Friday, September 13, 2013

Phylogenetic Tree of Caecums, Appendectomies, Microbiota Maintenance, and Anecdotal Failure of Fecal Transplants


Human Guts = Super-Organs

Human intestines are really part-carnivore, part-frugivore and part-microbe. As living entities, we are 'super organisms' or hybrids of microbes (over 100 trillion cells) + human (~10 trillion cells).  Did you do the arithmetic? (sorry -- I can't do math)

We are ~90% microbial cells. In fact all living organisms have gut flora microbes from termites, cockroaches to fish to frogs to birds to carnivores to omnivores.  Recall SFB (segmented filamentous bacteria; Firmicutes; Clostridia; Candidatus Savagella) the commensal (symbiotic) bacteria intimately residing in the ileum (small intestine) of insects, humans, chickens and rodents improving TH17 and immune system regulation and protecting against autoimmunity and T1DM.

The caecum and appendix (animals that have one -- see photo) may serve the job of storing and maintaining the microbiota that seed the gut (fore and hind). In a phylogenetic analysis of a variety of animals, evolutionary biologists have various theories that the appendix was retained for a functional purpose (Smith et al, 2010. Photo credit: PDF.)



The Human Appendix is Not Vestigial 

The appendix is not a vestigial organ. In modern healthcare, broad spectrum antibiotics are handed out carelessly and tonsils and appendices are removed without much thought -- acute symptoms or persistent infections precipate the surgery in otherwise healthy and young folks. However, a recent study shows that there is an un-ignorable and increased relative risk of unexpected sequelae (e.g. subsequent heart attack) in these people following surgery -- 44% and 33%, respectively.

Why? Tonsils and appendices are part of the hybrid microbiota-immune system and control of inflammation.  According to Smith et al, our ancient predecessors most likely had appendices for at least since 60 million years ago if not extensively longer, 80 mya.  Come on... 80 mya... that's a long time.
"The appendix has evolved independently at least twice
and has been extensively maintained, albeit not uniformly,
in at least three and perhaps four groups of
mammals; glires, primates, Diprotodont marsupials and
perhaps monotremes. The possibility that the appendix
occurred at the base of the primates suggests that the
appendix may have been preserved in that clade since
before the two primate suborders
, Strepsirrhini and
Haplorrhini, diverged an estimated 60–63 million years
ago (Gingerich, 1986; Shoshani et al., 1996; Pouydebat
et al., 2008). Similarly, the conclusion that the appendix
evolved at the base of the glires indicates that the
appendix has been maintained since before the K–T
extinction,
when rodents and lagomorphs diverged
approximately 80 million years ago (Bininda-Emonds
et al., 2007)."




Caecums, Carb/Fiber Digestion, VFAs

Caecams are organs at the juncture between small and large intestines. Mammals have one, gallinaceous birds (ground-feeding) two, and fish several.  Humans and primates have a small caecum and vermiform appendix (worm-like, blind pouch). Caecums appeared to have evolved as chambers for microbial fermentation. It has made multiple appearances in evolution. Sizes vary in the animal kingdom from none to some to fully functional appendices. In species without appendices, the great majority of microbial fermentation occurs in the stomach (ruminant herbivores).  Ruminants have evolved small caecum (no appendix) since most of the fermentation occurs in the foregut. Smith et al theorize "Thus, the evolution of small ceca in some species that are foregut fermenters seems likely to have involved loss of the digestive function of a cecum with an appendix, with maintenance of the immunologic function of the cecal appendix."

Certain herbivores do a HUGE amount fermentation in the caecum -- rabbits, pika, guinea pigs.  These vegan-animals also exclusively practice coprophagia to obtain nerve/brain nutrients (vitamin B12) from caecal protein and vitamin synthesis (e.g. poo consumption).  [Curiously, porcupines have big caecums but no  observed coprophagia behavior (though dogs and tortoises have been observed to eat porcupine poo).  Yet in one study 16% of energy requirements were produced in caecal fermentation (versus 4.7%, rat).  BTW resistant starch (RS -- corn) provides different volatile acids, caecum expansion and improved insulin and blood glucose profiles in rodent studies, compared to high GI wheat/gluten starch.]



Photo credit: talkorigins

Our caecum is microscopic (see below); herbivores, gargantuan.  The human caecum and appendix serve more of an immune function, reservoir for microbiota; the function for digestion is minor.  Both our caecums and large intestines can ferment carbs (fiber, resistant) then release the digested products into the blood circulation as volatile organic acids.  The small intestines should not... except under illness (SIBO, small intestinal bowel overgrowth).  We are not foregut fermenters.  These metabolites can be measured (propionate, acetate, butyrate, etc). GDX/Metametrix organic acids testing is available-- Nutri Eval, Organix, ION, ONE.  I favor the ONE -- requires only the first morning void urine (FMV) so non-invasive and you get the cancer/inflammatory marker 8OHdG, mineral/vitamin deficiencies are other functional metrics.


Photo credit: Smith et al, 2010
Fig. 1 The cecal appendix (a through l) or appendix-like structures (m through o) in a
variety of mammals. The cecum ⁄ appendix is oriented toward the top of each drawing,
the distal end of the small intestine toward the left and the proximal end of the largeintestine toward the bottom.
  (a) human, Homo sapiens;
  (b) Pongo pygmaeus, orangutan;
  (c) Lepilemur leucopus, sportive lemur;
  (d) Lasiorhinus latifrons, Southern hairy-nosed wombat;
  (e) Oryctolagus cuniculus, rabbit;
  (f) Phalanger gymnotis, ground cuscus;
  (g) Anomalurus derbianus, scaly-tailed flying squirrel;
  (h) Trichosurus vulpecula, common brushtail possum;
  (i) Bathyergus suillus, Cape dune mole-rat;
  (j) Atherurus africanus, brushtailed porcupine;
  (k) Castor canadensis, beaver;
  (l) Microtus pennsylvanicus, meadow vole, shown with a partially uncoiled large bowel//
  (m) Phascolarctos cinereus, koala;
  (n) Ornithorhynchus anatinus, platypus;
  (o) Tachyglossus aculeatus, echidna.


