins are ‘incomplete’, meaning they have a lower than ideal proportion of the essential amino acids.  Generally plant proteins have a lower proportion of the sulphur amino acids (methionine and cysteine), the BCAAs and/or lysine
·         Most protein sources are low in glycine, except connective tissue, skin and bones [1] [2]

Also, some amino acids are commonly supplemented for various benefits, such as:

·         Leucine to increase protein synthesis [3]
·         BCAAs to enhance exercise performance and/or protein synthesis [4]
·         Tryptophan to increase serotonin synthesis
·         Beta-alanine to increase carnosine [5]
·         Arginine (or nuts as they’re high in arginine) to increase nitric oxide
·         N-Acetylcysteine (NAC) for a number of effects including glutathione synthesis[6]
·         Glycine (or gelatin as it’s high in glycine) for a number of effects [2]

The metabolism of amino acids is more complex than fat and carbohydrate.  After being deaminated (removal of nitrogen), amino acids can also enter the TCA cycle in certain positions (see here) and then depending on the amino acid can either be broken down for ATP synthesis, converted into glucose or converted into ketones.  The removal of nitrogen as urea/uric acid is a limiting factor of protein intake and exceeding that capacity with a very high protein intake coupled with low fat and carbohydrate induces rabbit starvation.

Sunday, May 11, 2014

The Australian Paradox: Part 2

In the last post, I showed how in the Australian Paradox, the authors own data suggests it more likely that sugar and SSB consumption has increased and that the only way to conclude there has been a “consistent and substantial decline in total refined or added sugar consumption by Australians over the past 30 years” is to look at the (faulty) FAO data and ignore all the other results. 

RCTs > Ecological Studies 

Once the authors looked the FAO data and concluded the “consistent and substantial decline”, they turned their attention towards the implication of their ‘results’.  Essentially that reducing sugar or taxing SSBs may not reduce obesity: 

“The implication is that efforts to reduce sugar intake may reduce consumption but may not reduce the prevalence of obesity” 

“The findings challenge the implicit assumption that taxes and other measures to reduce intake of soft drinks will be an effective strategy in global efforts to reduce obesity” 

The problem is that even if there was the “consistent and substantial decline” the authors would be overstating their ‘results’.  The Australian Paradox is an ecological study, a type of observational study that looks at populations rather than individuals, and ecological studies shouldn’t be used to make inferences about the biological effects on individuals [1] (doing so is referred to as the ecological fallacy), a point which is made briefly by the authors 

“A limitation common to all ecological studies is that relationships observed for groups do not necessarily hold for individuals” 

The Australian Paradox can’t determine whether sugar and/or SSBs are obesogenic or whether taxes will reduce obesity.  RCTs will answer the first and other studies (most likely case studies) will inform the second 

Fortunately, at least for SSBs, there’s a number of RCTs investigating their relationship with weight.  Prior to 2011 (the Australian Paradox was published in 2011), there were six systematic reviews without a conflict of interest with the food industry, which examined the relationship between SSB and excess weight gain in observational studies and/or RCTs. Five out of those six systematic reviews found a positive association [2] 

However, in the discussion when the authors compared their findings to similar research (ecological, other observational and RCTs) they tended to cite studies that found a negative or no association between sugar/SSBs and excess weight gain, and only one study that found a positive association 

Who are the Authors? 

Alan Barclay, PhD (AWB) is an Accredited Practicing Dietician, the Head of Research at the Australian Diabetes Council and did his PhD thesis on the relationship between glycemic index (GI) and chronic disease (Australian Diabetes Council 2013). Jennie Brand-Miller, PhD (JBM) is a Professor of Biochemistry in the School of Molecular Bioscience at Sydney University and her research interests include the role of carbohydrates and GI on health

The authors disclosed some conflicts of interest: AWB is a co-author of one of the books in The New Glucose Revolution (NGR) book series and the chief scientific officer of the Glycemic Index Foundation (GIF); JBM is a co-author of the NGR book series and the director of the GIF 

What isn’t mentioned with these conflicts of interest is that: (1) The NRG book series makes claims of high GI bad, low GI good, sugar ok; and statements like: “There is an absolute consensus that sugar in food does not cause diabetes” [3] [4].  An absolute consensus means 100%.  You won’t need to look too hard to prove this statement wrong.  (2) The GIF promotes low GI whole foods (like fruit), lower GI alternatives (lower GI bread and potatoes), but also lower GI sugar and junk food [5] 

The authors did not disclose that some members of the food industry are corporate governors of the nutrition research foundation at Sydney University’s School of Molecular Bioscience (where JBM works) [6] 

Also, JBM was the guest editor of a special issue of Nutrients (the journal, only started in 2009) called Carbohydrates, which was the issue that the Australian Paradox was published in.  With all that’s been said, it’s likely the authors choose to publish in Nutrients, with JBM as guest editor, because under normal circumstances the paper would likely have not passed peer-review 

