Don't Blow Your WOD on Your First Snatch...

...Or First Jerk *ahhhh*
...Or First 2 Rounds of Tabata Torture


I don't know what attracted me to Crossfit first...

How Crossfit diet and health principles are aligned with TYP... The Paleo diet which 80-90% of all members and trainers follow for optimal performance, gains and superior health... Robb and Nicki's gym (ranked top 30 in the U.S. By Men's Health)... the HAWWT people at my gym... my first warrior trainer Luca who could rip your head off if he wanted to... the MLF who keep us safe (military, law enforcement, firefighters)... how T-Muscle (formerly known as T-Nation) tries to knock it but can't like HERE...

Or the raunchy, hilarious inside jokes about our workouts!

So here is my progress (in my tri Zoot suit)...



Finally my insulin is better controlled (no more tooth abscess b/c it was pulled and the synthetic progestin nearly out of my f*&#$(@ system) after a year of Hormone H*LL... and the 6-paks are re-emerging...again...

Insulin.

It can be your friend or your enemy. It can grow great hypertrophic muscles or screw your metabolism, jack your hsCRP and prevent loss of belly fat.

Low carb, mod-high fat Paleo and bursts of anaerobic exercise at Crossfit control insulin.

As does
--avoiding dental infections
--avoiding dental inflammation
--avoiding synthetic/FAKE hormones which increase inflammation and insulin

OK I learned the hard dumb way.

In my experience (and Robb Wolf's), Paleo and Crossfit control autoimmune diseases and chronic inflammation, the crux of today's modern illnesses including heart disease. Our gym has a story of normalization of NASH/fatty liver disease within ONLY 1 month of Crossfit/Paleo, in addition to stories of complete reversal of IBS cases and many fantastic stories of 30-50 lb-weight loss. Robb has a tale of two pharmacists *cough cough* with NASH/fatty liver (which is autoimmune) and resolution with Paleo eating and Crossfit (one case the liver tests were so high, he was on a liver transplant list), and numerous other stories including one painful/burning, autoimmune lower extremity vasculitis (who I met at his b-day party) and another lifelong cutaneous tarda.


Here are my studmuffin Xfit homeys. Our Diablo Crossfit affiliate gym came in 16th out of 100 Xfit gyms. Congrats babes and boys! Y'll R-O-C-K.



Today for Sunday's WOD (workout of the day) we did TABATA... torture... *haa*

Workout:
Tabata deadlift (135lb men, 95lb women, barbell deadlifts)
Tabata dumbbell push press (men 45lb dbs, women 25lb)
Tabata burpee

A "Tabata" is 20 seconds of work followed by 10 seconds of rest. 8 rounds total (4 minutes). Count reps for each round. Your 'score' for each exercise is the lowest number of reps completed in any one round.

My score: DL 43# 11 times; DB PP 15# b/c I suck 6 times; burpee 4

The key of course to Tabata is to pace yourself. Don't blow your WOD on the first one to two successive rounds.

Crestor Raises %-Small Dense LDL (Anti-Regressive)

"It takes a wise doctor to know when to prescribe, and at times the greater skill consists in not applying remedies."

B. Gracian
The Art Of Worldly Wisdom

Definition of %-sdLDL ('concentration' of sdLDL)

%-sdLDL = (small dense LDL)/(Total LDL)

Total LDL = large LDL + IDL + sdLDL + Lp(a)

What's Lp(a)? Large Lp(a) + small Lp(a)

Pattern A: Dominance of Large LDL (desirable)
Pattern BAD: Dominance of Small LDL (undesirable)



Over-Medication

Judicious use of medications can bring about therapeutic outcomes or can have dire consequences. In medicine, it is truly an art form to balance the two, more than a science. Science however can provide a better understanding of what ancient doctors like Hippocrates or others in the last half century have known as wisdom and deep experience showed them.





'Mindless Statinators'

(Thanks Barkeater for that phrase *WINK*) Growing evidence shows that statins have 'differential' effects on people who take them. The lower the insulin resistance, the less the small LDL particles are reduced. In fact, two studies have shown that the most potent statin Crestor/rosuvastatin in fact raises small LDL concentrations when Triglycerides (TG, Trig) are less than 120 mg/dl (see first table, above, Kostapanos MS et al. Clin Ther 2007).