Volative organic acids include polyamines, short chain fatty acids (VFA) and others.  These can be quantified on the GDX/Metametrix GI function stool test and blood/urine organic acids testing.  This test is the best on earth. It assesses both large and small intestine function, and additionally accurately pinpoints pathogenic overgrowth, parasites, and worms which are frequent invaders despite 'clean' air, water and soil in modern continents. If pathogens exist in the small intestines, caecum and/or large intestines, putrification of undigested fats, proteins and carbs occurs.  Certain volative by-products are highly odiferous-- cadaverine, putrescene, spermidine, etc.

Treatment includes pathogen killing (charcoal, clay, herbals), healing the broken gut/brush border/GI peritalsis/acidity/pH, and replacing lost gut flora (commensal Firmicutes, Bacteroides, facultative anaerobes, SBO, good yeasts, etc).

The entire human gut has only ~17% of surfaces for fermentation compared with 50% for an animal like guinea pig. (TO ME, this is like the diff betw a select post-harvest wine versus mass produced Coors light.)

Bergman talks in-depth about VFAs. "Current estimates are that VFA contribute approximately 70% to the caloric requirements of ruminants, such as sheep and cattle, approximately 10% for humans, and approximately 20-30% for several other omnivorous or herbivorous animals. The amount of fiber in the diet undoubtedly affects the amount of VFA produced, and thus the contribution of VFA to the energy needs of the body could become considerably greater as the dietary fiber increases."  I don't think we are gorillas (57.3% energy obtained from VFAs) though some humans may exist as such (functional..? debatable?).




Role of Appendix and Failed Fecal Transplants

Our comparatively tiny human appendix is nearly non-functional yet appears to serve a purpose for maintaining maternal, birth- and early life-derived microbiota and biofilms.  This is why -- I've heard -- that fecal transplants often fail 1-3 years post-transplant (anecdotal communication,  Metametrix/GDX Tony Hoffman).  Were these cases Paleo? Consuming fermented foods frequently? Root causes for dysbiosis/permeability identified and reversed?  Toxins, mercury, pathogens addressed??




Appendectomies, Gluten Sensitivity, Gallbladders, Nutrigenomics and TMI

Not all animals have an appendix...... including members of my family; two out of 4 siblings have had surgical removal of the appendix. We also have 3/4 (diagnosed) autoimmune disorders. And 2/4 have documented gliadin sensitivity (me, positive fecal anti-gliadin sIgA in 2011 on Metametrix GI fx stool testing). Is there a connection? You tell me.

I'm Paleo because I'm protecting my gallbladder, appendix and other precious ~~.  Not into chopped off organs, boobies, etc.

Integrative medicine, treatment and prevention for gallbladder disease HERE (Gaby 2009).

Recently my kids and I did 23andme genotype testing. Have you done it? It revealed many gluten-sensitivity related conditions we are susceptible to based on known SNP analysis (alkylosing spondylitis, primary biliary cirrhosis, T1DM, etc).  Not a shock. I'm grateful for discovering the Paleo and gluten free diet in 2007, then functional medicine and intestinal permeability/gut dysbiosis in 2010.  We have made appropriate changes and seen improvements -- some mild, some dramatic.

This is the year of personal nutrigenomics.  We are negative for MTHFR but have the GSTT1 (glutathione, detox, heavy metals), deletion and are heterozygous for COMT (methylation -- detox of toxins, metabolism of adrenaline, dopamine, estrogens, 4OHE1, cortisol, etc).

Gallbladder stones and removal are super super super common in primary biliary cirrhosis (one of many celiac/silent-celiac conditions -- just like fatty liver, fatty pancreas, fatty heart, blah blah blah). Why? Look how anatomically close they are together to the liver, portal vein, stomach and duodenum/small intestine. When intestinal permeability allows undigested gluten through (or gluten just opens zonulin), gluten causes immunogenic havoc, scarring and immune system activation.  Same with the appendix.  When gluten and resident microbes translocate from the caecum/small/large intestines to proximal and distal organs, they hit neighbors the hardest.  Appendectomies are mega-crazy-common (my dad's a surgeon; gluten paid for my college).


Often I hear stories that the spasms and pain remain despite surgery.  Despite diligently avoiding 'high fat diets', they suffer (eating wholehealthylectins).  It's not just the 'fat, forty, fertile female' (4F's) who are afflicted (as all hazed med students are taught).  Males are affected too. Children are now affected.

It's a silent epidemic across the world in sync with vegetarianism (vegetarian males: 3-fold; vegetarian +alcohol, 7-fold) and westernized, Big Agra crop-users (like Saudi Arabia).

Gluten? Dietary removal of gluten helps a ton as Gaby above reports (two studies in celiacs 1985 and 1999).  Gluten is heat/cooking resistant. The toxic gliadin peptides can resist GI enzymatic digestion when microvilli DPP-IV  is disabled (by mercury) and when brush border enzymes are missing (SIBO, gut dysbiosis, pathogens/parasites).  At least 60 gliadin protein sequences are immunotoxic, triggering immune system reactions for susceptible individuals.  These were in relatively low concentration in ancient wheat but 50-100 years ago, transgenic hydridization and GMO techniques have bred (pun, bread) the concentration of the toxic gliadins to an estimated 500-fold amplication.

Peter at Hyperlipid cogently discusses Gluten and Gallbladders (circa 2008); good stuff, good comments.





Safe Guarding Appendices?

Smith et al talks about how the caecum is a "‘safe-house’ for biofilms containing commensal bacteria." How does antibiotics affect this? Antibiotics in food, cattle/chicken feed, eggs and their products?  How do we revive extinct commensals and healthy biofilms....? Wish I knew definitively because there are few ways to test the contents of the caecum and appendix.

If I could repeat preconception, conception, birth, postnatal, and lactation periods with my kids, I would certainly do a million things differently from the gut and gut microbe perspectives.

