"It never gets easier, you just go faster." - Greg Lemond

Tuesday, March 26, 2013

Salt Matters

 The health outcomes associated with a high salt diet are generally negative, and include increased risk of cardiovascular disease risk, stroke, and kidney disease (1).  Because salt intake influences the total osmolarity of your blood, increased consumption of salt, aka sodium-chloride (NaCl), rich foods results in the body shunting more fluid to the blood, which requires various compensatory mechanisms, including increased workload on the cardiovascular system (2).  There is substantial evidence that those at risk for cardiovascular disease due to high blood pressure should reduce NaCl intake.  However, recent high impact studies have been published that demonstrate salt intake may also influence the progression of other diseases.
Salt sources in American diet (source NIH)
There has been a significant increase in the incidence and frequency of autoimmune disease in the American population over the last half-century (3).  Examples of these diseases include inflammatory bowel disease, rheumatoid arthritis, type I diabetes, multiple sclerosis, and lupus erythematosis.  In order to understand whether certain environmental factors may be responsible for the increased incidence of autoimmune disorders in the United States, researches have examined the relationship between changes in the Western diet and immune function.  Increased consumption of processed foods or “fast” foods containing copious amounts of NaCl has represented a significant dietary change over the past half-century (4), although the relationship between high NaCl intake and autoimmune disease has not been well characterized.

Cutting Edge
Recent studies published in Nature Letters have provided a solid foundation for future research focused on the relationship between NaCl intake and autoimmune immune disease.  A recently discovered immune cell, known as a Th17 T cell, has been suggested to play a role in the etiology of numerous autoimmune and proinflammatory diseases.  Th17 cells are known to heavily participate in chronic inflammatory diseases as well as hyperactivation of the immune system during immune responses to various pathogens such as influenza (5).  Because these cells are mediators of inflammation, they play a critical role in protecting the host from infectious agents, however, excessive activation of the immune system resulting in chronic inflammatory or hyperinflammatory responses has potentially lethal consequences to the host.

Thus under normal circumstances, Th17 cells are tightly regulated immune cells that are present at relatively low frequencies in the body.  In has been demonstrated that Th17 cells can be found at increased numbers during autoimmune disease, and deletion of Th17 cells using genetic ablation reduces the severity of autoimmunity (5, 6).  These observations reinforce the notion that Th17 cells are critical mediators of autoimmune disease.  Because our understanding of these cells is in its infancy, it is not quite understood what factors determine the production of Th17 cells.  However, among various cytokines, the inflammatory cytokine, interleukin 23 (IL-23), has been shown to stabilize and reinforce Th17 development (7).  

In two very timely publications, scientists show that high sodium (Na) plays a role in the development and pathogenic nature of Th17 cells.  Studying the molecular aspects of Th17 cell differentiation, Wu et al. show high Na concentrations induce the activation of signaling within T cells that supports development into Th17 cells (8).  This was shown to be related to the activation of an intracellular protein known as serum glucocorticoid kinase 1 (SGK1), a salt-sensitive protein, meaning its activation is highly dependent on salt concentrations.  Activation of SGK1 in T cells results in increased sensitivity to IL-23, which as mentioned earlier supports Th17 development.  

In the vary same issue of Nature Letters Kleinewietfeld et al. discovered culture of human T cells in media containing increasing NaCl concentrations promoted the development of Th17 cells in a dose dependent fashion (9).  Using an “experimental” model of autoimmunity, the authors of this study fed mice that were destined to develop autoimmune encephalitis (an autoimmune disease similar to multiple sclerosis) a high salt diet and found that mice fed a high NaCl diet presented with more severe autoimmunity than mice fed a normal NaCl diet (9).  Further studies by Wu et al. found that mice fed a high salt diet alone had marked increase in the frequency of Th17 cells in gut associated lymphoid tissues, and that mice harboring a genetic deletion of SGK1 had reduced Th17 cell development in response to a high salt diet.  Perhaps even more important, Wu et al. present data in agreement with Kleinewietfeld et al. in that mice fed a high salt diet exhibited more severe autoimmunity than mice fed a normal salt diet and that this severe autoimmunity was SGK1 dependent.  

Ok, great, but what does this all mean? 

I’m sure the media will blow most of this out of proportion... (Foxnews).   Do these studies say that having a high salt intake will result in autoimmune disease?  NO. 

These are experimental models of autoimmunity, in which mice are immunized with proteins that forcefully induce autoimmunity.  However, these two studies form an attractive hypothesis supporting the role of the Western diet in immune dysfunction.  Furthermore, these data provide framework for future studies examining the direct role of NaCl intake on the incidence of autoimmunity, especially in individuals who might be genetically predisposed to developing autoimmune disease.