Or if Trigs are less than 88 mg/dl (1.0 mmol/L)... (see below Caslake MJ et al. Atherosclerosis 2003)

Or if Trigs are less than 177 mg/dl (2.0 mmol/L)... (see below, significant data points sdLDL% increased)


WOWO.

Trigs are low in nearly all low-carb compliant TYP'ers! And definitely 100% of people on low carb PALEO.



Crestor is QUITE potent.

At 40mg daily it is THE most potent statin on the market for sledge-hammering down all the LDL particles (large v. small). Caslake et al (Table 2) found that for normotriglyceridemic individuals LDLIII (small dense) % increased from 15.3% to 21.9% (delta = +6.6% sdLDL%) after 8wks only on the maximum dose Crestor 40mg daily (see below graph with comments, the authors failed to put zero on the x-axis...wtf. So please look at how %-sdLDL increases as the Trigs are less than 88 mg/dl = 1.0 mmol/L and even for a great majority of data points less than 177 mg/dl = 2.0 mmol/L).


What a terrible, counterproduct, ANTI-REGRESSIVE adverse drug effect.





TYP Goal for Regression:
small LDL NEAR-ZERO or DOWNWARD TREND

The goal for combatting heart disease and to invoke regression/ reversal/ eradication of plaque is to achieve a lower concentration of small dense LDL. Surprising, regression on EBT is frequently reported even before all TYP goals are met! (Wonderful cases of late -- hillbrow, Lindybill, dcarrns!)

Like dense ignorant people, we want the least amount of density and a transformation to lighter, buoyant, more athero-protective LDL particles.

Statins can hurt people as we know (myositis, peripheral nerve effects, brain damage, depression, accidents, suicide, vision reduction, erectile dysfunction, want me to go and on...?! autoimmune disease, inflammation at the mitochondrial and cellular level, liver/kidney failure related to rhabdomyolysis, death, etc).

OK.

Statins in fact can hinder EBT regression I strongly believe and examples unfortunately exist (the REGRESSION 10yr-subanalysis is an example of higher cardiac mortality in the statin-arm in a sub-group that exhibited a phenotype/genotype for low triglyerides). When an individual temporarily stops or backs off on the dose, the large LDL re-appear and the concentration of small LDL decrease. The sdLDL may not be exceptionally great compared to sdLDL reductions promoted by low LOW carb, mod-high fat diets or ketotic diets, but they DO IMPROVE noticeably as a result from 'statin holidays'. An example of statin suppression of large LDL suppression is for instance if one had an %-sdLDL=300/300=100% improve to 200/400= 50% after stopping Crestor for 1-2mos (Trigs always stay low when a TYP'er stops their statin because nearly all TYP strategies are insulin sensitizing).

That makes sense, right? You don't have to be a 20-year trained cardiologist or lipidologist to understand this data. If Trigs are less than 120 mg/dl, then small LDL concentrations are going to start growing. The graph actually shows that the lower the Trigs go, the HIGHER THE SMALL DENSE LDL CONCENTRATION BECOMES.

What is the effect over time?

What is this effect month after month after month.

What is this effect year after year after year of statin-addiction.

I can't even imagine. F*ck me...it aint regression.



EBT Calcification Progression? Y E S .

Iatrogenic, drug-induced coronary calcifications? One study with Lipitor has shown increased coronary calcifications in aortic stenosis patients compared to the placebo. Unfortunately, I see statins as well associated with coronary calcification progression on EBT when individuals continue the statin therapy after Trigs hit Dr. Davis' TYP goal of less than 60 mg/dl. To achieve EBT regression (HATS trial NEJM 2001 91% reduction in coronary mortality/ events in 3yrs NIACIN NIACIN NIACIN + simva 40/d), some reduction in sdLDL concentration is mandatory. Not... necessarily a lot.

Most individuals with severe coronary disease have ALL small dense LDL particles. In fact 100% concentration of sdLDL is not uncommon at all, at the start of the TYP program.