Further Smith et al concludes on the relationship between the caecum (which contains a region of lymphoid tissue), gut microbiota and the immune system....
 'Although microbial biofilms in the proximal large
bowel are apparently a hallmark of immune support for
the microbial flora in a wide range of mammalian species,
the biofilm distribution in the gut of an outgroup for
mammals had not been evaluated previously. Thus, the
observation that biofilms are distributed in frogs in a
manner similar to mammals, with a preference for the
proximal large bowel (Fig. 4), strongly suggests an
ancient origin for a pro-microbial immune function in
the proximal large bowel. Specifically, this observation
suggests that the adaptations supporting biofilm growth
by commensal bacteria are more ancient than blind sacs
of the gut, such as the cecum, which are involved in
fermentation. In support of this idea, microbial biofilms
are not only strengthened by secretory Immunoglobulin
A (SIgA) produced by the adaptive immune system, but
can also be supported by mucin (Orndorff et al., 2004;
Bollinger et al., 2005), a major biomolecule produced by
the more ancient innate immune system. This finding
points toward increased immune support of the gut
microbes as one of the potential driving forces for the
evolution of blind sacs in the proximal large bowel.'



Our Gut Anatomy and Physiology:  Part Carnivore + Part Frugivore

The curious thing is that advanced hominids are not exclusive frugivores. Though it makes sense that we lost the capacity to synthesize Vitamin C and must find and outsource this to dietary Vitamin C, our digestive tract length, volume and capacity to produce low pH and secretions are akin to carnivores.  Additionally, our shrunken small intestines possess really exceptional digestive capacities and efficient absorptive surfaces synonymous with carnivores, not herbivores (3-5X our height, not 10X as in herbivores).

 Photo credit: Biocyclopedia.


Nearly ALL digestive work and absorption are concentrated in the small intestines, which varies in length by individuality, 15 -30 feet. This is why illness in the small intestines (SIBO/gut dysbiosis) disrupts all health, including even distant, peripheral tissues (brain, breasts, fat/belly, bones, joints, vasculature, gonads-b**ners), not only proximal (liver, pancreas, gallbladder). Energy dense food provide long acting fuel (fats, complex carbs). Our small intestines, gallbladder bile acids for fats and carbs, pancreatic enzymes (lipases, proteases, carb-ases) compensated.   Our carnivorous small intestines are the super gift we acquired through evolution.

Our immune system is 70-80% based in the gut. Despite, our immunity being outsourced to microbes (caecal, appendix, intestines), only a fraction of our nutrition is (~10% from VFAs) because we obtain the energy from broken down, digested high-energy bonded food (e.g. fatty acids, complex carbs) in the small intestines.  Our sophisticated and elite human small intestines suck all this energy up taking what first-pass at the liver misses. Human nutrition is super nutrient dense and fat based (my diet is 30-40% fat) allowing us to forgo chewing and grazing but only every 3-5 hours.

The remaining marginal allotment of our nutrition is brewed by symbiotic bacteria and yeasts... It's arguable that butyrate is both a nutrient for the intestinal cells as well as an extension of the ancient immune system for the entire body. Our hindgut (large intestines) continues methodical fermentation and microbial metabolite harvesting (organic acids, volatile fatty acids, B12, butyrate, other bacterial Firmicutes/Bacteroides end-products).  It's absolutely not necessary to produce heaps and heaps of dung like our four-legged herbivore friends all day post-digestion without anal control.

Tuesday, September 10, 2013

Korean Pepper Paste Burns Body Fat, Soil-Based Organisms (SBO), Gut Microbiota -- New Study 'Kochujang, fermented soybean-based red pepper paste, decreases visceral fat and improves blood lipid profiles in overweight adults'

Gochujang -- Staple at our House

When we first moved to Shanghai, we ate Bibimbap at least once or even twice every week.  It was our go-to comfort (Cali) food until our food sources diversified and expanded with the help of other expats and finding reliable organic/local/non-GMO purveyors.  Gochujang (which contains soil-based Firmicutes, B. subtilis, etc) is good for HEAT and tummies. The one on the right is a traditional product which I brought (eg smuggled) in from California (refridgerated area of the Korean shop in Albany, north of Berzerkeley). Both are Korean products but unfortunately the red one on the left is ubiquitious and popular in markets both in America and Shanghai, China. (BTW neither are gluten-free.) The first ingredient of the modern, processed version (red box) is guess?

Prior to 2008, apparently Korea didn't open its doors to GMO corn but that changed when the price of non-GMO corn went up to $400usd per ton (from $150); GMO corn was only $50usd per ton (source: ENN). Money talks and the grind of multinational corporations continues..?? Did this trump the price of cane sugar?!? GMO corn infiltrates internationally... Why does our food continue to become more and more perverted and unrecognizable (AND SUPRATASTY, ADDICTIVE, AND UNSUBTLE).




Ingredients (Right): Glutinous rice flour, Salt, (hopefully fermented and non-GMO) 
Soybean flour, Malt syrup, Hot Pepper Powder
Ingredients: (Left):  See below, it's the Korean SunChang brand 
(first ingredient: GMO CORN SYRUP; last ingredient 'seed malt')

Source :  Amazon




'Seed Malt' (?Arsenic, Heavy metals) in Modern Processed Gochujang

The tastiest ingredient is perhaps the most vile, seed malt. Even the traditionally prepared one contains malt syrup which is likely to come from gluten-containing barley malt.  I had to look up what seed malt is. In many Asian countries, the unami flavor is so desired and favored but hard to achieve from a food science perspective without time-consuming aging processes and fermentation.  Seed malt is the short cut.  Fast, cheap and full of nasties.  The starch that it is all germinated and cultured in is not specified but the food industry generally uses: corn, wheat, barley or the like.  Definition of seed malt (source: KFDA Korean Food Additives CodeThere are crude seed maltand powdered seed malt. Crude seed malt is obtained from a culture where starter of Aspergillus kawachii, Aspergillus oryzae, Aspergillus usamii, Aspergillus shirousamii, Aspergillus awamori or Rhizopus genus are separately or mixedly inoculated so that spores are inserted into a pasteurized raw material containing starch. Powdered seed malt is obtained by collecting pure spawn spores by a special method. 

Lot of fungal species...(but Aspergillus at least contains xylanases which break down gluten)

To eliminate the fungal species and 'clarify' I believe production of 'seed malt' uses an absorber which contains heavy metals and/or arsenic. This is a problem in German beer. Kieselguhr (diatomaceous earth) is used in beer processing to filter and remove yeasts, hops and particles (source: sciencedaily.com). How heavy metals and arsenic otherwise can test positive in a starch malt, I don't know. Fungicide-contaminated rice sources? HFCS (high fructose corn syrup) due to mercury containing chlor-alkali processing (Dufault et al, EH 2009)? Right: list of arsenic food contaminants (source: Codex Committee 2011).




