Showing posts with label Animalia. Show all posts
Showing posts with label Animalia. Show all posts

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.

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.

Tuesday, April 16, 2013

Babies and Mapping the Pollution in People: EWG's HUMAN TOXOME PROJECT

I think this is cool (...naught really).

This is a (user-friendly) compilation of the data collected in individual and large studies by the Environmental Working Group's Human Toxome Project. You can click on the right side on the study or an individual to review the toxic metals, pesticides, solvents, PCBs, POPs, and other chemicals found and at what level (low, mod, high).



The data below is from the EWG/Commonweal Study #1.



In each of these 9 adult participants over 150 chemicals, pesticides, solvents and heavy toxic metals were found. Fifty chemicals and metals that have been shown to cause dysfunction of the immune system were detected.  I talked about these factors above at AHS2011 'Rainforest of Your Gut' because not only do they disrupt our immunity but also intestinal barriers and permeability.  Researchers estimate that the intestinal system contains 70-80% of the immune cells.  Once chronic intestinal permeability occurs, all hell breaks loose.  Signs can be acute or terribly subtle....Bloating, dyspepsia, heartburn, hormonal disruptions (men become fem/moobies and grrrrls masculinize), inflammation, insulin resistance, suboptimal adrenals/thyroid, low HDL/high LDL, heart disease, endothelial hardening, penises softening, mental vulnerabilities, autoimmunity, autism spectrum, skin disorders, sinus disorders, candida overgrowth, allergies, oxidative DNA damage, and 50 Shades of F-Cked (cancer).

How do all these multiple industrial neolethal toxic factors influence our health?  From a systems biology perspective, do multiple factors amplify the depth of damage as each organ system one-by-one fails to accomplish what it is designed to do?

People eat whole foods, filtered water, organic, sustainable, ancestral, paleo, et cetera, but is it enough?  What if an individual has a low exposure but genetic variants for particular detox/antioxidant pathways which keeps an industrial toxin or metal hanging around? ApoE4, COMT, MTHFR, MT, and GST are just a few. Granted most of us have decent flux and adaptive mechanisms to survive most assaults but what are the thresholds for coping for multiple exogenous assaults combined with unique endogenous frailities?

On the other hand, what if a person just gets an accumulated butt-load of low exposure from frequent or daily soaked, arsenic- or lead-laced brown rice or heart-healthy omega-3 mercury/flame retardant- and selenium rich wild seafood?  Sorry -- I don't buy that urban mythology.

When I used to go for miles and miles jogging in the neighborhood, on weekdays I watched unprotected city workers spraying pesticides and herbicides on grass edges and around the municipal parks. Where does all the herbicide water run-off go? Where do contaminated water sources originating from Big Agro GMO Monsanto crop fields end up?  How is it tracked? Why not?

67% of the 9 individuals had 'high levels' of mercury detected and 22% 'low levels'.  Mercury used to be in our mouths; my kids and I are amalgam-free for one year now. We rarely eat wild fish with our histories and above is why.

Fukushima radiation is another now (here and here).

Before a first breath of air, 10 babies via cord blood lab analysis (EWG study #4) were found to have 287 heavy metals, pesticides and chemicals. All 10 had mercury (60% moderate levels, 40% low). 100% had dioxin. 100% had PCBs. 100% had organochlorine pesticides.





Recently pesticides from Bt GMO crops were found in 80% of fetuses and 93% of adults (healthy pregnant) randomly tested in one Canadian study (Aris and Leblanc, Reproductive Toxicology, 2011). This herbicide is used as a topical spray as well genetically spliced into the DNA of GMO crops with promoters for high-copy amplification and expression of of a bacterial toxin bacillus thuringiensis (Bt). Bt toxin is also known as Cry1Ab protein.  It is a gut specific delta-endotoxin which exerts toxicity through increasing larvae/insect intestinal permeability causing the death of crop pests like leaf- and needle-feeding caterpillars (lepidopteran insects --butterflies, moths), beetles (coleoptera--weevils, ladybugs, beetles), and the larvae (e.g. babies) of leaf-beetles. It has been designed to be toxic to mosquitoes (dipteran)now.  Fun, no?

Has lateral transfer of Bt DNA to our gut bacteria and microbial communities already occurred (or at least the unborn and adult Canadians in Aris and Leblanc's study)?  Are we transformed? Mutant gut-hybrids of GMO experiments gone awry?

Like advising pregnant moms to avoid fish and seafood to minimize exposure to bioaccumulation of mercury and other pollutants, the American Academy of Environment Medicine (AAEM) issued a GM Foods Position Paper on May 8, 2009 for everyone to avoid all GMO foods in their diets.  Why such adamant recommendations for exclusive GM-free diet prescriptions?



For physicians and healthcare practitioners, they encourage looking at the role of GM foods in health disorders and diseases in integrated medical evaluations.  Why are we fat?  Why does USA obesity trends track and follow herbicide use?  Why are hypothalamus and brain reward centers so SO BROKEN?  How is the global use of herbicides and Bt gut-perforating pesticides related to our health woes and epidemic cancer and diabesity/heart disease/strokes?



In 1998 two scientists fed mice for two weeks potatoes (a) soaked for 30min in a dilute suspension of harvested Bt toxin (from bacterial spores grown in the lab; 1 g/L concentration), (b) transgenic Bt potatoes, and (c) control potatoes. Mild structural changes in the microvilli of the ileum of the transgenic GMO Bt potatoes were seen in.However in the Bt delta-endotoxin soaked potato-fed mice, the ileum changes were quite substantially greater in scale -- '...basal lamina along the base of the enterocytes was damaged at several foci. Several disrupted microvilli appeared in association with variable-shaped cytoplasmic fragments.' The authors further report 'in the group of mice fed on the delta -endotoxin-treated potatoes, the Paneth cells of the crypts of Lieberku¨hn were highly activated and contained a large number of secretory granules. These cells are believed to have an important role in the activation of phagocytes and controlling the bacterial flora of the gut (Ariza et al., 1996; Fawcett, 1997). They contain elevated levels of lysozyme in their large eosinophilic secretory granules, an enzyme capable of digesting bacterial cells walls, and antibacterial peptides called cryptdins (Junqueira et al., 1998). Ouellette (1997) revealed that Paneth cell secretory products seem to contribute both to innate immunity of the crypt lumen and to defining the apical environment of neighboring cells....The antimicrobial polypeptides of the Paneth cell secretory products kill a wide range of organisms, including bacteria, fungi, viruses and tumor cells (Aley et al., 1995).'  Lysozymes are 'cutters' -- they cleave and cut things, for instance, tumour/cancer cells and cell walls of pathogens that take a ride in our food.