* I was fortunate (being familiar with Rory Robertson and Background Briefing) that the Australian Paradox was one of the papers we could use for an assignment called ‘critical analysis of the literature’, hence the subject of the blog posts.  From my experience, the papers they select for these types of assignments tend to be poorer quality.  The assessor liked the assignment, noted a few other issues with the paper that I hadn’t discussed and wondered whether the paper had previously gone under review at a different journal.  I discussed the paper with a few people and they had similar views on it.  If the Australian Paradox was presented in an academic setting I wonder what the audience response would be.  I certainly wouldn’t want to be the one presenting

Sunday, May 4, 2014

The Australian Paradox: Part 1

For those who don’t know, the Australian Paradox essentially says that there has been a “consistent and substantial decline in total refined or added sugar consumption by Australians over the past 30 years”, during which time the prevalence of obesity in Australia has tripled.  And concludes that “the findings challenge the implicit assumption that taxes and other measures to reduce intake of soft drinks will be an effective strategy in global efforts to reduce obesity”.  In other words: sugar down, obesity up, therefore sugar isn’t responsible 

Rory Robertson has already really thoroughly critically analysed the Australian Paradox.  Also in February, Wendy Carlisle did an investigation of the Australian Paradox for Background Briefing. 

In this post I’m just going to look at the results and save other points for the following post 

Obesity has increased over the last 30 years.  No surprises there

This is the FAO data, which has gotten its Australian data from the ABS Apparent Consumption of Foodstuffs up until 1999 as the ABS ceased that dataset after 1999.  In the years after 1999 there’s a flat line for ‘refined sucrose’ with a very low year-to-year variation.  It looks like the FAO made up the data for 2000 onwards (see here) 

Another issue is that when calculating apparent consumption of sugar, the ABS data didn’t include sugar contained in imported highly processed foods.  Between 1988 and 2010, imports of highly processed food containing sugar increased to a much greater extent than exports.  If the data on imports was added to the FAO dataset it would suggest an increase in sugar availability [1]* 

* On Background Briefing one of the authors says “my paper has not been criticised by any scientist”

Both these graphs suggest sugar intake has increased in both adults (F3) and children (F4)

In the discussion the authors say that per capita sales of sugar sweetened beverages (SSBs) decreased by 10% between 1994 and 2006, but per capita sales of SSBs increased by 30% and the reduction of 10% refers to market share.  This was corrected after background briefing in February, although the authors said this change, and another two, have no material impact on the conclusions of our paper”.  When your paper is supposed to look at trends in sugar consumption I don’t see the point of mentioning market share between SSBs and diet drinks (DDs) 

Volume Sold (L/person/year)

Market Share (%)

* The numbers in these tables are rough to make it easy for you to see the relationship between volume sold and market share (you don’t need a calculator)

If you wanted to look at 30 years trends I don’t understand the point of figure 6 as it only lists data from 1997-1998 to 2005-2006 (8 years).  In relation to this figure the authors say “overall, there was a decrease in sugar contribution from nutritively sweetened carbonated soft drinks to the Australian food supply, amounting to 12,402 tons (~600 g per person*, Figure 6) from 2002 to 2006.”.  That sounds like a lot of sugar, but on closer inspection, this impressive figure only amounts to an average reduction of 0.42 g/person/day** 

* Corrected here 

** 12.4 billion grams / 20 million people / 1461 days

It’s interesting that this data in children suggests no difference or a decrease in SSBs from 1995 to 2007, while F4 shows a more than doubling in SSBs over the same period and F5 shows a 30% increase in volume of SSBs sold among both adults and children

Bonus graph!  This one comes from The Australian Paradox Revisited.  Like the ABS data, the issue here is that this doesn’t include imports of sugar and sugar in processed foods, which have increased over time [1] 

Taking the results at face value: 

·         F2: Decrease in apparent sugar consumption
·         F3: Increase in sugar intake among adults
·         F4: Increase in sugar intake among children (overall)
·         F5: Increase in the volume SSBs sold
·         F6: No difference in sugar from SSBs between 1997-1998 to 2005-2006
·         F7: Decrease in SSBs consumption by children
·         B1: Increase in availability of refined sugar 

No Change
F3, F4, F5, B1
F6 (limited trend)
F2, F6

On balance, the results presented in the Australian Paradox suggest that sugar and SSB consumption has more likely increased rather than decreased.  This is even while ignoring issues with the data such as not accounting for sugar from increased imports of processed sugary foods and SSBs (F2, B1) 

In the discussion the authors say there has been a “consistent and substantial decline in total refined or added sugar consumption by Australians over the past 30 years”, which is clearly inconsistent with their own results and you could only make that conclusion if you looked at the FAO data and ignored all the other results 

* F4 and F7 suggest a decline in sugar and SSB consumption respectively between 1995 and 2007.  F1 suggests the incidence of obesity in children increased between 1985 and 1997 and between 1997 and 2004.  Being quite dissatisfied with the authors’ referencing and citations, I looked for information on trends in childhood obesity and came across this meta-analysis that found the trend in prevalence of childhood obesity plateaued from 1996 onwards [2].  If the data in children and the meta-analysis is true then sugar intake in children decreased between 1995 and 2007, which is the timeframe when the prevalence of obesity in children plateaued, suggesting there is no Australian paradox in children