Science Behind Ancestrally/Traditionally Fermented Gochujang

Being in Asia has certainly given me an appreciation of the variety of fermented foods in countries outside of the USA. We have always been fans of Korean food which has one of the most easily accessible sources because typically in the USA, every good Korean restaurant ferments their own variety of fermented tofu, beans, radishes, green beans, cabbage and raw crab/seafood... (as each family does in traditional homes that adhere to the old way... and after making our own hot pink sauerkraut HOT D**MN THIS IS A PART TIME JOB)

Good news, it is all worth it.

Fermented foods are packed with cheap prebiotics and even cheaper soil based organisms that make the gue microbiota a friendlier and happier place, crowding out overgrowths of yeast, parasites, worms and other un-friendlies and promoting growth of healthier gut epithelium and immunity (70-80% of our immune system is in the gut).





Brand Spanking New Study...
This clever study verifies many things that we know already.  Eating the poop/probiotics from healthy, lean people is perhaps not harmful for you...  It can make a mouse leaner, thinner and move from a fat phenotype to a leaner, less body fat profile.  Clostridia (Firmicutes) from Ln (lean) types invaded the guts' microbiota of Ob (obese) cagemates via copraphagia (eating of poo).

Recall, I like coprophagia... [cough cough] for B12-deficient vegans.  It's like a fecal transplant... (DIY fecal transplant: Silverman et al, 2010).






New Study: 'Kochujang [KCJ], fermented soybean-based red pepper paste, decreases visceral fat and improves blood lipid profiles in overweight adults'  (Cha et al, 2013)  [PDF HERE]

"The KCJ is produced by fermenting powder red peppers
combined with powdered meju (fermented soybean
powder), salt, malt-digested rice syrup, and rice flour for
about six months. The fermentation process extends the
storage period while increasing bioavailability of bioactive
ingredients [4] such as free amino acids, peptides,
alcohols, organic acids, capsaicin and flavonoids [5,6].
KCJ has unique flavors of sweet and hot red pepper
combined with savory soybean protein hydrolyzate and
nucleic acids. In recent years, KCJ has gained its popularity
outside Korea for its taste and health benefits derived from
the several ingredients [7-16] that are produced by the
fermentation process [17-22]. The functional substances
either singularly or in combinations have exhibited antiobesogenic,
anti-oxidative, and anti-mutagenic properties
in several in vitro experiments and in various murine
models [7-16]. Anti-obesogenic and anti-atherogenic properties
of fermented soy products have been demonstrated
in obese adults [23], possibly through modulation of
hepatic acyl-CoA synthase, carnitine palmitoyltransferase I,
and acyl-CoA oxidase [24]."

My Summary
  • The n=56 overweight subjects were given ~2 tablespoons of Kochujang daily (approx daily Korean consumption amount) as supplements in this RCT, and checked at 5 clinic weights during the 12-week long study duration.  Visceral fat was assessed by CT.
  • WHR (~0.9), BMI (~26-27%), body fat % (~33-34%), BP (~117-119/75) and HgbA1c (~5.4%) all did not change however both groups lost subcutaneous fat (47.9 cm2 v. 53.2 cm2, study v. control, respectively).
  • Visceral fat was dramatically dropped in the study group receiving the kochujang supplements (which were ++ in addition to regular daily amount) compared to placebo: -4.8 cm2 v. +0.4 cm2 (p=0.001).  ~~Ten-fold differences...
  • Interesting placebo effect on subcutaneous fat loss...
  • Perceptible changes in TG and apoB (which is super-tightly related to TG) were seen too (p=0.049). TG decreased.  It's hard to see HDL changes unless big weight, fat, dietary changes are seen, and that was the case.
  • Thankfully, none of the researchers were funded by SunChang (the modern, processed Kochujang manufacturer).


Thoughts? 

 I don't agree with their conclusions entirely. Yes, 'capsaicin in red pepper, isoflavon aglycones, and peptides from fermented soy' all are good things, but the placebo group probably ate these as well in small amounts (because they lost subcu body fat).  In fact, researchers admit they really are clueless stating 'However, the mechanisms responsible for these observed effects are yet to be elucidated.'




Evolution, Interspecies Guts, Soil-Based Organisms and Achieving Leanness

Discounting eating disorders and celebrity/model fanatics, most normal people can achieve leanness by normal lifestyle habits, balanced diets, fixing nutritional deficiencies, avoiding being 'germ-free' and broad spectrum antibiotics/antifungals, avoiding nutritional pitfalls (excess n6 pufa, excess refined starches, mercury, arsenic, PCB/pesticides/BPA/plastics and other estrogen-mimics), detoxing environmental toxins, avoiding stupid excesses (alcohol binges, brownie binges, sleep deprivation, chronic endurance sports, etc) and balancing hormones. All the above also fix the gut microbiota according to emerging pubmed data.

This study exemplifies it... though the research authors fail to identify the role of the gut, immune system, and microanimalia found in fermented kochujang.

Kim chee: The biome structure of kochujang's counterpart kim chee has been more deeply profiled.  Kim chee has been massively PCR microarrayed, and it does indeed also contain as one would expect (from dirt) archaebacteria and good yeasts (like Saccharomyces).  I cannot find in this article if the species S. boulardii  -- one of my favorite yeasts -- is listed but fermenting rice bran with S. boulardii yields  bioactive candidate metabolites that reduce B lymphoma growth in vitro.   Kim chee in most studies is characterized by 3 main genera LactobacillusLeuconostoc and Weissella. Particular species that are speculated to be found in kim chee cultures are: Leuconostoc species-- Le. mesenteroides, Le. kimchii, Le. citreum, Le. gasicomitatum, and Le. gelidum, the Lactobacillus species -- Lb. brevis, Lb. curvatus, Lb. plantarum, and Lb. sakei, Lactococcus lactis, Pediococcus pentosaceus, Weissella confusa, Weissella kimchii, and Weissella koreensis.