Damage to the ileum and small intestines can lead to changes in microbial population and the disorder known as SIBO (small intestinal bowel overgrowth).  An expanding body of knowledge links SIBO with nearly every chronic systemic and skin disease seen in outpatient medicine (John Hopkins Turnbull, Mullin et al)

Bt toxin appears to induce self-digestion -- (increased Paneth cell and lysozymal activity) and damage from the inside out.  Lovely! And it is present in unborn children and adults.




References

Nutrient tasting and signaling mechanisms in the gut. II. The intestine as a sensory organ: neural, endocrine, and immune responses.
Furness JB, Kunze WA, Clerc N.
Am J Physiol. 1999 Nov;277(5 Pt 1):G922-8.

Adult Women’s Blood Mercury Concentrations Vary Regionally in the United States: Association with Patterns of Fish Consumption (NHANES 1999–2004)
Kathryn R. Mahaffey, Robert P. Clickner, Rebecca A. Jeffries
Environ Health Perspect. 2009 January; 117(1): 47–53.

Blood mercury reporting in NHANES: identifying Asian, Pacific Islander, Native American, and multiracial groups.
Hightower JM, O'Hare A, Hernandez GT.
Environ Health Perspect. 2006 Feb;114(2):173-5.

Pesticides in Shanghai and Globally

Pesticides May Cause USA Insulin Resistance and Obesity Trends

Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada. (FREE PDF)
Aris A, Leblanc S.
Reprod Toxicol. 2011 May;31(4):528-33.

Fine structural changes in the ileum of mice fed on delta-endotoxin-treated potatoes and transgenic potatoes [GMO Bt toxin] Free PDF
Fares NH, El-Sayed AK.
Nat Toxins. 1998;6(6):219-33.

Principles of Integrative Gastroenterology, Systemic Signs of Underlying Digestive Dysfunction and Disease, Turnbull, Mullin, et al.

Assessing Cumulative Health Risks from Exposure to Environmental Mixtures—Three Fundamental Questions
Ken Sexton, Dale Hattis
Environ Health Perspect. 2007 May; 115(5): 825–832.

Combined toxic exposures and human health: biomarkers of exposure and effect.
Silins I, Högberg J.
Int J Environ Res Public Health. 2011 Mar;8(3):629-47.

Thursday, November 25, 2010

Human Zoo and How to Cheat... Nudeln and Teigwaren sind Gift* für unsere Tiere


Translation

'Pasta and pastries are poisonous to our animals.'

Feeding the animals are forbidden...
Human-animals...??!

* Gift [German] = toxin, venom, poison = LECTINS, PHYTATES, GLUTEN




Hagenbeck Zoo
We just finished visiting the aquarium and zoo at Hagenbeck in Hamburg, Germany, one of the few progressive, privately owned zoos in the world. Each cageless biotope enclosure displayed harmonious groups of animals, surrounded by watery moats. Curious combinations included orangatuans + sea otters; hairy cheeked rabbits, guinea pigs, sparrows; etc. Images, Chinese muntjacs which wandered around freely on the zoo campus, along with one peacock, many Australian cavies and free-ranging chickens. Muntjacs are extremely friendly allowing my daughters and I to pet them on their heads and neck like a dog. My daughter named a pair Otis and Otissa!



Hagenbeck, One of First Conservationists
Mr. Hagenbeck was one of the world's first naturalist and conservationist.

Interestingly, his zoo in 1897 was on of the first to hybridize a male lion and female tigress... LIGER cubs. In South Carolina earlier this month, a liger cub was again born at a wild animal preserve, see HERE. Ligers are gigantic, larger than both lion fathers and tigress mothers. Nutso!! Reminds of other hybrid births (e.g. Twilight... and Neanderthal+H.s.s.)




CHEATING... On GFCF Diets

Thank God for technology.

Biotechnology has matched our paleo, grain-free, dairy-free GFCF diets (gluten-free, casein-free).






GUT DYSBIOSIS: Passively Paleo, Neolithically Advanced

On this trip because we were eating out of the house daily, we relied on factory produced pancreatic enzymes to break down, degrade and render HARMLESS gluten from grains and casein from dairy. Enzymes are 'cutters' in biological systems. They 'cut' things into smaller pieces. DNA and RNA are broken down to nucleotides by DNAses and RNAses. Meat/protein degraded to amino acids by proteases, collagenases, elastases. Veggie fibers by cellulases... starches by amylases, glucoamylases, maltases, phytases, pectinases, beta glucanases, xylanases, etc. Lactose (milk), lactases, galactosidases. Gluten, DPP-IV. Fats to fatty acids, lipases. Etc.

Enzymes work the best under optimal situations which many of us damaged by the SAD and other environmental and epigenetic factors does not apply to: acidity/pH, temperature and cofactors. For every degree less than optimal 98.6F, approximately 20% less enzymatic activity occurs.

After food is broken down to constituent basic units, optimal digestion requires optimal ABSORPTION which requires acidity/pH, temperature, cofactors including good gut bacteria for conjugation of vitamins, nutrients and bile acids (cholesterol derived 'detergent' factors) from the gallbladder and enterohepatic circulation.

Who has these???! Few. Even children have suboptimal digestion these days.

Are you a hard-gainer?
Is your body temp less than 98.6 F?
Do you have a gallbladder?
What percent is your diet raw? 100% 75% 50% 25% None???!

Dr. Francis Pottenger (Brent's relative) in his Empire study with cats reported that in cats, apparently 50% of the diet as raw maintained fertility and health in the cats, obligate carnivores. In humans, marine carnivores (obligate?? I would argue, YES) require what percentage? For cats, 100% raw diet, thrived. Having a partially raw diet confers active, raw, and/or fermented components including enzymes which help nutrients to be digested. Pottenger cats: Price-Pottenger video.

Prior animal pharm: Marine-Based Carnivory in Early H.Sapiens





Cheating

My sister 'M' introduced us to the below products. SHE IS A GENIUS and constantly scans the spectrum/ASD boards, forums and networks.

Products we like to cheat with *wicked laugh!*: [ found at amazon.com, local health food store, iherb.com]
(1) Peptizyde = broad spectrum plus GLUTEN-enzymes and CASEIN-enzymes; available in chewables for children as well
(2) Trienza = GLUTEN-enzymes and CASEIN-enzymes
(3) Glutenease = GLUTEN-enzymes and CASEIN-enzymes
(4) Digest Gold = broad spectrum digestive enzymes, POWERFUL strength
(5) Now SUPER ENZYMES = broad spectrum digestive enzymes PLUS OX BILE for those without perfect gallbladders.


Shame? Hardly... we're passively paleo, neolithically sophisticated and advanced (because we have to be to SURVIVE)...



Our French Thanksgiving
Happy Turkey Day!

Menu:
Wine, wine, wine
Carpaccio
Salad with Gizzards and Pâté
Country Pâté
Lamb Chops with Herbs
Lemon Tart
Crème brûlée
Chocolate Mousse
Espresso with cream
PEPTIZYDE + GLUTENease




Alizee, French Pop Princess

SWEET, WICKED and hilarious
'I'M FED UP (!!)... with single-minded extremists...
Je me prelasse voici... relax... It's my aquatic state...
Content... everything's delicious...
mildly offensive...'
red HAAAWWT goldfish on her cute *ss...

Monday, July 5, 2010

Animal Amour and Metabolic Networks


Les Nubians: Amour à Mort [Love Unto Death]
Courtesy Youtube.com


Dogsitting

We're dogsitting this weekend, K, a 3-year old blond lab who has the most warm beautiful hazel eyes. My second daughter calls them 'copper hazelnut' eyes. She loves bossing him around... *haaa* Being the youngest, she finally has someone. He's a darling, patient and immensely playful.


My Animal Farm Growing Up

I grew up around animals but I look at them with different eyes knowing some science now. We lost our 12-14 year old 3 cats over the last 4 years to thyroid conditions -- 2 had Grave's and one had diabetes (and I think undiagnosed hypothyroidism). As a kid in Pennsylvania, we raised 2 rabbits and 3 turtles. My parents who grew up around pigs and animals for consumption really did not take to the idea of pets but we still had pets. After moving to Sacramento in 1979 my parents bought a farmhouse off of Florin Road which had geese, ducks, horse stable, rabbits and pigeons. We brought back 2 rabbits and 4 pigeons to our suburban home and raised them along with our 2 hamsters, 2 fox terriers Phillip and Fluffy, Tiger our red Irish setter, and a fresh-water aquarium. On and off we had 'pet' earth worms, praying mantis, dragon flies. tadpoles/frogs and other assorted backyard creatures. *haa* Pure happy mayhem may have been a good descriptor. Well we grew older, busy with school and tennis and had to find new homes for our furry, feathery and scaled friends.


Hiking

Taking K hiking through the wooded Sunol park today I forget how animalistic animals are. Yes we had feline pets before but they were entirely domesticated except for the birds or cute mice they'd bring back for us for show. Actually 2 of our 3 cats were good hunters and brought back quite a few kills. Lynx would attack dogs and when one dog-owner approached us to note that Lynx must be sick because he stopped attacking her dog. We took him to the vet afterwards to learn he had Grave's hyperthyroidism.

Our temporarily adopted dog K tried to mark/impart his SCENT on every snag of vegetation, garbage can and tree during our hiking excursion. How can dogs urinate all day long?? Is it just 1-2 Tbs at a time?? He apparently was not interested in any of the raccoon or horse scat, but only other canine remains. Is it so hard-wired to be aware of other canines in the vicinity? What purpose? Territorial and reproductive instincts alone??

Most feline and canine eat only once a day. They are quite suited to intermittently fast routinely. Humans, are we so different? I don't think so.


Cunnane and Domesticated Fox

Cunnane writes in his epic book 'Survival of the Fattest' an interesting anecdote about the adrenal glands of a line of fox which are domesticated. He notes that the size of the adrenals shrink with domestication. Perhaps the constant necessity for testosterone, cortisol, progesterone and estrogen are no longer mandatory when food and survival are not ubiquitious requirements?

Is this what happened to humans with the advent of agriculture and animal husbandry?


Animal Husbandry?

WTF. Why such a name??? *haaa*




Human's Best Friend

Khyber is a great jogging partner. I took him on a couple trail hike/runs at Sunol and he did wonderfully -- matching my pace despite an annoying leash to his harness, leading me while not smelling every f*cking mark left from previous dogs, and somewhat providing protection. If a rattlesnake or mountain lion intersected our path, I do believe Khyber would have kicked into predator mode without a doubt and kicked some *ss. When we were in Mt. Shasta last week, we came upon rattlesnakes not only directly on our horse ride through the hills (to a SECRET cave *FUN!!!*) but also when we went to the waterside, we were cautioned that a young rattlesnake was found the night very close to the camps. Apparently it is unusual for rattles this time of year and the region -- the rain and recent change in weather plays a part apparently.


Metabolic Networks

When we were in Shanghai earlier this year, we met up with researchers who do research on Metabolic Networks which requires a strong background in physics, genomics, evolutionary biology, systems biology, bioinformatics, mathematics, biochemistry and a variety of other disciplines.

[Thank you LePine for your insights]

What I realize that is that we share so much homology with all living organisms, and this may go back to the first archebacteria 4 BILLION years ago (bya). Our mitochondria are the remnants of bacteria that have been push forwarded into mammalian cells. We can track the DNA signatures of the first life forms on earth to our mitochondria DNA which comprise of a humble set of 37 genes. Without mitochondria for energy systems, we would not have evolved.



Homology v. Complexity of Higher Life Forms

I think this diagram says it all (it actually crashed my computer twice). See citation #6. Homology exists between all life forms. Complexity however increases with increased skills of predation, IMHO. Humans are apparently at the apex of predation -- have taken over the earth and colonized every imaginable niche. (sometimes I think the bacteria have us by the GUT, pun intended *HAA*) Unfortunately our life form is also damaging earth in every imaginable niche as well -- terrestial, aquatic, and atmospheric...