To reach Dr. Davis' goal of 10% concentration of sdLDL, 90% reduction in %-sdLDL would help to achieve regression. It is not the end all, however. It is demonstrated over and over that perfect lipoproteins (esp LDL=60mg/dl) doesn't guarantee SH*T when it's 100% sdLDL. Regression fails to occur in those who persist in over-statinating when the Trigs are excellent less than 120 mg/dl.





Persistently Elevated sdLDL-Concentrations

The signs and symptoms of over-statinating are subtle. They involve persistly high sdLDL-concentrations that do not decrease with TYP strategies, low carb dieting and even the addition of fats which normally remodel sdLDL into large buoyant beautific particles (omega-3, eggs, coconut oil, krill oil, etc). In fact, sometimes (yikes!) the statin effect appears to lead to HIGHER small LDL particle counts and concentrations. Sadly these individuals (to me... IMHO) have disappointing EBT progressions of 10-25% year after year, despite all their wonderful, hard work, good intentions and optimism... Despite spectacular, dramatic reductions in Lp(a).... Unfortunately the Lp(a) is all dense, all small, all drug-related Lp(a) which may actually be accelerating progressive damage.


Would've been better to not be on a statin at all in the first place? Well, perhaps there is value in the first 1-2 wks of the TYP program, but as you can see from post-CAD patients, insulin sensitivity and Trigs are easily controlled with no starch or ketotic diets within only 6 wks (Hays JH Mayo Clinic Proc 2003).

Six weeks... 42 days. Do you have 42 days?

Those who are statin-less at TYP (Mr. 'H', Mr. 'C', Dr. 'K') on the other hand witnessed large %-sdLDL reductions with each NMR or VAP lipoprotein test, perfect increases in large LDL and magnificent reductions in small LDL (even 'NONE') and consequently report EBT regression (Mr. 'C' and Dr. 'K' are pending, I have no doubt). 'Pretty lipoproteins' do not equal regression... it is how the pretty lipoproteins are achieved and the downward trends, with the minimization of iatrogenic, inflammatory drug effects.

Reduction in small dense LDL% is a very important goal to not ignore for atherosclerotic disease regression and eradication because small dense LDL reflects the internal inflammatory status.







ALL Statins Increase %-Small Dense LDL If Trigs Are Low

Crestor is not alone.

The other statins are NOT exempt.

Lipitor does it too.

They are certainly in fine company. The off-patent generic statins do it as well.





No Starches/High-Fat Diet Decreases %-sdLDL By 10%

I will review this in more detail later but this VERY short trial excellently demonstrates the efficacy and safety of a ketotic diet in post-CAD-event men and women, in producing dramatic lipoprotein changes in only 6wks. By eliminating starches and restricting fruit and increasing protein and dietary cholesterol and fat, concentrations of small dense LDL reduced from 35% to 25%. These patients were on lipid-lowering medications and the average LDL was 100 mg/dl (not high whopper doses of statins apparently). During the feeding diet, Trigs diminished from 147 mg/dl to only 88 mg/dl.

Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease. Hays JH, DiSabatino A, Gorman RT, Vincent S, Stillabower ME.Mayo Clin Proc. 2003 Nov;78(11):1331-6.



References

A 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemia. (A significant increase in mean LDL particle size after rosuvastatin treatment (mean [SD], from 26.4 [0.4] to 26.9 [0.4] rim; P = 0.02) was observed only in patients with baseline TG levels greater than or =120 mg/dL.)
Kostapanos MS, Milionis HJ, Filippatos TD, Nakou ES, Bairaktari ET, Tselepis AD, Elisaf MS.
Clin Ther. 2007 Jul;29(7):1403-14.
PMID: 17825691


Phenotype-dependent and -independent actions of rosuvastatin on atherogenic lipoprotein subfractions in hyperlipidaemia.
Caslake MJ, Stewart G, Day SP, Daly E, McTaggart F, Chapman MJ, Durrington P, Laggner P, Mackness M, Pears J, Packard CJ.
Atherosclerosis. 2003 Dec;171(2):245-53.
PMID: 14644393