Human GITs (gastrointestinal tracts) are part-carnivore and part-frugivore.  Our shrunken, medium-sized small intestines possess exceptional digestive capacities and hyper-efficient absorptive surfaces synonymous with carnivores, not herbivores (3-5X our height, not 10X as in herbivores).   We have enzymes to breakdown protein, fats and complex carbs to base, fundamental constituents (amino acid, fatty acids, glucose). The rest (soluble and insoluble fiber) is fermented in the hindgut by our friendlies into further end-products that we harvest and absorb (B12, butyrate, etc)...

Kochujang is special.

Maybe it is because it is fermented and digested by dirt-commensal microbial critters in carby, high protein/fat environment (rice + soybeans? ...which are fatty AND proteinous (complete proteins incidentally).  Why it sounds... SO ODDLY... OMNIVOROUS...

Our gut microbiota in the large intestines has the ability to manufacture enormous supplies of butyrate, a short chain fatty acid, that plays an imperative role in healthy guts for regulating and controlling inflammation.  Butyrate is mostly produced by Firmicutes species.  Butyrate not only enhances the integrity of the gut by inducing mucin synthesis but also is the main energy source for colonic epithelia. By lowering inflammation, I believe, butyrate and gut microbiota synergism/cross-talk with immune system lymphocytes and gut epithelia produced the lowering of the (minor) visceral fat compartment and improvements in metabolic flux in the test subjects with Kochujang supplements.

Previous animal pharm:
Burn Body Fat Loss with Saturated Fat (Butyrate and MCT Oil)







Kochujang Contains Mostly SBO, Soil Based Organisms (E.G. FROM DIRT)

Kochujang has been analyzed it contains more soil-based organisms (SBO) Bacillus versus kim chee's Lactobacillus genera.  The bacteria in Kochujang is predominantly Firmicutes (93.1%) species, simliar to the SFB (segmented filamentous bacteria) discussed in the last post.

"Through the analysis of 13524 bacterial pyrosequences, 223 bacterial species were identified, most of which converged on the phylum Firmicutes (average 93.1%). All of the kochujang samples were largely populated (90.9% of abundance) by 12 bacterial families, and Bacillaceae showed the highest abundance in all but one sample. Bacillus subtilis and B. licheniformis were the most dominant bacterial species and were broadly distributed among the kochujang samples. Each sample contained a high abundance of region-specific bacterial species, such as B. sonorensis, B. pumilus, Weissella salipiscis, and diverse unidentified Bacillus species. Phylotype- and phylogeny-based community comparison analysis showed that the microbial communities of the two commercial brands were different from those of the local brands. Moreover, each local brand kochujang sample had region-specific microbial community reflecting the manufacturing environment [e.g. probably not SunChang, Inc]."  Source : Nam et al, J of Food Science, 2012.




Please Pass Your Good Cuddies/Firmicutes -- SBO Also Breakdown Gluten

The two most dominating species found in this study of Kochujang are soil based organisms -- B subtilis and B. licheniformis.  In experiments, B subtilis and B. licheniformis, digest gluten; they're frequently found in sourdough ferments, naturally-occurring on rice straw, Japanese traditional natto, Chinese fermented black bean sauce, Nigerian fermented soy 'Daddawa', Thai fermented foods, Indian fermented soy Hawaijar, fermented shrimp heads, Korean fermented black soybean Chungkookjang, and raw dairy.

The undigested gluten peptide, that is most toxic to celiacs and induces immuno-triggering damage to the small intestine, is broken down by enzymes from either B. subtilis* or B. licheniformis*.  HLA DQ2/8 on APCs have extremely attractive binding affinity ('epitope') to undigested gluten (for example, 33-mer alpha-gliadin).  Consequently, APCs will present undigested gluten to CD4+ T-cells as invaders, thus setting off the cascade of TH1, Th17 and Treg hyperimmune responses.

Celiac is actually an autoimmune disease of the DQ2/8-gluten complex (IC, immune complex) in the small intestines and other affected organs.  At least 60 immunogenic gluten peptide sequences exist in modern-hybridized industrial wheat.



Conclusion

In gluten intolerant folks, TH17 is usually slightly or entirely j**cked up.  TH17 may lack training/regulation, and intestinal hyperpermeability is likely present.  Food antigen intolerances consequently pop up secondary to hyperpermeability.  The commensals in the gut microbiota shape immunity and prime and promote the proper differentiation of TH17 and other cell subsets.  Is this one of the primary differences between the obese and the lean?  The gluten intolerant and the gluten tolerant? The celiac HLA DQ2/8 and the non-celiac HLA DQ2/8?  What gut toxins prevent seeding of commensals? Bt GMO corn? Mercury and other DPP-IV inhibitors (microvilli DPP-IV digests gluten)?

SBO and their molecular components appear to play a great part in re-balancing the distribution between arms of the vast immune system: TH1 v. TH2 v. TH17 v. Treg.  When the gut barrier becomes tight and competent again, food intolerances reverse or disappear.  Undigested gluten won't pass through.  The gut epithelium is but one cell layer thick.

Permeability perhaps is the bane of advanced hominids. We diverged from primates with zonulin, the gate keeper of intestinal permeability.

Why?  For the the continuation of post-natal growth of the gigantic human brain?  For the extended longevity and flexibility of advanced hominids? I'm not certain but I suspect it has to do with ontogeny and how our premature babies require maternal immunoglobulins, IgM in breastmilk, for 18 months to 3 years old of age for the immunoprotection until their own immune systems mature, interact with the environment and develop.

For some individuals, soil-transmitted hookworms are solutions and the key... together, SBO/dirt, kochujang, coprophagia, and 'kraut may be fine, and problematic pathogenic (microbial/yeast) overgrowth and parasites can perish.





SBO Related Sources and Probiotics:

These are all shelf-stable because SBO are spore-forming and don't require refridgeration. In immunocompromised and susceptible individuals, probiotics can exacerbate the root problem. Introduction of lactobacillus organisms, bifida, SBO or other probiotics may increase gas and bloating if SIBO (small intestinal bowel overgrowth) is severe, just as introduction of fiber/inulin/FODMAPs can induce gas and bloating until gut initation and adaptation has gradually occurred.


Probiotic that includes B. licheniformis:  Body Biotic

Protiotics that include SBO:
Prescript Assist (B subtilis, etc)
FloraBalance, Bacillus Laterosporus BOD
Ultimate Acidophilus with Bacillus Coagulans
AOR Clostridium Butyricum
Thorne Bacillus Coagulans
Threelac (B subtilis, etc)
Primal Flora (B coagulans, etc)
Primal Defense (B subtilis etc)   [the wildly successful original formulation had both, ~ + B licheniformis]


Gluten-digesting Digestive Enzymes:
Devigest (B subtilis + enzymes from B licheniformis, etc)



Sources: ASSESS and CNSweb.com


Catch This:  Making Gluten-Free Korean Chili Paste Gochujang (CriticalMas blog)

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)

Ingredients
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.

Friday, June 7, 2013

(NSFW) B**bies, B**bies, B**bies... I see..chopped off b**bies

Sunny Tales
Sunlounger

If you know me (and this blog) you know I love racks and b**bies (incl mine).

So it is exxxtremely disheartening when I hear of individuals choosing to go through the agony of cortisol-spiking surgeries to remove their respective rack and b**bies. Now that Jolie' preventive bilateral mastectomay has hit the big news, I see chopped off b**bies and ovaries everywhere. [Cue: Sixth Sense movie music]

Sayonara b**bies


LOL. The horse and I will miss the real thang




Breasts and B**bies: Chock Full of Both Omega-3, MCT (medium chain triglycerides) and Taurine

Our breasts serve an evolutionary function as storage for all the goods things that need to be passed to the next generation, besides adipose storage and breastfeeding. Omega-3 fatty acids from seafood, grassfed game, herds, and free range poultry are selectively stored in breast, gluteal, abdominal and thigh fat. And the amount that gets stored in the breasts and other fatty tissues is governed in a dose-dependent fashion over time. The nutrients in the breast are important not only for lactation (year 1-2 for newborns) but also for gestation.  Our breasts become factories to feed the next generation all the things that nourish and grow the massive homo sapien brain and forward-gazing, stereoscopic, color vision, X-ray eyeballs, which doubles in physical size during the first 12 months of life. The contents of breast milk are super foods for newborns: MCTs (caprylic acid, lauric acid), omega-3 fatty acids (EPA + DHA), taurine, vitamin A, vitamin D, magnesium, zinc, iodine, colostrum, amino acids, galactose, IgM, immunoglobulins, protective enzymes, epidermal growth factor, etc. For certain nutrients, naturally, maternal supplementation also works when the mom cannot breastfeed (hormone imbalances, anatomical issues, neonatal twisted tongue, etc).

A baby is born with inherent 'leaky gut' (intestinal permeability) for the first few months in order for some of the larger protein molecules and mom's immunity to pass directly into their blood stream for immunoprotection. Since the baby has an underdeveloped and immature immune system, there is no point in vaccinations (full of toxic aluminum or mercury) on Day 1 of life (assinine).

Many factors in breastmilk subsequently raise of the IQ of newborns who breastfeed.  In one study, the breastmilk (not necessary connected with the close maternal-baby contact, milk in tube) was associated with a 8.3 point increase in IQ testing in preterm children at age 7.5-8 years of age compared with no breastmilk.

See prior animal pharm:  MCT Oil (coconut oil, breastmilk) kick the crapola out of olive oil

Credit: Celeb*tchy
higher? harder? pointier?
Good job Kristi Funk MD


On Nursing
"Its unique recipe of fatty acids boosts brain growth and results in babies with higher I.Q.'s than their formula-slurping counterparts. Nursing babies suffer from fewer infections, hospitalizations and cases of sudden infant death syndrome. For the mother, too, breast-feeding and its delicate plumbing of hormones afford protection against breast and ovarian cancers and stress. Despite exhaustion, the in-laws and dirty laundry, every time we nurse our babies, the love hormone oxytocin courses out of our pituitaries like a warm bath. Human milk is like ice cream, Valium and Ecstasy all wrapped up in two pretty packages."  Source:  NYT Toxic Breast Milk?




Breastfeeding: Good way to detox pesticides, metals and PCBs (flame retardants)

Unfortunately our breasts store both the good and the bad... our fatty breast tissues are magnets and reservoirs for fat-soluble toxins and heavy metals from our produce (pesticides), commercial meat (growth hormones, pesticides), marine fish and seafood, pharmaceuticals (aluminum antacids, mercury/Al from vaccines, etc), dental (mercury and other metals from amalgam and titanium dental implants), Teflon cookware and coated clothing (PFOA), and environment (flame retardants, mercury/arsenic from coal burning plants which supply 40-50% of USA energy, aluminum from municipal water, blah blah blah).  The individuals who are least likely to have the biochemical mechanisms to chaperone and eliminate these modern industrial toxins, are the individuals most highly likely to develop inflammatory conditions including cancer, autoimmune diseases and Western chronic diseases.

Some of the identified genetic variants are MTHFR (Amy Myers MD), GSTM1 (Mark Hyman MD), COMT, ApoE4, CBS, GSTT, BRCA1/2, and several other emerging ones. A functional medicine doctor and dietician, Dr. Elizabeth Boham MD talks about how she developed breast cancer in her 30's despite 'doing all the right things' eating low fat, exercising regularly, etc HERE. She talks about how to identify and remove toxins in our food, lifestyles and environment.  A functional medicine and SNP case study: 'George'. To see more on SNPs and diverse associated human diseases, go into OMIN (online Mendelian inheritance in man), RegulomeDB.org/GWAS and PrometheASE.

Who has pesticides and PCBs in their toxome?  Apparently everyone -- adults and newborns before even their first breath of air according to CDC, NHANES and EWG studies. Even the President's Panel reported so in 2008.

In the '80s and '90s apparently Europe cracked down and starting banning dousing all home furnishings and clothing products with flame retardants (PCB and its cogener, polybrominated diphenyl ethers, PCBEs). Not the case in the USA.  In California for several decades, PCBs were required on pajamas, pillows, mattresses, couches, etc and thus many other states (and China) have followed suit.  PCBs end up in the ocean and rivers and marine life especially large predators bioaccumulate PCBs, mercury, dioxins, and pesticides. Cats and other indoor pets (and children) inadvertently consume dust and lick their fur, subsequently becoming exposed to PCBs.  All of our cats unfortunately developed endocrine disorders and I can never be certain that it was not secondary to the PCBs in their seafood/tunafish soft food that we 'treated' them with (combined with BPA-lining of the catfood cans).  They were all healthy and fine until 3-9 months after introducing them to seafood canned catfood....

In 'A retrospective study of PBDEs and PCBs in human milk from the Faroe Islands' the authors tested and tracked flame retardants in the milk from women who live on the Faroe Islands. They concluded 'Although remote from pollution sources, the Faroe Islands show high concentrations of POPs in human milk, particularly PCBs, but also PBDEs. The PBDEs show increasing concentrations over time.'

From Dr. Pizzorno in Is Toxin Exposure Relevant?
We know that considering the effect of one chemical at a time is no longer suficient. The Centers for Disease Control (CDC) published data on the levels of selected persistent organic pollutants (POPs) – a category of toxins which includes dioxins, phthalates, PDBEs, PCBs, etc. – and found that among a representative sample of the US population, some toxins were present in essentially every individual over the age of 12, including, for example, p,p’-DDE and hexachlorobenzene.5 An analysis of NHANES data found up to a 38-fold adjusted increase in risk for diabetes prevalence in those with the highest levels of 6 POPs,6 and increased risk has also been documented for cardiovascular disease,7 insulin resistance, impaired neurological development, learning and attention deicit disorders, endometriosis, and deficits in the hypothalamic-pituitary-thyroid axis8,9,10,11 (Figure 1 shows the increasing concentration of PBDEs (polybrominated diphenyl ethers) in breast milk).12 While very little data for humans is available, current evidence suggests that PDBEs are likely to be developmental neurotoxins, and are likely to have synergistic effects with similar chemicals.13

In addition to exogenous toxins such as POPs and heavy metals, a number of endogenous substances also require efficient functioning of detoxification enzymes to prevent a build-up of harmful metabolites. For example, endotoxins from bowel flora have been associated with depression, chronic fatigue, inflammatory bowel disease, and atherosclerosis, effects partly influenced both by bacterial species as well as intestinal permeability.14,15,16,17,18 Also, catechol estrogens and estrogen quinones are estrogen derivatives associated with oxidative damage and reproductive tissue cancers, which accumulate due to alterations in enzymatic activity.19,20 Other examples are the build-up of methylmalonic acid and homocysteine - both metabolic by-products known to have vascular, renal, and neurological toxicity, consequences of genetic susceptibility and poor B vitamin status.21,22,23,24





What Can We Do?

We must do much.  The statistics for lifetime sporadic cancer risk is currently 1:3 and will exponentially increase to 1:2 by 2020 according to WHO statistics.  I believe it.  Our toxome is excessive and unfortunately no diet (even paleo or ancestral diets) frees us from the pollution and the body burden accumulated over generations (our mothers, their grandmothers and, particularly, this current one).  We can thank the World Wars which ushered in technology (nitrogen fertilizers, Agent Orange).  It is rather wicked and ironic that the best green for liver support and thus elimination of pesticides, metals and PCBs is dandelion greens (e.g. a weed) introduced to the Americas by the British.

Good luck as we shall all need it.





See other animal pharm:
BRCA 1/2 Myths and Measuring Oxidative DNA Damage, 8-OHdG
USA Cancer Management: 50 Shades of F%$*# UP

Other resources:
Our Feel-Good War on Breast Cancer
Dr. Cate, BRCA Testing: Are the Medical Options Sensible
Mercury: How to Get This Lethal Poison Out of Your Body
How to Rid Your Body of Mercury and Other Heavy Metals: A Three-Step Plan To Recover Your Health
Kaayla Daniel and Galen Knight (WAPF) -- Oral Chelation and Mercury/metal-free Living (How to Avoid Toxic Metals and Clear Them From The Body)
Soy Recovery: The Toxic Metal Component
The Little Known Soy Gluten Connection
WAPF -- Environmental Toxins (comprehensive list of Wise Tradition articles)
Toxic Ignorance and Right-To-Know Biomonitoring

Thursday, May 23, 2013

Death of the Great Cholesterol Diet Fairy Tale, Familial Hypercholesterolaemia, BRCA1/2 Myths, Insulin 101, Cancer and 50 Shades of F_cked (Sorry, Y E S Again)




Sorry for the delay.... Old scathing editorial in QJM (hat tip: Peter D'Adamo), by D.D. Adams 'The great cholesterol myth; unfortunate consequences of Brown and Goldstein’s mistake.'



The Mistaken Implication of FHC and Elevated Blood Cholesterol

Abstract  Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D.

Unfortunate consequences of Brown and Goldstein’s mistake
Brown and Goldstein’s burst of fascinating information dazzled the medical profession, most of whom consequently accepted the false cholesterol hypothesis. This has led to unfortunate consequences that include:

  • Waste of money on misdirected research.
  • Waste of money on blood cholesterol tests.
  • Waste of money on statins.
  • Malnutrition from lack of fat-soluble vitamins (A,D,K,E) present in butter, full-cream milk and animal fat but lacking in margarine and skim milk (green-top bottles in New Zealand).
  • Fear of eating eggs, contributing to unhealthy, starchy diets.
  • Ricketts in middle-aged men from lack of vitamin D due to use of margarine and skim-milk.
  • Distortion of the Dairy Industry, causing unnecessary marketing of skim milk.
  • Distortion of the Meat Industry with unnecessary production of lean meat.



The author concludes 'The fact that of the thousands of people involved in achieving this spurious result did not include a single elementary mathematician with intellectual independence is in accord with the whole sorry story of the great cholesterol myth, starting with the false statistics used in analysing the Framingham data.10 The meta-analysis of Ray et al.,13 showing no prolongation of life by use of statins in randomized controlled trials involving 65 229 participants, is the final nail in the coffin of the great cholesterol myth.'



Insulin 101, Diabesity and Cancer Malignancies....

The lifetime risk of developing any invasive cancer is over 1:3 (males nearly 1:2) currently and by 2020, the WHO estimates, the stats will be 1:2 for both males and females.  The XX chromosomes no longer will protect us gals.

Why?

Does it have anything to do with 'Great Cholesterol Diet Myth' that the above authors have dispelled on unfounded, false scientific interpretations?  The refined whole-wheat-unhealthy-heart debacle may be nearing its end after this editorial, perhaps.

