Thursday, September 5, 2013

Hot Pink Kraut in The New Kitchen

Hot Pink 'Kraut!
Made by My Kids

We moved and it's been hectic. This past summer, my kids were so fortunate to attend the most jiving cooking class at the Albany Community Center in Northern California, where their sweet teacher Ilah Jarvis is not only a Baumann College Nutrition graduate but also an integrated practitioner. They learned all the basics for soaking and cooking nuts, (GF) grains and legumes, dairy-free pesto, meats, salads, dressings, sides, and spent ONE WHOLE DAY on the benefits and techniques of fermenting vegetables (kim chee, sauerkraut, pickles).

Their second batch of hot pink kraut is in the crock (gift from our Fujian ayi) and bowl. You fill the moat at the top with water to provide a tight seal that allows anaerobic fermentation.  Formed gas can escape one-way across the seal.  I used the old 'kraut as a starter for our inaugural batch at the new abode in the burbs.  (Yes we are outta the grind and grime of the Shanghai Pudong city...) This recipe below is my daughters' favorite because it tastes like kim chee but sans spiciness.  I had no idea how easy, inexpensive and gratifying it is to eat your own 'kraut... In the States, I fell in love with Sonoma Brinery's RAW SAUERKRAUT this summer.  Was so pleased I could find it in fresh supply everywhere (WH, Andronico's, etc).  Though we love it but kraut is a bit of work -- need a minimum 3 hours to prepare 1-2 weeks worth (one person; for 2 kids = 2 hours + undisclosed hours clean up (MOM)).  However, it's so guuuuud...we eat it almost as fast as it's made...

Tickled Pink Ginger Kraut (adapted from HERE)

1 Head Green Cabbage
2 Heads Purple Cabbage
6 Carrots
4-5 tbsp Sea Salt
2-4 tbsp Fresh Garlic
1 Lemon Squeezed

Combine and squeeze squeeze squeeze.  Minimizes the juicing out and 'organic explosions' later, as my kids told me.  If you add a starter, days on the counter is shortened to only 3 days, otherwise 5-7 days at room temp is needed to get a good ferment going.  Sander Katz's book Wild Fermentation is awesome for more ideas.

New science media on the microbiome and evolution...

(1) Convergent Evolution of Hyperswarming Leads to Impaired Biofilm Formation in Pathogenic Bacteria (hat tip: NB)

Cell Reports, Volume 4, Issue 4, 697-708, 15 August 2013
AuthorsDave van Ditmarsch, Kerry E. Boyle, Hassan Sakhtah, Jennifer E. Oyler, Carey D. Nadell, Éric Déziel, Lars E.P. Dietrich, Joao B. Xavier
HighlightsExperimental evolution of swarming in P. aeruginosa generates hyperswarmers
Parallel evolution in the flagellar regulator FleN is causal for hyperswarming
Point mutations in FleN produce multiflagellated hyperswimming bacteria
There is an evolutionary trade-off between motility and biofilm formation
SummaryMost bacteria in nature live in surface-associated communities rather than planktonic populations. Nonetheless, how surface-associated environments shape bacterial evolutionary adaptation remains poorly understood. Here, we show that subjecting Pseudomonas aeruginosa to repeated rounds of swarming, a collective form of surface migration, drives remarkable parallel evolution toward a hyperswarmer phenotype. In all independently evolved hyperswarmers, the reproducible hyperswarming phenotype is caused by parallel point mutations in a flagellar synthesis regulator, FleN, which locks the naturally monoflagellated bacteria in a multiflagellated state and confers a growth rate-independent advantage in swarming. Although hyperswarmers outcompete the ancestral strain in swarming competitions, they are strongly outcompeted in biofilm formation, which is an essential trait for P. aeruginosa in environmental and clinical settings. The finding that evolution in swarming colonies reliably produces evolution of poor biofilm formers supports the existence of an evolutionary trade-off between motility and biofilm formation.

(2) How hormones and microbes drive the gender bias in autoimmune diseases (hat tip: Angela)

Immunity, Yurkovetsky et al.: "Gender bias in autoimmunity is influenced by microbiota." Free PDF.
Sex hormones are known to play an important role in the gender bias of autoimmune diseases. But studies have shown that environmental influences and other non-hormonal factors also make a difference. For instance, animals that lack gut microbes because they were raised in a germ-free environment do not show a pronounced gender bias in type 1 diabetes, which is generally considered to be an autoimmune disorder. Until now, it has not been clear how hormones and microbes work together to influence the gender bias in type 1 diabetes and other autoimmune diseases.
In the new study, Chervonsky and his team found that microbial communities in male and female mice became different once the mice reached puberty, whereas microbes in females and castrated males were more similar to each other. These results suggest that sex hormones contribute to gender-specific changes in microbial communities. When the researchers raised mice in a germ-free environment and then exposed them to different types of bacteria, they discovered that only certain microbes specifically protected males against type 1 diabetes.
Taken together, the findings suggest that hormones and microbes cooperate with each other to protect males against autoimmune diseases. "Our study has helped to establish the general principles of how hormones and microbes interact with the immune system, which is the first significant step to get to the stage of developing new therapies."