Comparative effects on lipid levels of combination therapy with a statin and extended-release niacin or ezetimibe versus a statin alone (the COMPELL study). (Lipitor raises sdLDL% W T F... Crestor largely does not lower sdLDL concentrations much UNLESS NIACIN IS ON BOARD; Both Crestor and Lipitor wtf raise Lp(a), the most toxic, atherosclerosis-accelerating blood component carried by 17-25% of the general population)
McKenney JM, Jones PH, Bays HE, Knopp RH, Kashyap ML, Ruoff GE, McGovern ME.
Atherosclerosis. 2007 Jun;192(2):432-7. Epub 2007 Jan 19.
PMID: 17239888


Baseline triglyceride levels and insulin sensitivity are major determinants of the increase of LDL particle size and buoyancy induced by rosuvastatin treatment in patients with primary hyperlipidemia.
Kostapanos MS, Milionis HJ, Lagos KG, Rizos CB, Tselepis AD, Elisaf MS.
Eur J Pharmacol. 2008 Aug 20;590(1-3):327-32. Epub 2008 Jun 7.
PMID: 18585701


Effects of maximal doses of atorvastatin versus rosuvastatin on small dense low-density lipoprotein cholesterol levels. (Table 3 shows Lipitor INCREASES wtf sdLDL% +10% and Crestor 40mg makes virtually no change in sdLDL% at this dose (-5%))
Ai M, Otokozawa S, Asztalos BF, Nakajima K, Stein E, Jones PH, Schaefer EJ.
Am J Cardiol. 2008 Feb 1;101(3):315-8. Epub 2007 Dec 20.
PMID: 18237592

Vitiligo: Autoimmune Silent and Overt Celiac Sign

(Picture courtesy: wikipedia)

At my children's elementary school, I'd conservatively estimate that at least 25% of the children have vitiligo the skin condition that the late Mr. Michael Jackson suffered from (or...self-induced?) that caused loss of skin pigmentation (melanocytes). Small patches of whitish areas on their tan or darker-toned faces are the tell-tale signs. I'm not a dermatologist but this is easy to diagnosis. Vitiligo is yet another autoimmune disease with high association with several HLA immune types which leads to destruction of target cells (T-cell cytotoxic lymphocyte destruction of skin melanocytes). This condition is obviously more apparent in darker-skinned individuals (like my daughter) of Asian, African, Indo-Asian and Middle Eastern descent but paler-toned individuals who have a risk of melanoma can also share the same pathology.

Common treatment is immunosuppressants which dampen the body's own immune responses. In fact we were given steroid creams to apply to the lightened spots on my daughter's face. Does these work? Perhaps for some, but in our case, none worked and we ended up just giving up. We had been on vitamin D (which cured hers and my intermittent asthma) and omega-3s for half-year but noticed no real changes on the white spots until we went gluten-free. Yes, apparently I've ruined my daughter's life since we stopped wheat and gluten (we are the 'weirdos' in her school and understandably she's horribly embarrassed).

The trade-off for ruining her life? Within 4wks of our family going gluten-free, her skin toned completely evened out and ALL the few mild white spots disappeared. Now they only re-appear to a limited extent if my babysitter tries to toxify her or if we give in to her whining for wheat.

Where did vitiligo come from?? Neither my parents or my in-laws have ever been affected by this skin condition? It's not contagious. It's inherent in the DNA.