Is our diabesity and cancer epidemics related to the growth over the last few decades of 'low fat,' government-sanctioned, high refined carbs, grain-based propaganda and GMO (Bt-gut busting zonulin-opening lectins), pesticide laced grains and grain-fed commercial meat, poultry, dairy and eggs?  And the environmental havoc that plays out...?  Our original gut flora are nearly extinct much like most of the rainforest species.  Compound this with other endocrine- and gut-disrupting toxins like mercury and arsenic that  rain out from coal burners which still supply greater than 50% of USA energy.  BTW China is now #1 globally for coal utilization, eeking out over the USA in recent years. Go China for exceeding USA's giant industrial pollution footprints.

http://www.avonbreastcare.org/files/SusanLuckWebinar.pdf



BRCA1/2 and Chopping Off B**bies

Breast cancer is complex, yet it is quite simple. Is it necessary to contemplate IMHO surgical removal and reconstruction of any beautiful body part that may fall to cancer? Where does one logically start? Where does one end because everything that undergoes DNA replication and editing may fall to cancer and mutations...?  Ms. Angelina Jolie, I lurrv u, please stop. Your message is IMHO short-sighted and not sustainable.




Pardon, Let's Look at A Couple of BRCA1/2 Facts: 

BRCA1/2 is a defect in DNA repair and fails to fix 8OHdG (oxidative DNA damage product, 8-hydroxy-2'deoxyguanosine)

BRCA1/2 raises risk in men of breast, prostate, pancreatic, gastric and hematologic cancers

BRCA1/2 raises risk in women of breast (73%), ovarian (41%), colon (2-fold), pancreas (3-fold), stomach (4-fold) and fallopian tube (120-fold) cancers

BRCA1/2 like all mutation genes is under epigenetically controlled regulation -- for example, silencing of the gene occurs with polyaromatic hydrocarbons (pollution), insulin, and hypomethylation (lack of methyl donors -- either depletion or dietary deficiency -- or COMT, MTHFR, etc variants). Best food sourced methyl donors are methylB12, choline and methylfolates (free range egg yolks, liver, meat, seafood -- sorry no plant sources you crazy vegans).  Insulin 101: Insulin is a growth hormone and one function is to induce stimulation of female ovaries to increase testosterone secretion.  Unfortunately, in both men and women, normal levels and excess testosterone may be converted into estrogens under insulin induction by P450-aromatase (aka, CYP19), in many tissues including fat tissues, breast cells, endothelial cells and prostate cells.... Certain gene variants accumulate significantly more estrogens than non-carriers (COMT, CYP19).
  • Compared with noncarriers, women carrying at least one CYP19 8r allele had 20% higher estrone (P = 0.003), 18% higher estradiol (P = 0.02), and 21% higher free estradiol concentrations (P = 0.01). Women with the COMT Met/Met genotype had 28% higher 2-hydroxyestrone (P = 0.08) and 31% higher 16α-hydroxyestrone concentrations (P = 0.02), compared with Val/Val women. Cancer Epidemiol Biomarkers Prev13; 94.

BRCA1/2 silencing may be epigenetically avoided by diet, resveratrol and other antioxidants

BRCA1/2 needs a genetic 'cofactor' like MTHFR, COMT, CYP19 (aromatase which converts testosterone to estrogens), CYP1B1 (pathway increases 16OHE1, estrogen carcinogen adduct) and CYP1A1 to be carcinogenic according to emerging evidence. These genetic polymorphisms are all related to raised toxic estrogen metabolites and creation of estrogen dominant states.





Functional Medicine and Tracking/Lowering 8OHdG

GDX/Metametrix Labs and other functional medicine lab testing centers offer a wonderful test that measures and helps practitioners to track oxidative DNA damage, the 8OHdG biomarker.  This goes up and down with oxidative damage. Many things have been shown to lower and raise 8OHdG.  Diet and supplements (melatonin, vitamin C, berry extracts, resveratrol, etc) have been shown to lower 8OHdG.  Please check out more HERE and HERE (p. 361 of 'Lab evals for integrative and functional medicine' 2nd ed, 2008).

In a hepatitis C trial in participants at risk for hepatic carcinoma and iron overload, a low-iron diet and phlebotomy lowered 8OHdG to near normal 8OHdG rates after 6 yrs. Additional observed benefits were improvements in liver function: lower ALT and liver function tests, improved scarring and hepatitis, no progression to carcinoma. Viral Hep C titers remained the same but cancer was avoided despite originally sky-high 8OHdG six years prior at trial onset.



Prior animal pharm:

Pesticides May Be Behind USA Diabesity, Disrupting Insulin and Tissue Insulin Resistance
50 Shades of F_cked Up (Cancer medical management in the USA)



Other Citations:

http://www.ultrawellnesscenter.com/files/2010/05/Functional-Diagnostics-Redefining-Disease.pdf
http://www.ultrawellnesscenter.com/files/2010/05/Cholesterol-AT.pdf
http://www.cancer.org/cancer/cancerbasics/lifetime-probability-of-developing-or-dying-from-cancer
http://whattofeedyourkids.blogspot.jp/2009/10/xenoestrogens-and-breast-cancer-why-we.html
http://www.scientificamerican.com/article.cfm?id=earth-talk-the-coal-truth
http://www.lef.org/magazine/mag2012/nov2012_Epigenetics_Breast_Cancer_01.htm
Aromatase up-regulation, insulin and raised intracellular oestrogens in men, induce adiposity, metabolic syndrome and prostate disease, via aberrant ER-α and GPER signalling.
MTHFR Polymorphisms, Dietary Folate Intake, and Breast Cancer Risk Results from the Shanghai Breast Cancer Study [hat tip: Todd Lepine MD]
Breast. 2008 Oct;17(5):441-50. Counseling for male BRCA mutation carriers: a review.
Methionine-Dependence Phenotype in the de novo Pathway in BRCA1 and BRCA2 Mutation Carriers with and without Breast Cancer. [need for methyl donors]
Epigenetic diet: impact on the epigenome and cancer.
Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.
Epigenetic impact of dietary polyphenols in cancer chemoprevention: Lifelong remodeling of our epigenomes.