I find this umbrella publication of multiple mouse experiments really fascinating and neat as it found robust and vigorous testosterone levels to be protective for male mice against the Type 1 Diabete (T1D)  mouse model (usually it is high estrogens -- E1 E2 4OHE1 16OHE1 etc).  I wish these researchers measured the estrogens in these mice because the picture seems incomplete...

Segmented filamentous bacteria (SFB) were the population found to be not only most protective but also associated with the highest testosterone levels in male mice.  It appeared to elevate mouse androgen concentrations to a threshold necessary for autoimmunity protection.  Can poor gut flora knock out your T?  Also interestingly, the commercial VSL #3 frequently used therapeutically for IBS, Crohn's and other GI disorders was found (again, remember, in mice) to be associated with lower T.  That was an odd finding as VSL #3 is high in Lactobacillus and other strains typically associated with balanced flora.

SFB and Autoimmunity
Photo Credit: Ivanov, Littman 2010

We know already that gut dysbiosis and anything excessively taxing raises cortisol which can sap and suck the steroids out testosterone (for males) and progesterones (for females), if chronic and enduring.  When this dysregulation occurs, inflammatory estrogens are favored over metabolism of anti-inflammatory estrogen moieties. Estrogen has a role as a stress signal across both plant and animal kingdoms. Some of our best antioxidants (EGCG, curcumin, genistein, resveratrol) are weak phytoestrogens synthesized by plants in response to stressors.  In every chronic disease -- prostate cancer, breast cancer, hypertension, heart disease (TACT), osteoporosis, PCOS, infertility, autoimmunity -- endogenous inflammatory hydroxyestrogens and/or xenoestrogens/metallo-estrogens are either elevated or outweigh the beneficial the estrogens (2-OHE1, etc).

Intimate Crosstalk Between SFB
With Intestinal Cells
(photo credit: Nature)

Heretofore virtually undiscovered in humans (only insects and many mammals), earlier this year 2013, Yin et al in Hangzhou, China characterized one of the earliest human commensal SFB. Via 16S rRNA-specific PCR detection, the intestinal contents of 251 humans, 92 mice and 72 chickens were analyzed. The researchers state "The results showed SFB colonization to be age-dependent in humans, with the majority of individuals colonized within the first 2 years of life, but this colonization disappeared by the age of 3 years... In summary, our results showed that SFB display host specificity, and SFB colonization, which occurs early in human life, declines in an age-dependent manner." Formerly known as 'Candidatus Arthromitis' , like 80-90% or more of our intestinal microbiota, they are unculturable anaerobic bacteria.  SFB hail from the Firmicutes phylum (Order: Clostridia). Like many of the good gut flora they appear to play instructive roles in stimulating proper TH17 and Treg responses in for immune fitness. We need some Firmicutes -- not a ton as it is overdistributed in nearly every obesity microbiota analysis compared with Bacteroides (or it can be too low and eclipsed by Bacteroides) -- but an adequate and sufficient amount it seems and the right kind appear good. Might there be a spectrum of good v. bad Firmicutes like all things? Can 'kraut and other fermented veggies help add the good anaerobic micro critters?  I hope so.

One analysis using pyrosequencing techniques to quantify and identify the microbial composition of traditional Korean fermented kochujang which is a ubiquitious condiment made of of red pepper, glutinous rice, salt, soybean and the naturally occurring microanimalia (e.g. dirt organisms). Of the 223 species discovered, 93.1% were Firmicutes, including Bacillus subtilis, a strain known to digest gluten and casein (as also found in traditional sourdough and other fermented foods). YUM! Gochujang is the hot pepper paste for bibimbap.  Modern, post-industrial gochujang actually is tainted by high amounts of gluten/wheat as a filler, flavor, preservative and 'spice' unfortunately.  FYI, for the real stuff, find a Korean market and look in the refridgerated area.

1 comment:

Unknown said...

A few times I've fermented a big green cabbage and a small red one, and it comes out a beautiful bright fuchsia. I likened the juice to a salty fruit punch (but less sweet and more sour).
Time- and hand-saving tip: If you mix in the salt and then let it sit for 12-24 hours, it becomes much easier to squeeze.