My parents are Hakka and their ancestors grew up for hundreds of years on the Pacific-Rim island, Taiwan. They grew up eating grains like rice (which is of course non-gluten containing) and had very little wheat or flour products. With the Japanese occupation their diet in fact probably improved -- consuming more miso (fermented soy bean), varied seafood, dried small fishes, buckwheat (again not gluten), etc. Growing up we ate sashimi from a young age and rare little bread or cereal (except the little breads for succulent roasted Peking duck at restaurants). As kids we snacked on dried cuttlefish and glutinous rice balls made with Pork or Fish Sung (see picture, courtesy of wikipedia). Pemmican is a shredded, dried meat like flaked jerky eaten by native American Indians. Our Asian/Taiwanese version is Pork and Fish Sung (with a little added sugar... HHHhhhMMhh.... and lots of LARD... yum). A frequent staple was pork spareib/bone soup with seawood, mushrooms, certain Chinese berries (ginko)/nuts, and bamboo shoots. It is pretty neat imo how many ethnic foods coincide in derivations and are just mutations of the 'Paleo' diet. I don't eat much sweet potatoes but my parents love that stuff. The shape of Taiwan's geography resembles a sweet potato and it's considered one of the national foods. (I do like yam noodles which are slivery smooth and delicious and very high in protein but I think those are more Korean.) Interestingly, traditional Japanese and Taiwanese dishes are incrediblely Paleo... with the exception of the ubiquitious rice...which probably explains the extreme myopia and short stature of meat-seafood-deprived parts of Asia (btw I'm not myopic or short since I grew up here in NE, PA and Cali eating like the carnivore/omnivore that my parents raised... quite frankly, my sisters and I are Amazonian in height/size relative to all of our *wink* vertically-challenged relatives and Asian friends...some... who forbid me to wear platform high-heels near them *haa*).


FYI... Below is an excerpt from the WSJ of what modern Taiwanese eat -- many cook traditional Japanese foods like my parents.

"...much of what you find in Taiwan that's truly Japanese is a relic of sorts from its days as a colony of the empire of the sun. From 1895 to 1945, Japan occupied Taiwan and the nearby Pescadore Islands -- its spoils of victory over the Chinese in the Sino-Japanese War (1894-95). During that time, the Japanese turned an agrarian backwater into one of the most modern -- and well-educated -- societies in Asia.

The Japanese built grand public buildings, turned the harbors of Kaohsiung and Keelung into key shipping ports, and laid a railroad that stretched along the western coast of the island. In Taipei, they tore down the old city walls and built a grid pattern for the city's streets. Eventually, they extended primary education -- in Japanese, of course -- to ordinary Taiwanese, an effort to nurture literate workers."

Another article appeared highlighting restaurants that serve traditional Japanese fare in popular hot spots in Taiwan in the WSJ today.... My mouth is watering!

"After the Japanese defeat in World War II in 1945, the Chinese reclaimed the island... But the rebranding of Taiwan, which continued after the Nationalists fled the Chinese mainland in 1949, wasn’t entirely successful. There are many Japanophiles living in Taiwan, and many places offering tourists in Taipei a less-expensive alternative to a trip to Japan. The roots of Japanese culture are still on display in Taipei, in a warren of alleys that locals call “Little Tokyo,” just south of Nanjing Road.

Today, these alleys are virtually indistinguishable from Tokyo’s Kabuki-cho nightlife district, lined with brightly lit Japanese signs advertising countless tiny hostess bars hidden behind doors not quite thick enough to contain the warbling of off-key karaoke. At the bar, you’re likely to find groups of middle-aged salarymen similar to those you’d see in Tokyo, except the hostesses—sitting beside them and keeping the drinks and conversation flowing—speak Japanese with a Taiwanese accent.

The Japanese-style grilled eel at the restaurant Fei-qian-wu is far better than its bar-alley location would suggest. The smoky flavor of the eel counters the slightly sweet basting sauce, just as you’d expect in Tokyo’s finest unagi (grilled eel) restaurants.

As at most casual eateries in Japan, the menu at Fei-qian-wu hangs on plaques around the walls (laminated menus in Chinese and English are also available). Order in Japanese or Mandarin—the restaurant was founded 35 years ago by a Japanese-Taiwanese family. You won’t even find the ubiquitous Taiwan-brand beer here. Instead ale drinkers are expected to order Kirin. A regular size unajyu (grilled eel over rice served in a lacquered bento box) and a Kirin costs about $6, a small fraction of the several thousand yen you’d expect to pay at an eel restaurant in Tokyo.

It’s not just the physical manifestations of Japanese culture that survive. Taiwan is one of the few places that can successfully duplicate the tipsy camaraderie of an izakaya eatery, where Japanese kick back and relax over drinks and small dishes of food after a hard day at the office.

At Wa-ko, the specialty is fresh seafood, and it offers an excellent variety of sashimi and grilled fish, served in small portions to go with drinks. Like most izakaya joints, the restaurant has two rooms: one with tables and chairs, the other with pillows or low-benches around tables in sunken recesses—old-style Japanese. On a recent visit, the traditionally styled room was full of Taiwanese customers. Owner Asato Satoshi, 55 years old, hails from the southern Japanese islands of Okinawa, and opened Wa-ko nearly two decades ago. The most popular dish is an Okinawan xia jiu cai—tofu with small fish and lemon on top. Be sure to try the roast chicken wings and squid with tarako, a kind of fish roe.

Oden is so much a part of Japanese food culture that a steaming pot of the stuff can be found right next to the cash register in many Japanese convenience stores. A simple, lightly flavored broth with root vegetables, egg, tofu and fish paste, oden dates back hundreds of years. Besides the modern convenience-store variety, oden traditionally was consumed at sidewalk stalls, along with the requisite glass of sake or beer, as a late-night snack. Taiwan sports its own homegrown version of oden bars—called heilun in Mandarin—that date back to its occupation-era days, and it has some traditional Japanese versions as well."

Gene expression skipping between generations? What promoted the sudden gene expression of vitiligo when in previous generations it had not appeared (as far as I am aware)?

Well... I don't need to go far... I just look in the mirror. *haa* In utero wheat intoxification probably caused triggers for my poor little helpless offspring. I remember doing the prescribed Pedi progression of starches... rice meal... oats... barley meal (ding ding... GLUTEN)... then of course wheat. Like Martha Stewart, I did produce some good food processed homemade lamb stew baby food and other tasties... but at daycare she received the usual gluten/wheat drivel like goldfish crackers, hearthealthywholegrain-Cheerios, mac-n-cheese, cookies, etc. We provided our share of wheat as well. I only hope now we can make repairs and prevent damage to her children and their grandchildren... Certainly I'm in awe of the power and scope of epigenetics and yet... completely horrified.

Horrified.





I have been seeing an older 70-something year old gentleman with all 3 diabetic complications -- retinopathy, nephropathy and neuropathy. High Lp(a) and vitiligo exist as well. Lp(a) progressess ALL diabetic complications -- specific organ damage, microvascular disease as well as macrovascular disease of the coronary, peripheral and renal arteries. Tissue and cellular damage all occur faster, deeper and harder. He declined insulin (which is good b/c Lantus insulin is now associated with a 31% increased cancer risk). Therefore, at visits we hammered and hammered the diet and negotiated a few vitamins. He was already very active spending most days working around the house and helping his wife with grandchildren.

New diet:
Breakfast -- 3-6 eggs, bacon occ (nitrate free, organic), menudo (no starches, no hominy, no corn)
Lunch -- salad with protein and olive oil
Dinner -- protein, little starch (yams, few small potatoes (no corn tortillas which are all contaminated with flour/wheat; no bread)

Nutrional Deficiencies and Correction:
Magnesium 2-4 daily (all Metabolic Syndrome are depleted)
Taurine (in 3mos -- this + glycemic control resolved all diabetic neuropathic pain symptoms and lowered BGs and BPs; he stopped Neurontin, Actos and cut BP meds by half)
Omega-3: BOATLOADS of EPA DHA 6-8 g daily (for Lp(a), insulin resistance, autoimmunity, PVD, etc)
Vitamin D to achieve 25OHD 70 ng/ml
Vitamin A for skin and deficiency
Slo-niacin (vitamin B3 -- vitiligo a sign of Pellagra? Perhaps Y-E-S) 500 mg/d and gradually titrated to 1.5 g/d over sev mos


After 3-6 mos, the Creatinine (kidney measurement) improved from 1.5 to 1.2 (maybe better now -- that was 12/08), BP reduced from 160s/80s to 116/60s, HDL increased from 33-35 to 48 mg/dl (again probably better now -- 12/08 labs), he lost 4-6 inches on his large expansive belly, and his sugars were well controlled (no insulin EVAH; last a1c 6.9% from 8%). In fact, the oral medications have all had to be cut back (Prinzide, Norvasc, Glipizide); Actos and Neurontin entirely stopped. Simvastatin 20mg cut back to once weekly... yeah... the dose: a couple licks of the tablet once a week. He also conceded that he felt younger, more energetic and glad for the diet changes. We actually had some ... ummm... disagreements for the first 3 mos! He brought his daughter on two occasions to articulate his displeasure and frustration with the new meal plan. Didn't work. *evil laugh* We ended up hammering the diet with his daughter as well, much to his general disgust. Giving up food he had been eating for 70+ yrs was ahhh... let's say DIFFICULT.

