Sunday, November 16, 2014

Carnitine and Cardiovascular Disease

Since we ‘know’ red meat increases cardiovascular disease (CVD)* researchers have been investigating possible mechanisms.  Attention has recently turned to carnitine (and choline but this post will focus on carnitine) as the components in red meat responsible for red meat supposedly increasing CVD [1]
 
Essentially the argument is that carnitine and choline increase TMAO in the blood, which is associated with CVD and in high amounts of TMAO can induce CVD in genetically susceptible mice [1].  (Which sounds an awful lot like the arguments against SFA, such as SFA >> LDL-C >> CVD)
 
* Even though a recent (2010) systematic review and meta-analysis found that no RCTs were identified that evaluated effects of red, processed, or total meat consumption on CVD or diabetes events” and in prospective cohort studies “red meat intake was not associated with CHD” [2], which is consistent with data from the NHANES III survey [3]
 
What is Carnitine?
 
Carnitine is a compound that is found almost exclusively in meat (hence ‘carn-’) and can be synthesised by humans from methionine and lysine using vitamin C dependent enzymes.  However, vegetarians tend to have slightly lower blood carnitine levels [4]
 
The main function of carnitine is to transport fatty acids into the mitochondrial matrix to be metabolised*.  Carnitine also functions as an antioxidant and supports mitochondrial function.
 
Examine has a page on the evidence regarding the effects of carnitine supplementation and it seems carnitine is beneficial compound in a variety of contexts [5].  For example, carnitine reduces blood pressure [5], improves insulin sensitivity [5] and reduces cognitive decline in the elderly [5]
 
* Due to this function, carnitine has been promoted as a ‘fat burner’.  However, it doesn’t appear to increase fat oxidation unless one has inadequate carnitine [5]
 
Does Carnitine cause CVD?
 
The proposed mechanism of carnitine >> TMAO >> CVD (therefore red meat >> TMAO >> CVD) has been thoroughly critiqued by Chris Masterjohn [6].  Other people have also critiqued the study (though not as well as Chris Masterjohn), but almost all these critiques have focussed on the study design and/or the mechanisms, with very little attention paid to the real question: ‘does carnitine increase the risk of CVD?’  Fortunately we have some fairly good evidence to help us answer that question
 
A systematic review and meta-analysis of clinical trials (13 trials, N = 3629) was conducted in 2012 looking at the effects of carnitine supplementation on CVD events and total mortality in secondary prevention (people who have had a heart attack) [7].  It found that carnitine associated with:
 
·         “A significant 27% reduction in all-cause mortality
(odds ratio, 0.73; 95% CI, 0.54-0.99; P=.05; risk ratio [RR], 0.78; 95% CI, 0.60-1.00; P=.05)”
·         “A highly significant 65% reduction in ventricular arrhythmias
(RR, 0.35; 95% CI, 0.21-0.58; P<.0001)”
·         “A significant 40% reduction in the development of angina
(RR, 0.60; 95% CI, 0.50-0.72; P<.00001)”
·         “No reduction in the development of heart failure
(RR, 0.85; 95% CI, 0.67-1.09; P=.21)
or myocardial reinfarction*
(RR, 0.78; 95% CI, 0.41-1.48; P=.45)”
 
These results are superior to statins (see table below), and unlike statins (which increase the risk of type 2 diabetes [8] and may impair cognitive function), carnitine seems to improve cognitive function and insulin resistance [5].  Carnitine supplements are fairly cheap, so I don’t see much reason why they aren’t prescribed to people who have had a heart attack
 
The Number Needed to Treat (NNT)
(lower is better)
Statins [8]
Carnitine [7]
Total Mortality
83
38
Non-Fatal Heart Attack
39
NS*
Ventricular Arrhythmias**
?
4
Angina**
?
3
 
This is secondary prevention so it’s unknown whether carnitine will have a similar beneficial effect in primary prevention (people who have not had a heart attack).  However, based on these results and overall effects of carnitine (see the Examine article) it’s likely that carnitine is beneficial for primary prevention as well.  At the very least, it would be surprising if something which is beneficial for secondary prevention is harmful for primary prevention
 
* There were only 38 myocardial reinfarctions which makes the study pretty underpowered (by comparison there were 250 deaths)
 