What can be taken away from these studies is that there is some evidence that excess salt in the diet can alter immune cell development, which has dangerous implications if one is predisposed to developing autoimmunity (such as in these mice).  The authors conclude that determining whether a “true low-salt diet, representing the conditions in which Homo sapiens were environmentally selected in Africa” has the potential to reduce risk of autoimmunity will be very difficult because of Western culture, which to me is a truly disappointing conclusion (obviously they’ve never heard of Paleo!).  Instead the authors suggest looking for pharmacological agents that block the molecular pathways described above (yay, just give people more drugs and lets continue to eat like crap!).  I think based on these studies there is real evidence that high salt diets have the potential to further exacerbate inflammatory responses which are clearly detrimental to human health.   

Works Cited

1.         Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health. Int J Epidemiol. 2009 Jun;38:791-813.
2.         Appel LJ, Frohlich ED, Hall JE, Pearson TA, Sacco RL, Seals DR, Sacks FM, Smith SC, Jr., Vafiadis DK, Van Horn LV. The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: a call to action from the American Heart Association. Circulation.  Mar 15;123:1138-43.
3.        Ascherio A, Munger KL. Environmental risk factors for multiple sclerosis. Part II: Noninfectious factors. Ann Neurol. 2007 Jun;61:504-13.
4.         McGuire S. Institute of Medicine. 2010. Strategies to Reduce Sodium Intake in the United States. Washington, DC: The National Academies Press. Adv Nutr.  Nov;1:49-50.
5.         Korn T, Bettelli E, Oukka M, Kuchroo VK. IL-17 and Th17 Cells. Annu Rev Immunol. 2009;27:485-517.
6.         Lee Y, Awasthi A, Yosef N, Quintana FJ, Xiao S, Peters A, Wu C, Kleinewietfeld M, Kunder S, et al. Induction and molecular signature of pathogenic TH17 cells. Nat Immunol.  Oct;13:991-9.
7.         Aggarwal S, Ghilardi N, Xie MH, de Sauvage FJ, Gurney AL. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem. 2003 Jan 17;278:1910-4.
8.         Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, Regev A, Kuchroo VK. Induction of pathogenic T17 cells by inducible salt-sensing kinase SGK1. Nature.  Mar 6.
9.         Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA. Sodium chloride drives autoimmune disease by the induction of pathogenic T17 cells. Nature.  Mar 6.

Monday, March 11, 2013

Review of Ultimate Direction AK Race Vest

Like a lot of my ultrarunning friends, I am a sucker for anything Anton related.  Something about that guy just oozes cool.  So when I saw that he was designing a race vest I knew that I would end up buying it.  I ordered it wayyy back in December, the second I saw it was available, which is lucky because it sold out FAST.  I think you can find them now, or at least pre-order them.  As spring approaches and the weather heats up, it will be time to start thinking about carrying bottles again, and the Ultimate Direction AK signature vest certainly offers up an alternative method for carrying two 20oz bottles.

Making it look cool

I think the main utility of this vest is the opportunity to use bottles, but not have to carry them in your hands.   I've definitely run into problems carrying handhelds during races before; lack of dexterity is MY major issue during a race.  Other problems include falling down and not having free hands to catch myself, sweaty sweaty sweaty hands glued to bottles, and tired shoulders and arms after 12 hours of carrying bottles.  So why not wear a pack?  Well I have also been at races, rather exhausted and pulled off my hydration pack, been unable to get it open myself, or handed it to a volunteer to be filled, not realizing they had no idea how to open it, fill it, or close it (not their fault, its just confusing sometimes). 
UD stock photo

So when I saw the AK vest, I was very intrigued, the Eurostyle bottles in the front definitely has application for us Americans, but you generally see US runners carrying bottles or wearing hydration packs with bladders.  

I was very excited when I first opened up the package and put on my size S/M vest.  It fits very well.  Super snug, incredibly lightweight, and it didn't seem to rub me in any strange places.  And then I put the bottles in - Sweet!  This is going to be a great piece of gear for race day.  One problem, the bottles weren't filled with water yet.

Filling the bottles with water soon revealed that it was not as comfortable as I initially thought.  There was quite a bit of bouncing.  I tried to adjust the pack in multiple different fashion, and eventually settled on a fit that seemed to work out OK.  The one thing I quickly realized is that the front of my pack (and thus the bottles) looked to ride quite a bit lower on my chest than it did when Krupicka is wearing it in pictures. 

I went for an 18 mile run in the winter with 2 filled bottles, more to test out the pack rather than actually needing the water.  Besides the slightly annoying bouncing and sloshing noises, it seemed to work ok.  Then towards the end of the run, I noticed myself getting more and more sore across my chest.  My man boobs were really not liking having full water bottles strapped across them for miles and miles.  I quickly drank down the bottles, and once they were empty, I wasn't bothered anymore. 