Results? Standard.



Mild vitiligo on his face completely disappeared.

The extensive vitiligo on his hands and fingertips (similar to the wiki picture posted above) stabilized and did not worsen. Skin become sealed, soft, and smooth.

He attended several large family reunions and get togethers and he reported to me that many were shocked and surprised... they told him he looked so much younger. He told me that he doesn't miss eating corn, rice, bread, oatmeal or tortillas. Or upset that he has to wear suspenders to keep his pants from falling off of his tight skinny little *ss... (ok latter's my clinical assessment and physical evaluation... *ehe*).



References:

Genetic variation of promoter sequence modulates XBP1 expression and genetic risk for vitiligo.
Ren Y, Yang S, Xu S, Gao M, Huang W, Gao T, Fang Q, Quan C, Zhang C, Sun L, Liang Y, Han J, Wang Z, Zhang F, Zhou Y, Liu J, Zhang X.
PLoS Genet. 2009 Jun;5(6):e1000523. Epub 2009 Jun 19.

Vitiligo and melanoma-associated hypopigmentation (MAH): shared and discriminative features.
Hartmann A, Bedenk C, Keikavoussi P, Becker JC, Hamm H, Bröcker EB.
J Dtsch Dermatol Ges. 2008 Dec;6(12):1053-9.

Autoimmune etiology of generalized vitiligo.
Le Poole IC, Luiten RM.
Curr Dir Autoimmun. 2008;10:227-43. Review.

Recognition and management of the cutaneous manifestations of celiac disease: a guide for dermatologists.
Collin P, Reunala T.
Am J Clin Dermatol. 2003;4(1):13-20. Review.

Lack of functionally active Melan-A(26-35)-specific T cells in the blood of HLA-A2+ vitiligo patients.
Adams S, Lowes MA, O'Neill DW, Schachterle S, Romero P, Bhardwaj N.
J Invest Dermatol. 2008 Aug;128(8):1977-80. Epub 2008 Mar 13.

[ssociation of HLA class I and II alleles with generalized vitiligo in Chinese Hans in north China]
Wang J, Zhao YM, Wang Y, Xiao Y, Wang YK, Chen HD.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2007 Apr;24(2):221-3. Chinese.

Association of HLA loci alleles and antigens in Saudi patients with vitiligo.
Abanmi A, Al Harthi F, Al Baqami R, Al Assaf S, Zouman A, Arfin M, Tariq M.
Arch Dermatol Res. 2006 Dec;298(7):347-52. Epub 2006 Sep 22.

Linkage and association of HLA class II genes with vitiligo in a Dutch population.
Zamani M, Spaepen M, Sghar SS, Huang C, Westerhof W, Nieuweboer-Krobotova L, Cassiman JJ.
Br J Dermatol. 2001 Jul;145(1):90-4.

HLA class II haplotype DRB1*04-DQB1*0301 contributes to risk of familial generalized vitiligo and early disease onset.
Fain PR, Babu SR, Bennett DC, Spritz RA.
Pigment Cell Res. 2006 Feb;19(1):51-7.

Autoimmune diseases in vitiligo: do anti-nuclear antibodies decrease thyroid volume?
Zettinig G, Tanew A, Fischer G, Mayr W, Dudczak R, Weissel M.
Clin Exp Immunol. 2003 Feb;131(2):347-54.

Possible transfer of vitiligo by allogeneic bone marrow transplantation: A case report.
Mellouli F, Ksouri H, Dhouib N, Torjmen L, Abdelkefi A, Ladeb S, Othman TB, Hmida S, Hassen AB, Béjaoui M.
Pediatr Transplant. 2008 Nov 18.