** Ventricular arrhythmias and angina would be expected to have a lower NNT (due to higher incidence) and therefore shouldn’t be compared to the statin NNT for non-fatal heart attack.  I included those two figures just to emphasise how therapeutic carnitine seems to be
 
The Limitation of Mechanisms
 
The take away from this is that biological mechanisms are just hypotheses for what happens in real world.  If we reduce most mechanisms to A >> B >> C*, then logic tells us that we can only be certain that A causes C if at least one of these conditions is true:
 
·         A only causes B
·         B only causes C
 
This is rarely the case in biology, as biological systems are highly interconnected and biologically active compounds have many effects**.  In this case, although carnitine may have some adverse effect by increasing TMAO, carnitine also has many beneficial effects, resulting in a net positive effect for CVD events and total mortality in secondary prevention.  The only way to test this is to do clinical trials
 
* Carnitine >> TMAO >> CVD
Saturated fat >> LDL-C >> CVD
 
** Also, when we get carnitine from meat we are also ingesting many other nutrients and various compounds in meat, all of which have their own biological effects.  With this in mind, reducing a given food (or food group) to one nutrient (or several) ignores the net biological effect of all the nutrients and compounds in a given food, not to mention any nutrient interactions.  A good example of this is demonising fruit by reducing it to sugar
 
Summary
 
·         There have been no clinical trials to examine the effect of red meat on CVD
·         Red meat is not associated with CVD in observational studies
·         Carnitine is a beneficial nutrient in a variety of contexts
·         Carnitine reduces CVD events and total mortality in secondary prevention
·        Just because A causes B and B causes C doesn't mean A causes C
 
If you haven’t already, I recommend you read the Examine article on carnitine and Chris Masterjohn’s critique

Sunday, November 9, 2014

The Narrative

The Narrative
 
People make decisions based on costs and benefits.  Given the detrimental effects that poor health has on quality of life, why is it that poor health is so common in western societies?  We are often told that by changing our diet and/or lifestyle we can reduce our risk of disease, and yet despite this many people continue to knowingly make poor diet and lifestyle decisions.  It’s not like we are oblivious to the prevalence and impact of poor health in the community as awareness campaigns by health bodies and the ubiquity of poor health in our social circles tell us that poor health is both common and has an adverse effect on quality of life.  However, this is also a negative, since poor health is so widespread it has become normalised.  We are then exposed to with a far more powerful message, one of hopelessness:
 
·         ‘That’s the sort of thing that happens when you get older’
·         ‘It’s genetic/runs in the family’
·         ‘No one knows why/these things just happen/just because’
·         ‘Diets (or other lifestyle interventions) are unsustainable’
·         ‘There is no cure’
 
The narrative is essentially a self-fulfilling prophecy: the narrative promotes hopelessness, hopelessness leads to inaction and inaction on a large scale leads to the ubiquity of poor health the current population faces, that then gives rise to the narrative
 
Challenging the Narrative
 
These statements avoid blaming the other person for their poor health (which is often unproductive), but simultaneously reinforce that the other person is powerless.  Also, these statements are often false and intellectually lazy.
 
‘That’s the sort of thing that happens when you get older’
 
Weight gain, the development of chronic disease and loss of independence is almost seen as an inevitable part of the aging process, but it doesn’t have to be:
 
·         Hunter-gatherers, who had an average life expectancy of 65-70 at 45 [1], are almost completely free of chronic degenerative diseases [2]
·         Similarly, the traditional cultures studied by Western A Price were almost completely free of chronic degenerative diseases [3]
·         Those living in the mid-Victorian era had a life expectancy at 5 that is similar to ours today and had 90% less incidence of degenerative disease [4] (and the remaining 10% could probably be explained by smoking/poor diet)
·         The incidence of coronary heart disease was very low in the early 20th century, that is not due to shorter life expectancy [5]
 
‘It’s genetic/runs in the family’
 
The points above also provide evidence against most poor health being solely due to genetics (some diseases are genetically determined, but most are not).  Chris Masterjohn made a point that one of the strengths of Weston A. Price’s work is that he found among populations free of chronic disease, the most vulnerable and the least vulnerable members are protected from chronic disease.  A saying goes ‘genes load the gun, but the environment pulls the trigger’
 
‘No one knows why/these things just happen/just because’
 
This type of statement may be made by the type of academic who waits for all the evidence to come in or by a doctor/layperson who is unaware of current research.  Ideally we would know everything about a particular disease and have multiple RCTs testing the efficacy of various therapies.  But this is the real world, where poor health/chronic disease is prevalent, current therapies aren’t good enough.  We have some understanding about the causes of chronic disease and their underlying pathologies and should use that to develop some logical, low risk, non-dogmatic approaches to preventing and treating/reversing chronic disease.
 
‘Diets (or other lifestyle interventions) are unsustainable’
 
In my opinion much of the problem here comes from the popular diet and fitness community where bland, low calorie diets (or highly restrictive diets) and/or grueling, high volumes of exercise are presented the only path to weight loss and subsequently improvements in health, which is often unsustainable.  People try it, but give up because it’s too difficult, then feel powerless to take back control of their health.  The traditional CICO approach to weight loss (simply ‘eat less, exercise more’) is harmful not because it’s wrong, but because it’s so difficult to sustain [6].  It forces people who are only aware of that method of weight loss to make a choice (to some degree) between being overweight and otherwise feeling good or having a normal weight and feeling hungry and tried.
 
An alternative is to devise a delicious and nutritious diet that improves food quality with the goal to normalise the body fat setpoint.  Similarly, to recommend lifestyle approaches that Recommendations for both diet and lifestyle could also be framed differently: as improving quality of life/making you feel better, rather than something fairly intangible like 20% reduced risk of disease
 
‘There is no cure’
 
This implies to some extent that you can’t do anything about it.  The way medicine is currently practiced is about ‘disease management’ and treating the symptoms even when potential cures exist (for example diet and type 2 diabetes).  Similar to the third point this may also be said when someone is unaware of potential cures
 
An Alternative to the Narrative
 
The narrative seems to be reinforced by:
 
·         The ubiquity of chronic, degenerative diseases that few people successfully reverse
·         People saying either 1, 2 or 3 to be sympathetic and avoid blaming the other person
·         Ineffective and/or unsustainable diet and lifestyle interventions that are promoted as ‘cure alls’
·         Doctors and researchers protecting others from the false hope of the latest lemon juice fast
 
Therefore to shift the narrative we need to:
 
·         Be sympathetic to those with health problems and avoid blaming the other person without making them feel hopeless
·         Don’t fanatically promote something as cure all with insufficient evidence, poor reasoning and without discussing the limitations, but also don’t be too sceptical about new approaches with some evidence and logical arguments supporting them.  There is a middle ground where the pros and cons of a variety of proposed therapeutic approaches can be discussed in a balanced manner
 
An empowering thing to consider is that there is an explanation for everything*.  Sometimes the explanation is simple, other times it is very complex, but there is often some level of understanding in even the more complex problems.  If you have a health issue a good place to start is identifying and fixing your weakest link(s), which is/are likely to be an underlying cause.
 
I think the Paleo community is great for shifting the narrative as many people have great success with Paleo (weight less, autoimmune disease remission, etc) and some the core messages include the very low prevalence of chronic disease in hunter-gatherers and traditional cultures and that ‘humans are not broken by default’.  This is part of what got me interested in health as I’ve always had a pretty optimistic view of the human body (I’m not generally an optimist), and I didn’t identify with the negativity in the mainstream health community.
 
* This is doesn’t mean there is a purpose for everything.  Explanation is to how as purpose is to why.  Science aims to answer the ‘how’ questions, but not the ‘why’ questions.

Sunday, November 2, 2014

The DAA on the Paleo Diet

The DAA recently did a three part series on the Paleo diet.  Here are my thoughts on it
 
What is Paleo
 
Part 1 opens up with a description of (Boyd Eaton’s) Paleo followed by some cliché criticisms and implies that Paleo is a re-enactment
 
·         There was not one Paleo diet
·         People kept changing and adapting after the Paleo period
·         Paleo is expensive and hard to sustain.
 
That there was not one Paleo diet isn’t really an argument against Paleo, but rather against dogmatic, one-size-fits-all approaches (such as the Australian dietary guidelines).  Even though there have been adaptations following agriculture, it’s important to recognise that anatomically modern humans have been hunter-gatherers for ~95% of our time on earth and that not all people have had much adaptation to the foods from agriculture.  Both of these points have been acknowledged and discussed in the Paleo community.
 
They cite this paper as evidence that Paleo is expensive and that a 9.3% increase in income is needed to achieve nutrient targets (except calcium).  The title of the paper is ‘the feasibility of a Paleolithic diet for low-income consumers’, which tells you they are modelling for on low income consumers.  They set a budget of $3.89 per day (US dollars in 2001, equal to $4.91 US dollars in 2010) for food made at home.  They found that by choosing low cost foods you would need 9.3% more ($4.25 per day) in the budget to meet micronutrient requirements (except calcium).  The authors of the paper then conclude that you need a 9.3% increase in income, but an increase of 9.3% in the food budget wouldn’t translate into an increase of 9.3% in income, unless 100% of earnings were spent on food.  So income would only need to increase by a fraction of 9.3%, perhaps 2-3%.  It should also go without saying (but doesn’t) that this study was modelled on low-income consumers and does not necessarily apply to the middle-class.
 
They finish off part 1 with ‘Australians need to eat more fruit and veg’, which I agree with, but what’s the relevance?  If anything this is an argument in favour of Paleo.  Grains are the centrepiece of the standard Australian diet (cereal for breakfast, sandwiches for lunch and often a pasta/rice dish for dinner).  When grains are substantially reduced it creates a void that needs to be filled.  Paleo can be thought of as meat and veg with a piece of fruit at 2 or all 3 meals, which would greatly increase fruit and veg intake.  Also, in the clinical trials the Paleo group ate more fruit and/or veg [1] [2].
 
Food Groups
 
The first section of part 2 discusses the pros and cons of Paleo in relation to the food groups.  It’s what you would expect: grouping legumes with vegetables, SFA is bad, some evidence from observational studies against fatty meats and in favour of whole grains and the ‘dairy is important for calcium’
 
The evidence used against SFA in relation to CHD shows no benefit when SFA is replacing with carbohydrate or MUFA only found a benefit when SFA is replaced by PUFA.  However, the evidence for this is very poor as the trials that suggest a benefit in replacing SFA with PUFA for CHD were poorly controlled and have confounding variables or were part of a multifactorial intervention (see here).  Also, the Cochrane and the Mozaffarian meta-analyses (which are used in favour of replacing SFA with PUFA) didn’t find any benefit in replacing SFA with PUFA for total mortality [3] [4].
 
In the summary they say “…the diet fails to provide all nutrients as per current recommendations and excludes foods and whole food groups”.
 
Paleo may often not meet the RDI for calcium without dairy, but the RDI for calcium is set in context of sub-optimal vitamin D levels and vitamin K2 intake.  Getting more sunlight would increase vitamin D, which would improve calcium absorption and Paleo would often be higher in vitamin K2 (found almost exclusively in animal fats), which is far more effective than calcium at reducing fractures in RCTs [5] [6].  On the other hand, since the dietary guidelines don’t recommend many eggs and much meat, and don’t emphasise organ meats, a diet based on the dietary guidelines is likely to have insufficient choline.
 
If the purpose of food groups is to group foods with similar nutrient profiles together so one could get adequate nutrient intake by eating foods from food groups with complementary nutrient profiles, then the current food groups don’t make sense.  Mature legumes shouldn’t be grouped with vegetables, grains aren’t unique and can be easily substituted and meat and dairy substitutes poorly match the nutrient profile of the thing they are meant to be (I discussed this a while ago (legumes, dairy, meat)).
 
Paleo Diet Studies
 
At the end of part 2 they mention the Paleo diet trials and how they are few and small in number, which is a problem I agree with.  They discuss this trial in more detail, saying:
 
“The authors concluded that the Paleo diet was found to be more difficult to adhere to and each diet was found to be equally satiating, although there were per calorie differences. Weight loss was not recorded in this study.”
 
This is either incorrect or misleading.  The trial the author is talking about had two publications, but the author seemed to have only read the second, as the first publication reports weight and BMI [2].
 
Yes, the participants were “equally satiated on both diets” [7], but since the Paleo diet group were consuming fewer calories [2] they experienced greater satiety per calorie eaten [7].  This measure of satiety per calorie is extremely relevant to the obesity epidemic as a limiting factor of weight loss is that people get hungry, therefore you would expect foods/diets with greater satiety per calorie to aid weight loss and maintenance.  But the DAA ignore that and merely say: although there were per calorie differences”.
 