'Red' Hotspots for Conservation of Individual Metabolic Pathways Between Archebacteria and all other Life Forms: Carb, Energy, Amino Acid, Nucleotide, and Lipid Metabolism

The 'red' color indicates greater than 90% of enzymes with significant DNA and protein sequence similarity. To appreciate our evolutionary past to 4 billion years ago, it is hard to escape our bacterial foundations that interact with our biology on every level: our metabolism, our gut, our pathogens, our immunity.


Longevity and Curing Cancer, Chronic Conditions and CAD

I would consider myself a strategist for conceiving longevity... I didn't plan it this way but by ameliorating a chronic condition with either pharmaceuticals or diet/lifestyle means, we are trying to improve longevity.

Mitochondria hold the the key between the balance between mTOR, SIRT-1, AMPK, and PPAR, as we've discussed before. These mini nuclear powerplants of energy production represent the link from our primordial past to the neolithic new world.

We are only as strong as our weakest mitochrondria...




Prior posts (Dr. Tourgeman, Dr. BG):

SIRT-1 -- (1) SIRT-1 (2) Aging and SIRT-1 (3) Evolutionary Skin and Muscles




References

1. Unusual pathways and enzymes of central carbohydrate metabolism in Archaea.
Siebers B, Schönheit P.
Curr Opin Microbiol. 2005 Dec;8(6):695-705. Epub 2005 Oct 26. Review.

2. Evolutionary aspects of whole-genome biology.
Doolittle RF.
Curr Opin Struct Biol. 2005 Jun;15(3):248-53. Review.

3. Distribution and phylogenies of enzymes of the Embden-Meyerhof-Parnas pathway from archaea and hyperthermophilic bacteria support a gluconeogenic origin of metabolism.
Ronimus RS, Morgan HW.

4. The unique features of glycolytic pathways in Archaea.
Verhees CH, Kengen SW, Tuininga JE, Schut GJ, Adams MW, De Vos WM, Van Der Oost J.
Biochem J. 2003 Oct 15;375(Pt 2):231-46.

5. Microbial behavior in a heterogeneous world.
Fenchel T.
Science. 2002 May 10;296(5570):1068-71. Review.

6. The conservation and evolutionary modularity of metabolism.
Peregrín-Alvarez JM, Sanford C, Parkinson J.
Genome Biol. 2009;10(6):R63. [Free PDF here.]

Sunday, January 10, 2010

(NSFW) Evolutionary Muscles, Skin, Fat

Fascinated Remix
(Offer Nissim, Courtesy of Youtube.com)



Questionable Trade-Off Between Sex and Longevity

I've wondered about this dichotomy -- can humans and other mammals have both sex and longevity? Nick Lane, author of Life Ascending, gives his deep, refined thoughts on this apparent contrast. 'The idea of a trade-off between sex and longevity was laid out by the British gerontologist Tom Kirkwood pictured exactly such a 'choice', on the economic grounds that ENERGY is limited and everything has a cost. The energetic cost of bodily maintenance must be subtracted from the energetic cost of sex, and organisms that try to do both simultaneously will fare less well than organisms that apportion their resources...'

This change that occurred in evolution when mammals internalized pregnancy and increased child-rearing from a few weeks to a few years may explain how the priorities in energetics shifted. It reminds me of other predators... bears, wolves and coyotes. Just like them, we invest a great deal of resources into teaching, reinforcing, enrolling into chest club, swimming lessons, golf camp, piano lessons and other preparations necessary for optimal success in life. Actually we invest VERY LITTLE in sex but MUCH MUCHO MORE in maintenance phases. The higher up the supposed predator food chain, the balance is FAR shifted toward maintenance phases, less sex. Nick Lane's theory is that 'In all cases, though, there is a choice, and in animals that choice is normally controlled by the insulin hormones.'



Behavioral budgeting by wild coyotes: The influence of food resources

Coyotes and wolves are quintessential survivors and clever companions. Dogs are pretty close. My daughter is reading a wonderful series called 'Wolf Brother' by Michelle Paver.

Coyote populations display a very curious 'negative relationship between coyote abundance and population growth' as these authors noted. Though increased litter size occurs with food abundance, 'There was also a hint that mean litter size may be correlated with food conditions under which females are reared, as opposed to conditions leading up to specific reproductive seasons (Knowlton and Stoddart 1983).'

COYOTE POPULATION PROCESSES REVISITED, Knowlton and Gese


Energy balance of the female of the species explains a lot. Certainly gender-specific nutrigenomics play a role. We are definitely more sensitive to the insulin resistant, pro-inflammatory effects of glucocorticoids and n-6 PUFAs than our male counterparts. Vitamin D (e.g. duration photoperiods), probably as well, esp if you believe the female-forager theories and division of labor.

Prior post (read end): n-6 PUFAs Cause Inflammation and Cancer: Israeli Experience



Energy Balance: Relates to Priorities in Mammalian Physiological Functions (SEX v. maintenance v. decreased population growth)

Bronson describes energy balance affecting reproduction in all animals. If the priority is survival and forwarding genetic material to the next generation, this all makes incredible and wonderful sense. Everything appears clear in light of evolution.

Climate change and seasonal reproduction in mammals. PDF free.



Evolutionary Skin

Recently, I started bikram yoga and... oh boy. It's H-O-T. One hundred four degrees F to be precise, in 40% humidity which grows during the 90min sessions. Skin is a big excretory organ (bigger than the KIDNEYS... *wink*). Sweating is a stellar way to detox whether it is during exercise or in a sauna -- the Japanese and Korean spend a lot of time in sauna-like hot baths; the Greeks luxuriate in hot mineral baths. After the class starts, within 5-10min every person in the room is dripping bodily fluids. Every sweat gland gets a workout. Even. My belly button's. In fact, it's gross but I discovered my knees SWEAT too.


Under My Skin: Subcutaneous Fat

Subcutaneous fat stores are anatomically located under the skin. Pinch an inch or grab a slab? (after holidays, the later for me) The quantity and quality of our storage fat and skin fluxes with the same hormones that affect our muscles.

See NephroPal: Evolutionary Muscles and Skin



Heat Shock Hormesis

I've discussed hormesis and how cold showers relate in an earlier post. Being BIONIC. This winter I've enjoyed much less cold showers... which last... OHHHH... ~1.4 seconds long. *haa*

Hot bikram yoga is a much more preferable way for me to achieve hormesis because both cold and heat shock induce mTOR changes.