I feel like this chick is about to be in a world of chest pain
I ended up with some bruises on my ribcage/pectoral area, and haven't tried to run with full 20oz UD bottles in the pack since then.  Maybe its my running form, maybe its my build, maybe its the fact that its sold as a S/M size, rather than allowing for someone who needs a small to get a small, but I just can't get it to fit quite right.  I dunno why, but its a serious flaw and drawback.
Back view

What I have used the pack for is to carry stuff (camera, gels, jacket, etc.) because it is so light and fits great.  Further experiment has lead me to conclude that I can get away with either small 10oz nutrition flasks in the chest pockets, Salomon softflasks, and I have heard other people (who have had similar bruises as mine) mention that the Amphipod style bottles seem to work.

Notice the lack of bottles
Stuff anything you dont want into the back sleeve

In the end I am kinda disappointed, If I'm stuck using two 10oz bottles, that's not really enough water to get between aid stations that are spread out.  Perhaps it will suffice as a training tool.  The vest has nice pockets, including 2 zipper pockets in the back and Velcro pocket in the front.  There are also two sleeve-like pockets that can be found in the shoulder area.   These are great for stuffing gel into.  Be warned using the Velcro pocket, car keys can fall out!  The back of the pack also features one giant pocket, which is what I generally stick things in if I know I don't need them for a while.  Part of me is considering putting a 1.5L hydration bladder in it, and using that, combined with two 10oz bottles up front, could provide ample hydration for long outings and also allowing me to customize fuels in the front bottles.

Tuesday, March 5, 2013

Time off, Time on, Back at it

Return of the Jedi Toe

It has been a long 5-6 weeks.  Knee pain began Thursday Jan 24th and lasted until March 1st-ish.  I've been hesitating to write this post so as not to jinx my recovery.  But here I am, typing away, that must mean something good has happened in the past 3-4 days.  

Friday I found myself angry for missing out on winter base building, and having just bought a pair of Newtons, I decided to run around Ann Arbor.  When the first mile clicked off at 7:15 I though, woah, a little fast there buddy, probably should slow it down a bit.  Then 6:58, then 6:50, then a 6:33, etc.  I could feel a little tightness on the top of my knee, but it was less than whisper, and I needed to run.  I found myself weaving in and out of students downtown, then jumping over curbs and snow banks on the outskirts of Ann Arbor/Scio Township.  Things I haven't been able to do in over a month.  The Newtons required more force from my hamstrings than my typical road shoes, so while I felt a noticeable tightness there, my aerobic system seemed to be intact.  I finished the 14 miler at a 6:40 pace, having run a couple sub 6:20s.  

The next day I was incredibly sore.  Hah.  I talked Jenny into running 4 miles with me and called it a day.  Sunday rolled around and I felt ready to test out my knee again.  12 miles later, things were feeling damn good.  It was a beautiful day (sunshine) so I grabbed my camera and decided to go for a hike to help loosen up my legs.  Then yesterday I had what I feel like was my first totally pain-free, completely forgot about my knee, run in a long time.  So I'm ready to write about the experience.  

98% sure it was petallar tendonitis.  On the top of your knee is a tendon that helps keep the knee-cap in line.    This tendon functions to help the knee act like a fulcrum as it bends and transfers force, so if it does become inflamed  you're gonna notice it when bending your knee and transferring power, such as going up and down stairs or running.  

So what to do?  I tried icing like crazy, but usually that caused my the tendon running over my kneecap to become so tight that it was very uncomfortable to bend it.  I did find that I could run on the treadmill at incline, like 15% incline so I tried to do this to maintain fitness to some degree.  It was...  very boring at best.  Probably the best therapy I found for the knee was to use a butter knife to scrape across the tendon when the knee was at a slight angle.  It simulates a Grastons-like therapy, and seemed to help relieve the inflammation.  I suspect because tendons receive very little blood flow that if they become agitated or inflamed it requires some artificial manipulation to help loosen up and force new fluid in and old fluid out.  I also have to admit to taking quite a bit of ibuprofen, normally I avoid the stuff like poison (I feel it diminishes training gains), but it seemed to provide relief and I wasn't training very hard.

So now I'm back, at least I hope so, and I have to figure out my racing schedule for the spring, summer and fall.  Last year at this time I was logging 100 mile weeks all month long, but I'm skeptical of my ability to do that right now, and not sure if it would be the best idea.  So instead I think I'll build my mileage back up, and hopefully retain some speed in my rested legs.  I'm thinking about a spring marathon or two, and I'll run a couple Ultras.  I'll hopefully run 1 or 2 100s, and currently thinking about Keys 100 mile, Kettle Moraine 100 mile, Mohican 100 mile ,or Burning River 100 mile, I guess only time will tell.  For now, I'll be preparing with the mentally of trying to run a fast marathon or two in April, maybe and maybe a 50-100 miler in May and June.  Honestly, I'm just happy to be running again, racing isn't calling my name quite yet.

Pictures from my hike: