The Travis Corner

[ecstatichamster]

@Travis Dr. Peat says raw vegetables are indigestible. To me it stands to reason that they rot in the colon and create a legion of bacteria and fungus. I think you may be fine because you are hyper thyroid and fast gut motility, but older people probably shouldn't have raw veggies in these quantities, I wouldn't think, as the rotting would overwhelm their livers with the endotoxins. That's how I understand it. Not well obviously, LOL.

 

[Optimus]

....and like to cut all vegetables into long strands and eat them with chopstix.

I wonder if this is helpful (as also in case of raw carrot longitudinal shreds) because once we chew it aren’t we anyway breaking them down much further?

 

[Travis]

@Travis Dr. Peat says raw vegetables are indigestible. To me it stands to reason that they rot in the colon and create a legion of bacteria and fungus. I think you may be fine because you are hyper thyroid and fast gut motility, but older people probably shouldn't have raw veggies in these quantities, I wouldn't think, as the rotting would overwhelm their livers with the endotoxins. That's how I understand it. Not well obviously, LOL.

Sir,

It is certainly true that not everything is digested. Everybody knows this, my sad cat informs me of that. However: the differential digestibility of certain fractions of fibre has been thoroughly investigated with the thoughtful collaboration from intubated out-tubated patients, sans ileum, and others described as being 'normal.' It had been eventually determined from this scientific inquiry that cellose had been digested by 80% and hemicellulose by 96%. This of course has implications for food value charts, those which generally consider β-linked polysaccharides as indigestible and thus contribute no energy. Cellulose is composed of β-linked glucose units with no branching: Hemicellulose, though not strictly defined, consists of a mixed-bag of various β-linked constructs of every monosaccharide imaginable besides kitchen sinccharide: i.e. xylose, mannose, galactose, rhamnose, arabinose. I feel that it's worth noting that humans don't have instructions for a cellulase enzyme in their dNA, implying of course that some undefined microbe is responsible for this. Yet the question remains: What species microbe had been responsible for this hydrolysis of β-linked glucose in entero?

Holloway, W. D. "Digestion of certain fractions of dietary fiber in humans." The American journal of clinical nutrition (1978)

Lignin had not been digested at all. Structurally: lignin is a radical departure from the other two dietary fibres, consisting of crosslinked phenols and being similar to melanin in form. The monomers are reminiscent of deaminated tyrosine alcohols with various degrees of ring-hydroxylation; these are given such names as coniferyl and sinapyl alcohol. And like melanin, it has the appearance of being a photocatalyzed polymer. The phenol ring absorbs energy in the UV region, thereby exciting electrons into higher-energy bonding orbitals. Lignin is somewhat like a natural UV-cured polyurethane, and we cannot ever expect any person or anything—and not even heat—to ever break it down. Lignin is used in paper making.

'I have consulted my crystal ball, and it informs me the end of the world will occur when life becomes fully-displaced by sheets-upon-sheets of indestructible lignin polymer.' ​

Besides the microbiota shift that can be result from a frequent ingestion of certain strands of indigestible fibre, and 'indigestible'-yet-really-80%-digestible fibre, we also have to consider the effects of cooking. My impression is that while cooking could perhaps nudge cellulose digestibility towards the perfect 100%, it would almost surely collapse the native food matrix and liberate bound oxygen. I would imagine that cooking could result in a more hypoxic food matrix, shifting the normal microbiome from the aerobic towards and anaerobic. Native bacterial leaf-flora would most surely be killed, transforming the Lactobacilli-rich cabbage into a sterile wilt. Resulting from this heat process: what could have previously been considered a Gram-negative inhibiting probiotic leaf becomes Gram-negative neutral, and fair game for just about any enteral strain of bacteria.

Endotoxin derives solely from Gram-negative bacteria and does so by definition. The endotoxin is specifically what repels the famous Gram strain which most bacteria readily assimilate. Endotoxin stimulates neutrophils to attack, and even serves as a chemotactic agent. For this reason, you could expect endotoxin-rich intestines to have increased concentrations of neutrophils and their characteristic protein products, such as calprotectin. Considering calprotectin concentrations to be convenient, reliable, and proportional estimations for neutrophil activity: endotoxin concentrations can be inferred by calprotectin.

Poullis, Andrew. "Bowel inflammation as measured by fecal calprotectin: a link between lifestyle factors and colorectal cancer risk." Cancer Epidemiology and Prevention Biomarkers (2004)

Andrew Poullis also takes the view that calprotectin is a useful proxy for neutrophil activity, and measured its levels in 325 Londoners who'd previously completed a lifestyle questionnaire. Included therein had been questions concerning food, notably the intake of 'fruit' and 'vegetables'—excluding the potato. Excreted calprotectin had varied greatly, yet it had been crudely correlated with age and activity. After adjusting for age and aspirin use, two considerable confounders, he had teased-out a better correlation between 'fibre intake' and calprotectin.

'Fruit and vegetable consumption was classified as number of pieces/portions/servings per day; potatoes were not included.' ―Poillis

'The consistency of the results of repeat testing on different days suggests that fecal calprotectin levels are stable on a day-to-day basis and a reflection of a chronic process.' ―Poillis

'The fecal calprotectin levels in our study population were lower than published levels in subjects with IBD, but they do overlap, with 24.7% of our population having fecal calprotectin levels above the reference range.' ―Poillis

'These relationships are demonstrated in Fig. 2. After correction for age, sex, stool form, NSAID use, and serum CRP the relationship of fecal calprotectin and BMI was lost, and the relationships found for fiber intake, physical activity, and age all remained.' ―Poillis​

'The colon is a reservoir to a huge volume and number of bacteria; dietary fiber reaches the colon where it is fermented by bacteria causing changes to the species distribution of the bacterial flora. A diet low in fiber and vegetables may promote the growth of more unfavorable microbial species.' ―Poillis

'The discovery that an easily measurable fecal protein reflects a number of lifestyle risk factors for CRC gives insight into the possible mechanism behind which the environment host interaction leads to CRC and provides a means by which environmental risk factors for CRC may be dissected from confounding factors.' ―Poillis

'Role of Funding Source. The study was funded by a private research study fund. [Whose?]The funding source had no involvement in the design, collection, and analysis of data or interpretation of results.' ―Poillis

'Physical activity could result in reduced levels of bowel inflammation due to enhanced vagal and reduced basal sympathetic tone.' ―Poillis​

I had initially thought that endogenous Bacteroides fragilis could have something to do with this. This is a normal Gram-negative anerobic bacteria found in the human digestive tract, yet it's endotoxin has an apparent reduced antigenicity—as compared to your classic Neisseria meningitidis endotoxin.

Kasper, Dennis L. "Surface antigens as virulence factors in infection with Bacteroides fragilis." Reviews of infectious diseases (1979)​

Yet Klebsiella pneumoniae is also considered a 'normal' Gram-negative inhabitant of humans, yet this one having considerable endotoxic activity. Klebsiella pneumoniae can kill people—if you consider alcoholics 'people' like I sometimes do—and hence could reasonably be considered a potential candidate:

Jong, Gou-Mou. "Rapidly fatal outcome of bacteremic Klebsiella pneumoniae pneumonia in alcoholics." Chest (1995)

'The overall mortality was 64.3% . The most dramatic group was that of ll patients (39.3% ) with bacteremic Klebsiella pneumoniae pneumonia, which had high mortality rate (100% ), short onset of illness before hospital admission (42.6 ± 8.2 h), and short survival time after the admission (24.6 ± 7.9 h). ―Jong

'High virulence of the microorganism, altered immune response, and increased susceptibility to infection may all have contributed to the fulminancy in this group of patients.' ―Jong
​