More Hormesis

Skin is our largest organ (yes, it is). Surface area ~ 27 sq ft (2.5 sq meter) and weighs about 9 lbs. Each square inch contains about 230 ft (70 m) of nerves and 16 ft (~5 m) of blood arteries and veins. More vitamin D synthesis occurs in our skin when we are heated (no sunlight involved, just temperature factors alone). According to the below authors "The skin locally synthesizes significant amounts of sexual hormones with intracrine or paracrine actions. The local level of each sexual steroid depends upon the expression of each of the androgen- and estrogen-synthesizing enzymes in each cell type, with sebaceous glands and sweat glands being the major contributors." I think we can have it both ways... sex/hormones... and quality, disease-minimized lifespans... (1) controlling insulin (2) keeping mitochondria happy. Hormones and hormesis are indeed key players for power, sex and survival.

Sexual hormones in human skin.

Sunday, April 12, 2009

Coyotes and Shooting Stars

My offspring have been enjoying this Maple Story about a mother's love for her child (see end). Exactly... it's big tear-jerker. We love this story. (Wonderful music as well.)

Why are mammals primed to protect and sacrifice for offspring? Preservation and survival of the young are so deeply rooted and ancestral in the most highest functioning species. Remember hunting-with-implement dolphins?

Coyotes have been on my mind (!!sighted one in my neighborhood 1-2 mos ago *veryCOOL* Don't worry...my children are too big for them to attack/hunt... Our cat... on the other hand would make a nice meal). Are humans like coyotes... or domesticated dogs...? Does civilization makes us soft... like dogs (sorry, dog-lovers)?

  • "Coyotes (like other wild Canis species) have a complex and unusual mating strategy not often found in mammals; they are socially and perennially monogamous, and males assist in pup-rearing.... Coyotes maintain an evolved mating strategy that is uncommon among mammals (and absent in dogs in particular)." Quoted from the REPRODUCTIVE BIOLOGY OF THE COYOTE (CANIS LATRANS): INTEGRATION OF BEHAVIOR AND PHYSIOLOGY (click HERE) by Debra A. Carlson for her PhD degree in Wildlife Biology in Utah examined wild coyote reproductive behavior. An entire 'village' of coyotes support the rearing, feeding and growth of the pups born to the dominant male and dominant female of pack. "Among wild canines, it is thought that the strategic role of pseudopregnancy may facilitate the alloparental care given to pups by subordinate adult females residing with the parents (Asa 1997; Asa and Valdespino 1998; Kreeger et al. 1991; Mech 1970). Helper females bring food back to the den and defend the offspring of the dominant female; but more remarkably, in some species, they also have the capacity to suckle the infant young (coyote: Camenzind 1978; dwarf mongoose: Creel 1996)."
As I trek my kids to gymnastics, piano, drawing, Mandarin lessons and make hot breakfast/lunch/dinners (Paleo, gluten-free) and forage at Whole Foods market, I think, boy, an inordinate amount of resources are sure devoted to ensuring species continuation (well, theirs anyway). Right? Heart disease certainly seems counter-evolutionary in every respect for humans... as well as other predators like coyotes.Paleo-styled life provides the best insurance to progress, survive and evolve in these uncertain times.



BTW... wild coyotes have integrated dog mitochondrial DNA... In forensic medicine (eg, CSI stuff), analyzing mitochondrial DNA (mtDNA) is employed to identify human tissue and remains.

"Sequence analysis of the mitochondrial DNA control region from 112 southeastern US coyotes (Canis latrans) revealed 12 individuals with a haplotype closely related to those in domestic dogs. Phylogenetic analyses grouped this new haplotype in the dog/grey wolf (Canis familiaris/Canis lupus) clade with 98% bootstrap support." These researchers in Idaho however conclude that "The introgression of domestic dog genes into the southeastern coyote population does not appear to have substantially affected the coyote's genetic, morphological, or behavioural integrity. (Waits LP. Mol Ecol. 2003 Feb;12(2):541-6.)" Really...?


Happy Easter :)

My Eye: Maple Story

Kristine Mirelle - Magic
No Secrets - I'll Remember
Michelle Branch - Goodbye to You

Saturday, January 10, 2009

Brain: Be an Evolver

Recently the Wall Street Journal reported findings from marine biologists studying dolphins in Australia's Shark Bay. They found that a group of bottle-nosed dolphins had learned 'fishing' behavior, employing cone-shaped, net-like sponges to capture bottom-dwelling fish. Interestingly, another curious observation was that the mother dolphins taught this foraging/hunting behavior to both her male and female offspring, however only the female dolphins apparently picked up the behavior and continued to display the behavior.
Among Dolphins, Tool-Using Handymen Are Women: In a Sign of Animal Ingenuity, the Marine Mammals -- and One Cross-Dresser -- Are Seen Making Hunting Implements


In the deep, lucid channels of Australia's Shark Bay, wild bottlenose dolphins have discovered tools, raising provocative questions about the origins of intelligent behavior, the nature of learning and the birth of technology.

There, dolphins in one extended family routinely use sponges to protect their noses as they forage for fish hidden in the abrasive seafloor sand, Georgetown University scientists reported earlier this month.

As best the researchers can tell, a single dolphin may have invented the technique relatively recently and taught it to her kin. The simple innovation dramatically changed their behavior, hunting habits and social life, the researchers found. Those that adopted it became loners who spend much more time on the hunt than others and dive more deeply in search of prey. The sponging dolphins teach the technique to all their young, but only the females seem to grasp the idea. (Picture, quote: Courtesy of WSJonline.)


Does the ability to learn and adapt short-term to our ever-changing environment affect survival? Our personal survival? Our progenies' survival?


Be an... E V O L V E R.


Be teachable -- receptive to guidance.

The technology for disease reversal and the tools for lifespan extension already exist. Take advantage! Don't be a de-evolver. Or worse... extinct.

Don't struggle, failing to learn life's soft lessons.

Be blissfully better/bionic...brain...body...being...booty (j/k...NOT).

Stop slowing killing your kids... Here's Richard's take on this topic... (and... we have all been there!)


Consider:
--Grain-free eating (no wheat, no corn/rice, no gluten)
--Going Eat Wild (grassfed meat, wild seafood) and grain-free
--Grafting functional and muscle intense movement into your life
--Globally assessing health markers and optimizing to your specific youthful levels
--Guard against toxins (environmental, dietary, pharmaceutical, mind, etc)




Album: EVOLVER
John Legend "I love... you love..."

Courtesy of Youtube.com

Sunday, December 14, 2008

Vitamin D: SEX AND SURVIVAL

One the largest full moon will be observed next Friday night, it's reported. I still can't get wolves off my mind...esp since my children and I are completely mesmerized by the Planet Earth DVD series right now. One of my daughters was born in August -- the busiest time of the year for most OB/GYN/maternity wards around the country. As you know, we celebrated our first Paleo b-day party for her this year. Apparently she is hardly alone in celebrating a birthday in this month! In the U.S., August is the month with the highest birth rates according to a report by ABC News (we concur -- nearly got kicked out and diverted to another hospital the night of the impending birth since all the beds were full -- luckily one opened up *wink*):
Summertime Mystery: More Born, Less Die in August

If human mammals have 40-week gestation periods (10-lunar months) and you do the math....there are a lot of us participating in uuuummm...reproductive activities during this month of cheer, festivities, and mirth, December. How is Vitamin D vital to some of these uuummm 'processes' do you ever wonder?

Are we so different from wolves and bears? Obviously we are different species (bears, 38 chromosomes; wolves, 39; humans, 23) however hormonally we are very very similar:
--melatonin (from the pineal gland)
--testosterone
--estrogen
--progesterone (the 'pregnancy' hormone)
--vitamin D (sourced from sun and rich salmon catches; IDEAL: 60-70s ng/ml)
--PTH (breaks down bone to modulate blood calcium, esp when vitamin D is low; IDEAL PTH levels imo 10-20)
--thyroid hormones T3 T4 and related TRH (thyrotropin-releasing hormone) and TSH (thyrotropin)




Sex Hormones in Black Bears

Researchers of black bears compared sex hormone concentrations between between summer and winter seasons as well as pregnant v. non-pregnant bears. Guess what 3 things they discovered?

  • "We found that serum sex steroids measured in black and polar bears change independent of torpor. Therefore, our results suggest that photoperiod may be a more important regulator of serum steroid levels and reproduction than metabolic condition." (Bahr JM (no joke on the name) et al Biol Reprod. 1988 Jun;38(5):1044-50.)

  • "During starvation in summer, the bears could not inhibit the net production of urea but used lean body mass...The ability to preserve lean body mass during winter sleep apparently is a special mechanism associated with the induction of winter sleep. Bears cannot duplicate this feat during summertime starvation. In winter sleep, urea is formed and degraded but the nitrogen produced is conserved in some manner that maintains the total nitrogen pool constant....Arginase activity in liver increased in winter sleep; hepatic steatosis and inflammatory reactions were also noted." (Code CF et al. Mayo Clin Proc. 1975 Mar;50(3):141-6.)

  • "During winter sleep the black bear has decreased levels of serum total and free thyroxine (T4) and triiodothyronine (T3) and a prolonged, delayed response of serum thyrotropin (TSH) (bioassay) to thyrotropin-releasing hormone (TRH). Four weeks after the end of winter sleep, levels of serum thyroid hormones increase, and TSH response to TRH is short and brisk. Serum T4 and T3 rise after TRH administration both during and after winter sleep; however, the maximum increment in serum T3 is greater during winter sleep when the TSH rise is also prolonged and exaggerated. These observations suggest that transient hypothyroidism of possible hypothalamic origin occurs in bears during winter sleep." Nelson RA et al Effect of winter sleep on pituitary-thyroid axis in American black bear. Am J Physiol. 1979 Sep;237(3):E227-30.



Seasonality, Sex and Survival

The length of the day (photoperiod) triggers activation of Thyroid hormone in both the hypothalamus and the pituitary glands in the birds and the bees...well...specifically QUAILS as demonstrated in the latest scientific breakthrough in Nature (below). The same research group shows a similar outcome in mice...here in the prestigious PNAS Nov 2008.

  • Thyrotrophin in the pars tuberalis (PITUITARY) triggers photoperiodic response. "Molecular mechanisms regulating animal seasonal breeding in response to changing photoperiod are not well understood... Here we show cascades of gene expression in the quail MBH (hypothalamus) associated with the initiation of photoinduced secretion (read: UVB sunlight which also triggers vitamin D synthesis) of luteinizing hormone...Increased TSH in the pars tuberalis therefore seems to trigger long-day photoinduced seasonal breeding." Yoshimura T et al Nature. 2008 Mar 20;452(7185):317-22.

And yes in case you are wondering humans have VDRs (vitamin D receptors) all over the brain -- in the hypothalamus (McGrath JJ, J Chem Neuroanat 2005)and of course the pituitary (Diguez C Life Sci. 1997).

So what may signal an increase in Thyroid hormone in bears and humans? What extends the photoperiods and those warm, long, lazy summer days?

Did you know in humans, seasonality of Thyroid hormones are observed as they are in the above bear studies? HERE, HERE and HERE. The Pituitary-Thyroid-Hypothalamus-Gonad axis potently controls reproduction. I talk about the Pituitary and Hypothalamus a lot because these are the endocrine glands which produce the signals that impact the sex organs (gonads) to produce Estrogen, Progesterone, DHEA, Testosterone, etc. The sypmphony of hormone music is truly a monumental miracle -- all geared to produce one single event. Yes, it truly breaks down to one thing.

No...not the 'O'... silly, which aint a bad event...

Conception.

NON-IMMACULATE.

Survival of the species...

More and more trials and studies are coming out demonstrating how Vitamin D synergistically affects this awesome baby-making health axis.

Dr. Davis has now discussed how both the hormone of light (Vitamin D) and the hormone of darkness (Melatonin) controls and optimizes the cardiovascular system. Indeed, they actually optimize every system including the reproductive.



Degeneration Associated with Vitamin D Deficiency

The role of vitamin D to me appears central and pivotal for signalling mammalian bodies to prepare for reproduction/survival. By survival, I'm referring to survival of our lineage and paternal/maternal DNA. There are a few things non-conducive to that achievement...for instance, death is one. Death of either parent would diminish chances of passing on beneficial genes I would guess. Myocardial infarction or erectile dysfunction might be another. How is our survival linked to nutrients and optimization of survival? Dr. Bruce Ames has discussed the importance of achieving optimal levels of ALL micro- and macronutritients to prevent DNA damage and cancer here in his famous/infamous PNAS article (Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage.PNAS 2006 Nov 21;103(47):17589-94.); Magnesium deficiency accelerates cellular senescence in cultured human fibroblasts. Killilea DW et al. Proc Natl Acad Sci U S A. 2008). His research has shown that if even one nutrient (like, let's say folic acid) is omitted, DNA damage occurs in the lab animal just as if the lab animal sustained significant radiation damage. For heart disease, we at TYP understand the importance of obtaining nutrients for the benefits of reversal of atherosclerosis and plaque. This also absolutely extends to fertility and reproduction. I loved Dr. Schwalfenberg's organ review and the role of Vitamin D in every organ system HERE. Reproduction is one of the most important functions for survival (right?) and it was another organ system that unfortunately failed to get a mention (in addition to Parathyroid and Thyroid). So..."let's talk about S*X baby..." *wink*



Vitamin D From Sunlight

Do you feel sexier in the summer? High vitamin D (eg, long photoperiods/sunlight) appears to be correlated with high reproductive activities and characteristics which are conducive to reproduction, for example great skin/hair (estrogen), great muscles and physique (testosterone), amorous displays (testosterone) and libido (testosterone). Did you know that Vitamin D supplementation normalizes estrogen and testosterone (via aromatase)? In men with low testosterone, supplemenation can modulate and raise blood testosterone. In women, the same, with estrogen.

But let's be reasonable. Taking supplemental vitamin D is not going to make you an immortal god/goddess overnight.

But it will sure help.




Fertility and Survival

Both long-term survival (species) and short-term survival (individual) appear assured when both vitamin D and sex hormones are set within normal limits. At TYP, hormone replacement with vitamin D, bio-identical estrogen and testosterone have been shown to allow regression and eradication of plaque and heart disease successfully. Vitamin D of course is vital for reproductive health, and deficiency may have long-range survival consequences as we are finding out globally.

How many infertile couples do you know of? How many moms with PCOS (eg, wheat intolerance, insulin resistant, fish oil/vit D deficient) who can't naturally conceive? How many celebrity twins can you count being born annually? Or just the ones among your friends, family, acquaintenances and neighbors?



Vitamin D Deficiency Linked to Infertility, Low Sperm Counts, Maternal Pre-eclampsia, Pre-emies, and Premature Births, SIDS, Infant Mortality

FEMALE INFERTILITY AND MALE LOW SPERM COUNTS
Vitamin D is necessary for optimal health. Unfortunately the corollary is true and supported by the established and emerging medical literature. Deficiency leads to suboptimal health and particularly poor reproductive health...which translates to discontinuation of genetic information for some folks. At the end of October, researchers from Australia prospectively showed that Vitamin D supplementation increased sperm counts in infertile males. A year ago, my OB had told me about the use of Vitamin D in the fertility clinics to improve sperm counts. I couldn't find any prospective studies at the time and just forgot about it. Until now. It entirely makes sense to me.

Vitamin D Plays Major Role in Male InfertilityIn a paper presented to this week's Fertility Society of Australia conference (10/21/2008 reported here by ABC), Dr Anne Clark shows Vitamin D deficiency may play a major role in male infertility. Clark, medical director at the Fertility First assisted reproduction clinic in Sydney, says blood screening of 794 men who visited the unit found more than a third of them had vitamin D deficiency.

They were also found to be deficient in folate and had elevated levels of homocysteine, an amino acid in the blood associated with cell toxicity.
Among the couples where the male completed treatment for their nutritional deficiencies, just over half conceived naturally or with minimal treatment.


The finding comes out of a study by
University of Sydney doctoral student Laura Thomson who is investigating DNA fragmentation of sperm, a significant factor in male infertility. DNA fragmentation of sperm is most often the result of cellular damage resulting from infection, smoking or advanced paternal age.

Clark says their findings add weight to a European study earlier this year that shows women's vitamin D levels strongly correlate with their ability to conceive.


Surprise"Vitamin D and folate deficiency are known to be associated with infertility in **women**, but the outcomes of the screening among men in our study group came as a complete surprise," she says.
She says concerns about skin cancer resulting from exposure to ultraviolet rays could be a contributing factor to vitamin D deficiency among men, along with work and lifestyle choices to avoid too much direct exposure to sunlight. "The amount of sun needed is just 10 to 15 minutes a day outside the heat of the day," she says. If workers had their morning tea break outside with their sleeves rolled up they would absorb sufficient vitamin D, Clark says. In response to the screening results, Clark says 123 of the men agreed to a program that included changes in lifestyle and diet such as quitting smoking, reducing caffeine and alcohol intake, and losing weight.

Results (sorry--couldn't find the paper -- don't know the vitamin D dose)
The men were also asked to take antioxidants and a multi-vitamin for two to three months, Clark says.
--She says the lifestyle changes led to a 75% reduction in the level of sperm fragmentation among the 123 men.
--"We also observed improvement in the shape of sperm, which can enhance conception," Clark says.
--Forty pregnancies had been achieved among the group, with more than half of those pregnancies occurring naturally or with minimal intervention such as intrauterine insemination.
--Clark says there were only three miscarriages (6%) among those pregnancies. This compares with an average 22% miscarriage rate among women using fertility treatment, she says.



Animal studies have long supported the important role of vitamin D in reproduction:



MATERNAL PRE-ECLAMPSIA
Pre-eclampsia is on the rise...like vitamin D deficiency is. Connection? yes. Preventable? absolutely yes. Pre-ecampsia is a life-threatening condition leading to hypertension and early kidney damage in pregnant women usually presenting in the 2nd or 3rd trimester. BP drugs and strict bedrest (eg, not even getting out of bed to pee, no joke).


If vitamin D is a steroid and during pregnancy, the pregnant woman is making 10-TIMES more steroids to grow, sustain, and harbor a growing fetus, what do you think occurs if the mom starts out vitamin D deficient? Or what if she starts out critically vitamin D deficient -- like many women who abhor the sun for vanity (I may be part of this group *wink* and because I was deathly allergic to sun when I was wheat-addicted) and/or wear sunscreen and makeup...what might occur? Can you imagine what might occur as the mom's body starts to run out of the raw materials (cholesterol and vitamin D) to make estrogen, progesterone and oxytocin?