Although more participants found the Paleo diet more difficult to adhere to (P = 0.02), more participants thought the Paleo diet was effective for weight loss (P = 0.02) and almost significantly more participants found the Paleo diet to be more satiating (P = 0.06) and more effective at reducing blood glucose (P = 0.08) [7].  It’s important to not view the perception of ‘difficulty to adhere to’ in isolation.  People make decisions based on costs and benefits.  The path of least resistance often isn’t the best one and achieving results usually takes some work.  The far more relevant question is: do the ends (weight loss, etc) justify the means (adhering to a diet)?  That hasn’t been asked in this study but my guess it that the outcome would be a lot less negative than what the DAA depict and probably even positive.  Also in my opinion the Paleo diet used in those trials is unnecessarily restrictive (salt, fatty meat, starchy vegetables) and I would like to see the results (weight loss, metabolic markers, etc) and perceptions of adherence in a Paleo trial that doesn’t include unnecessary restrictions, not that I’m holding my breath.
 
“…it must be recognised that these positive changes were not independent of weight loss”
 
I don’t understand why this is considered so important.  If a given diet promotes weight loss, thereby improving improves metabolic risk factors, because it is more satiating per calorie, then the effect is still causally related to the diet rather than deliberate calorie restriction.  In this instance you can say ‘not independent of weight loss’, but should also emphasise how the weight loss occurred (deliberate vs. spontaneous) so as to have a balanced commentary.
 
There are problems with the dietary methodology in these studies (i.e. no nuts included in the control Mediterranean diet)…”
 
I agree that the Paleo diet trials have limitations, but I challenge you to find a diet trial that doesn’t.  Anyway, I found it odd that of all the differences between the Paleo and Mediterranean diet (the author is now discussing this trial) they chose nuts.  In this trial the Paleo group did eat significantly more nuts (P = 0.02) but it was such an insignificant part of both diets (Paleo 10±12g, Mediterranean 1±3g) [1].  Whereas the main dietary differences in this trial were higher fruit and meat in the Paleo group and higher grains and dairy in the Mediterranean group [1].
 
The ‘High’ Protein Australian Diet
 
There isn’t much to say about part 3, except for this:
 
“While the Paleo diet focuses on fresh foods, as do the ADGs, there is too much emphasis on protein foods for most people. It is rare that individuals need more than 1g of protein per kilogram of lean body mass and currently most Aussies eat double this recommendation! The focus in Australia should be on getting enough high iron food choices in our diets, because while we all seem to get enough protein, there are some key population groups (mostly girls and young women) who do not get enough iron.”
 
The RDI is the “usual intake at or above this level has a low probability of inadequacy” [8] and the RDI for protein is approximately 10% of total calories.  Australians eat about 16.5% protein [9], which is why the standard Australian diet is often described as ‘high protein’.  However, in the same document as the RDI there’s also a range of protein intake recommended for reducing chronic disease risk which is between 15-25% of total calories.  As the average Australian intake is at the lower end of this range, you could argue that it would be better if we got more protein.  I also thought this was an odd comment to make given that: (1) iron is plentiful in most Paleo diets; (2) legumes were promoted as being high in protein; and (3) obesity was discussed at the end and high protein diets aid in weight loss

Friday, October 31, 2014

Summary of the Low Carb Diet Trials: Part 2

This is just a reminder of the results in the previous post
 
Y = Low carb had significantly better result than low fat
- = Not significantly different regarding low carb vs. low fat
N = Low carb had significantly worse result than low fat
 
Low Carb Diet Myths
 
These results may not be particularly exciting but these trials debunk myths about low carb diets and weight loss
 
1)      Low carb, high fat diets adversely affect blood lipids
 
As you can see in the table above there was often no difference in the changes in blood lipids between the low fat and low carb groups and in some trials the changes in blood lipids were better in low carb group compared to the low fat group
 
This would be expected as other clinical trials have found that replacing carbohydrate with fat decreases both the total cholesterol:HDL-C ratio and triglycerides [1].  Articles that criticise low carb diets based on supposed adverse effects on blood lipids may be forgetting that even though SFA (except stearic acid) increases the total cholesterol:HDL-C ratio, fats in foods are a combination of SFA, MUFA and PUFA and it’s the overall effect is a reduction in the ratio.  Alternatively they may be basing their assessment of CHD risk exclusively on LDL-C or even worse, total cholesterol, despite the total cholesterol:HDL-C ratio being a better predictor of CHD risk than total cholesterol and LDL-C [2]; and non-HDL-C being a better measure of LDL-P than LDL-C (see my rant here). 
 
2)      Low carb, high fat diets adversely affect body composition
 
Often when critics of low carb diets concede that low carb diets can cause weight loss their next argument is essentially ‘yes, you can lose weight on low carb diets, but this just glycogen and/or muscle loss (muscle wasting because of the idea that low carb >> gluconeogenesis from amino acids in muscle >> muscle loss).  Some trials measured body composition (Gardner, Brinkworth and Bazzano) and found nothing that would suggest that the proportion of weight loss from muscle was higher in the low carb group, whereas the low fat diet had an adverse effect on body composition in Bazzano.
 
Also, in case anyone was concerned about bone mineral density, the Foster trial found no difference between the groups regarding the change in bone mineral density
 
3)      Weight loss requires deliberate calorie restriction and induces ‘the starvation response’
 
One of the most unfortunate beliefs regarding weight loss it that it requires deliberate calorie restriction.  However, in many instances with these trials (both low carb and low fat, but mainly low carb) significant weight loss occurred without advice to deliberately reduce calories.  Although whether this statistically significant weight loss is clinically significant is debatable and depends on the trial.
 
 
Low Carb
Low Fat
Calorie Restriction
Significant Weight Loss
Calorie Restriction
Significant Weight Loss
Stern
 
Y
Y
Y
Dansinger
 
Y
Y
Y
Gardner
 
Y
Y
Y
Shai
 
Y
Y
Y
Davis
 
Y
 
Y
Brinkworth
Y
Y
Y
Y
Lim
Y
Y
Y
Y
Foster
 
Y
Y
Y
Iqbal
 
Y
Y
 
Bazzano
 
Y
 
Y
 
Another common belief regarding weight loss is that it induces ‘the starvation response’ (hunger, low metabolic rate, etc).  Dansinger measured the metabolic rate and found it didn’t decrease in any diet group at any time point

Adherence 

Most of the trials followed a design whereby the participants received an intensive intervention for the first 2-3 months then were largely left alone with a few follow-ups afterwards.  Not surprisingly, adherence to the diets was much better during the first 2-3 months and seemed to fall immediately after the intensive support was no longer provided.  In most trials the participants in the low carb diet ended up eating ~30-40% carbs and the low fat diet ~30-35% fat. 

Generally adherence to the diet was equally poor at the final time point, though there were some exceptions.  The Brinkworth trial was a high intensity intervention for the whole period and the participants adhered very well to the diets, which is reflected by their weight loss and metabolic markers improving to a far greater degree than participants in the other trials.  Another exception is the Stern trial, where the low carb group adhered better to the diet (251g to 120g carbs at 12 months) compared to other trials, whereas the low fat group really didn’t change at all (74g to 69g fat at 12 months).
 
Considering that the participants were overweight or obese and some of them also had type 2 diabetes, you would think that one of the best times to start a serious attempt at weight loss would be while participating in a diet trial with all the support you’re given.  So the big question is: why was adherence so poor?  This should be studied with the aim to find a solution to this problem.
 
Diet Quality
 
The focus on these trials was macronutrients, but this doesn’t give much indication of diet quality (with the possible exception of protein).  Most of the trials measured fibre intake which is perhaps not a bad measure of whole plant foods (and therefore diet quality).  The participants had an average intake of ~15g of fibre at baseline, which is similar to the US average (~15g) [3].  Fibre declined in the low carb group in some of the studies, but often only at 2-3 months when carbohydrate intake was more like 20-30% as opposed to 30-40%.  The real surprise was that the low fat group often didn’t increase fibre intake.  The Bazzano trial also measured folate and vitamin C intake and found that baseline intakes were just above the RDI (considering how easy the RDI for vitamin C is to meet, this is pretty bad), which didn’t really change during the trial (even though you would expect both to increase in the low fat group).  Altogether this suggests that baseline diet quality of the participants was poor and didn’t improve in these trials. 

Change in Fibre Intake
Low Carb
Low Fat
Stern
-
Dansinger
↓ (transient)
-
Gardner
↓ (transient)
-
Shai
Davis
↓ (transient)
↑ (transient)
Brinkworth
?
?
Lim
↓ (transient)
↑ (transient)
Foster
?
?
Iqbal
-
-
Bazzano
-
-