Highsmith, Anita. "Klebsiella pneumoniae: selected virulence factors that contribute to pathogenicity." Infection Control & Hospital Epidemiology (1985)​

'Mice that are resistant to the lethal effects of endotoxin have a generalized defect of their B lymphocytes, macrophages and fibroblasts that render them incapable of responding to endotoxin.' ―Highsmith

'The role of endotoxin in virulence is unclear. Recent studies have shown that strains of K. pneumoniae differ in the quantity of endotoxin produced and that these differences correlate with the amount of low molecular weight lipid A produced. Differences in endotoxin production or in lipid A or LPS structure may be associated with differences in virulence because even minor differences in lipid A structure can profoundly alter endotoxin activity.' ―Highsmith​

'...because even minor differences in lipid A structure can profoundly alter endotoxin activity.' ―Highsmith

'...even minor differences in lipid A structure can profoundly alter endotoxin activity.' ―Highsmith​

I have noticed a trend between omega−6 fatty acids and immunogenicity, and endotoxin composition could be one of them. For instance: leukotriene B₄ has 5000 × the chemotactic potency as leukotriene B₅; the former is the lipoxygenase product of arachidonic acid (20∶4ω−6), and the latter analogously derives from eicosapentaenoic acid (20∶5ω−3). Leukotriene B₃ is a product of Mead Acid (20∶3ω−9), and this has a fourfold reduced potency as compared to leukotriene B₄. Even the barely-modified 13-hydroxylinoleic acid has substantial chemotactic activity for neutrophils. Endotoxin has a lipid end, and should it's antigenicity be determined by its fatty acid composition I would bet omega−6 fatty acids—e.g. arachidonic, linoleic, γ-linolenic—would tend towards enhancing it.

 

[Travis]

Why not eat macadamias instead?

I have, and these are great; a good place to buy them, in my opinion, is from Ebay.com. Hawaiian farmers sell them by the pound, and once you master the ancient Judo triple-tap hammer technique the opening becomes a joy. I had since given up on almonds completely, and now often buy whole coconuts from the grocery store. I would imagine that I am getting rather low in omega−6 fatty acids by now, and could perhaps even be synthesizing Mead Acid at this point. I wish individual fatty acids were easier to measure, as I'd be fun to make a contest out of Mead Acid levels.

 

[Wagner83]

@Travis what do you think are the specific roles of dietary fat which cannot be fulfilled by glucose intake?

 

[Travis]

I have read that mk-4 stimulates the expression of interleukin-6. I understand it's necessary in the realization of the adaptation stimulated by mechanical stress of skeletal muscle, but is there a chance supplementing k2 could cause an issue with too much IL-6?

I don't think so, not after reading this:

Reddi, K. "Interleukin 6 production by lipopolysaccharide-stimulated human fibroblasts is potently inhibited by naphthoquinone (vitamin K) compounds." Cytokine (1995)​

 

[Travis]

@Travis what do you think are the specific roles of dietary fat which cannot be fulfilled by glucose intake?

There is only one exogenous fatty acid that appears essential, and that is for producing cell membrane DHA. The entire spectrum of saturated fatty acids can be synthesized directly from either fructose and glucose, and a full set of omega−9 fatty acids can be then desaturated from those. Most cell membrane fatty acids appear to be phosphoglyceride esters of: myristate, palmitate, stearate, and oleate; while myelin lipids appear composed primarily of: stearate, sterols, and serine. All but serine can be produced de novo from glucose, and serine needs merely a spare amino group to be a Krebs cycle spin-off.

We have elongation and desaturation enzymes in place with high affinity towards omega−3 fatty acids. Upon ingestion of α-linolenic acid (18∶3ω−3), this will eventually be elongated and desaturated to such an extent as to become full-length docosahexaenoic acid (22∶6ω−3). This lipid actually appears necessary to maintain a low-density and relatively-hydrophilic membrane needed for high glucose flux, and also has the high-kinetic energy tip—ranging from ω to ω−3—needed for maximum sterol exclusion. The alternative to DHA is osbond acid (22∶5ω−6), a linoleic acid elongation product that becomes progressively incorporated as DHA content falls. Osbond acid lacks some of DHA's sterol-excluding functionality, and also has precursors of heightened immunogenicity. The requirement for fatty acids, as far as I can tell, boils down to trace amounts of α-linolenic acid (18∶3ω−3). The amount necessary is practically unavoidable, and the real danger is consuming enough ω−6 as to dilute & displace it through competition for elongation and desaturation enzymes.

 

[Wagner83]

Thanks!

 

[ecstatichamster]

Thank you @Travis !

 

[nwo2012]

@Travis you are something a little special around here for sure.

 

[Travis]

@Travis you are something a little special around here for sure.

(Tommy has just told a story that's cracked up the entire company of gangsters at a table)

Henry: (laughing hard) Really special. Really special.
Tommy: Whattya mean I'm special?
Henry: You're just special, y'know, the story. It's special. You're a special guy.
Tommy: Whattya mean? They way I talk? What?
Henry: It's just, y'know, it's just special, you know the way you tell the story and everything ...
Tommy: Special how? I mean, what's special about it?
Anthony: (worried) Tommy, no, you got it all wrong ...
Tommy: Whoa, whoa Anthony! He's a big boy, he knows what he said. What'd you say? Special how? What?
Henry: Just you know you're special.
Tommy: You mean, let me understand this ... cuz I ... maybe its me, maybe I'm a little ****88 up maybe. I'm special how, I mean special, like Down syndrome? I amuse you. I make you laugh? I'm here to ******' amuse you? Whattya you mean special? Special how? How am I special?
Henry: I don't know just ... you know how you tell the story. What?
Tommy: No, no I don't know. You said it. How do I know? You said I'm special. (yelling now) How the **** am I special? What the **** is so special about me? Tell me. Tell me what's special?
(Long suspenseful pause.)
Henry (cracking up): Get the **** outta here!
(everyone laughs, the tension is gone)
Tommy: Ya ************, I almost had him! I almost had him! You stuttering prick here! Frankie, was he shaking? I wonder about you sometimes, Henry. You may fold under questioning!!

 

[tfcjesse]

Now go home and get your shinebox

 

[Wagner83]

Do you think a lack of dietary fat could clog the gallbladder?

---
For no particular reason I stumbled on this:
Octanoic acid prevents reduction of striatal dopamine in the MPTP mouse model of Parkinson's disease. - PubMed - NCBI

 

[Travis]

Now go home and get your shinebox

I was thinking if Joe Pesci were a verb, it would necessarily have to be reserved for a pen-stabbing event. For example:

Inmate #1: What had gotten you into solitary confinement?
Inmate #2: I, uh.. . I Joe Peschied the ***t out of my lawyer.
Inmate #1: Oh god, Jesus. I hope it wasn't a Montblanc Classique or Dixon Ticonderoga? We need all those we can get!
Inmate #2: Nope. It was a, uh.. . It was a Uniball Classic, with a, uh.. . a fine .7 mm tip.
Inmate #1: What color?

 

[Travis]

Do you think a lack of dietary fat could clog the gallbladder?

Clog it with what?

 

[Wagner83]

Clog it with what?

By not stimulating bile release enough so it stagnates I guess:

(courtesy of tca300)
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI
--
Eating LOW FAT Leads To Serious Gall Bladder Problems

I guess there are more than one way to stimulate bile flow.

 

[Inaut]

off topic once again..my apologies

@Travis what do you think about coconut or black vinegar over apple cider?

 

[Travis]

By not stimulating bile release enough so it stagnates I guess:

(courtesy of tca300)
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI
--
Eating LOW FAT Leads To Serious Gall Bladder Problems

I guess there are more than one way to stimulate bile flow.