Not good things?

Pre-eclampsia, pregnany-related hypertension, proteinuria, kidney failure, and potential maternal and/or fetal death to name a few.

Fetal neurologic and autoimmune disorders.

Perhaps sowing the seeds for future heart disease? Perhaps the vitamin D deficiency of OUR mothers is currently affecting OUR generation? And future generations.

As we reviewed in the last post, vitamin D regulates our blood pressure by affecting the angiotension-renin-kidney system. Pre-eclampsia is basically a critical hormone and vitamin D imbalance.

  • [Vitamin D deficiency in recently pregnant women] The authors enrolled n=89 pregnant and new moms and found 80% were vitamin D deficient with 25(OH)D less than 30 ng/ml (which means 99% were PROBABLY low less than 60 ng/ml). The scientists conclude that "Our data show that vitamin D supplementation of pregnant women (400 IU/day) is not enough and that 25VTD deficiency is not diagnosed in this high-risk population. Children born from deficient mothers will present a higher risk of suffering from bone mineral diseases as well as other pathologies, as type 1 diabetes or neurological disorders. Of course, this insufficiency will also have an impact on mother's bone reserve, but these mothers will also be at higher risk for preeclampsia." Emonts P et al. Rev Med Liege. 2008 Feb;63(2):87-91.

  • Vitamin D deficiency in pregnant New Zealand women. "RESULTS: 87% of women had 25-hydroxy vitamin D levels below 50 nmol/L (20 ng/ml). 61.2% of women had a vitamin D level below 25 nmol/L consistent with severe vitamin D deficiency. 10 women had an elevated parathyroid hormone consistent with secondary hyperparathyroidism. Only 22% of our patients were veiled, and included a diverse ethnic population, including African, Maori, European, Middle Eastern, and Polynesian women. CONCLUSIONS: Vitamin D deficiency is common in young pregnant women in this general practice, and it was not only confined to veiled women or women with dark skin. This highlights the magnitude of vitamin D deficiency in the pregnant population in a New Zealand setting; this vitamin D deficiency is responsible for the re-emergence of childhood rickets." Eagleton C et al N Z Med J. 2006 Sep 8;119(1241):U2144.
  • Pre-eclampsia: A challenge to public health teams worldwide to ensure that maternal diets contain adequate levels of folic acid, n3 polyunsaturated fatty acids and vitamin D at conception. Garratt FN.
    Public Health. 2008 Dec 4. [Epub ahead of print] No abstract available.
    PMID: 19058819 [PubMed - as supplied by publisher]
  • Does vitamin D supplementation in infancy reduce the risk of pre-eclampsia? The authors in Finland showed that: "We used data on 2969 women born in the Northern Finland Birth Cohort 1966 of whom 68 (2.3%) had pre-eclampsia in their first pregnancy. Risk of pre-eclampsia was halved (OR 0.49, 95% confidence interval (CI) 0.26-0.92) in participants who had received vitamin D supplementation regularly during the first year of life and this association was not affected by adjustment for own birth order, birth weight, gestational age, social class in 1966 and hospitalizations or pregnancy-induced hypertension of their mothers. Together with earlier observations on a reduced risk of type 1 diabetes after vitamin D supplementation, these data suggest that vitamin D intake in infancy may affect long-term programming of the immune response pattern." Pouta A et al. Eur J Clin Nutr. 2007 Sep;61(9):1136-9.
  • Prevention of preeclampsia with calcium supplementation and vitamin D3 in an antenatal protocol. Japanese researchers prospectively reduced 37% of pre-eclampsia in high risk cases (as identified by an angiontensin test) with calcium 152-312 mg/day and vitamin D3 supplementation (sorry--didn't understand their dosing 0.5 micrograms per/3 day?) Int J Gynaecol Obstet. 1994 Nov;47(2):115-20.



INCREASED FETAL MORTALITY, PRE-EMIES, SUDDEN INFANT DEATH SYNDROME
Actually little literature exists specifically on this subject (that I could find). SIDS is probably multi-factorial. In utero development of the innervation of the lungs and brain are likely key to susceptilibity factors. I did however find one report which showed low vitamin D levels in all cases of premature and infant death cases.

  • Serum 25-hydroxyvitamin D concentrations in sudden infant death syndrome. The lower the vitamin D blood concentrations, the lower the survival rate in these unfortunate babies studied. The author was trying to show no association but if normal 25(OH)D is 60-70 ng/ml then these babies had severe vitamin D deficiency. The levels measured were: "25-OHD was 19.0 +/- 7.9 mg/ml in SIDS, 16.9 +/- 5.2 ng/ml in acute death control infants, and 11.9 +/- 4.4 ng/ml in in-hospital deaths. For four "near miss" infants the mean serum 25-OHD concentration was 21.1 +/- 4.1 ng/ml. The mean serum 25-OHD concentration of 39 living premature or small-for-gestational-age infants at 3 months of age was 26 +/- 9.9. " Haddad JG et al Pediatrics. 1980 Jun;65(6):1137-9.




Perez-Lopez ties it up well for me (Gynecol Endocrinol. 2007 Jan;23(1):13-24)

Vitamin D: the secosteroid hormone and human reproduction
"Vitamin D is a secosteroid with an endocrine mechanism of action which is sequentially synthesized in humans in the skin, liver and kidneys. The active hormone, 1alpha,25-dihydrocholecalciferol [1,25(OH)2D3], is often considered only in terms of its role in controlling calcium and phosphorus homeostasis. However, cumulative evidence points to the presence of vitamin D receptors in many tissues. The present article summarizes key points regarding the participation of vitamin D in pregnancy and breastfeeding. During pregnancy, sufficient vitamin D concentrations are needed not only to address the growing demand for calcium on the part of the fetus, but also to participate in fetal growth, development of the nervous system, lung maturation and fetal immune system function. Hypovitaminosis D has been related to the development of diabetes, pre-eclampsia and fetal neurological disorders. During pregnancy and lactation, calcium from the maternal skeleton is mobilized, with a rise in bone turnover and a reduction in bone mass. It is advisable for pregnant and nursing women to maintain adequate levels of vitamin D, through small doses of solar exposure to facilitate natural formation of the hormone or by ingesting appropriate vitamin supplements."


Next post: More Vitamin D Dosing and Non-toxicity