That's anecdotal. This study here uses 390 people, and gallstones had been confirmed via ultrasonography.

Misciagna, Giovanni. "Diet, physical activity, and gallstones—a population-based, case-control study in southern Italy." The American journal of clinical nutrition (1999)​

 

[Travis]

off topic once again..my apologies

@Travis what do you think about coconut or black vinegar over apple cider?

Oh no, this is all perfectly relevant. This runs into endotoxin territory and, uh.. . The Primo Pizza of Miami Beach really does use Balsamic vinegar in their 'Joe Pesci' sandwich.

Acetobacter are a Gram-positive aerobic genus completely compatible with humans. They completely lack endotoxin and macrophages do not recognize their cell wall polysaccharides. Acetobacter are so nonimmunogenic that calling them 'friendly' would be an understatement, and on account of alcohol dehydrogenase expression they can be seen to enhance clarity. Ethanol, tryptophol, and tyrosol are three such yeast alcohols that can be retro-converted back into their corresponding carboxylic acids—i.e. acetic acid, 4-HIAA, 4-hydroxyphenylacetate—through the action of Acetobacter's alcohol dehydrogenase.

Daneshmandi, Saeed. "Modulatory effect of Acetobacter xylinum cellulose on peritoneal macrophages." Immunopharmacology and immunotoxicology (2011)

Apple cider vinegar, above all, is sieg-heiled to überstatus among authors of articles on alternative health and diverse diet gurus. I can see no logical reason for this, at all, since every raw fruit vinegar has the exact same Acetobacter species in similar proportions. As long as a particular fruit vinegar has not been pasteurized, it should be more-or-less similar in biotic composition to every other unpasteurized vinegar. The differences in small molecule classes such as: flavonoids, terpenoids, and coumarins could be seen as insignificant; even if they somehow were, they cannot account for apple cider cultism because such considerations are never found in their scripture or used to justify cider superiority in any way. Although bacterial cell counts could certainly be higher in certain batches, I wouldn't think this could be reliably ascertained through scientific publications currently available.

Yet coconut vinegar and black vinegar are not fruit vinegars, and thus might be assumed to be radically different in microbial demographics. Let us examine these two vinegar forms further:

Perumpuli, P. A.."Identification and characterization of thermotolerant acetic acid bacteria strains isolated from coconut water vinegar in Sri Lanka." Bioscience, biotechnology, and biochemistry (2014)

'From the pellicle formed on top of brewing coconut water vinegar in Sri Lanka, three Acetobacter strains that grow at 42 °C and four Gluconobacter strains grow at 37 °C were identified as Acetobacter pasteurianus and Gluconobacter frateurii, respectively. Acetic acid production by the isolated Acetobacter strains was examined. All three strains gave 4% acetic acid from 6% initial ethanol at 37 °C, and 2.5% acetic acid from 4% initial ethanol at 40 °C.' ―Perumpuli​

Okay: coconut water vinegar seems very similar to fruit vinegars, so close that I would assume them practically equivalent. Of course, this says nothing about its organoleptic properties: I do like drinking coconuts when they don't taste 'off,' yet I cannot even comprehend what coconut vinegar would taste like.

Black rice vinegar a different animal with a new twist. Just as with you run-of-the-mill fruit vinegar, that made from rice also involves Saccharomyces cerevisiae followed by Acetobacter aceti. Yet even before that, however, rice vinegar production involves Aspergillus oryzae: The infamous Japanese soy sauce mold. [Sound of thunderstrike.. . being progressively diluted by the screams of Japanese in stomach pain.] Endotoxins have been described in black rice vinegar, especially in 'Brand A.' If you ever see the vinegar labeled as 'Brand B' at your local grocery store it could be very well to buy that one:

Hashimoto, Masahito. "Separation and characterization of the immunostimulatory components in unpolished rice black vinegar (kurozu)." Journal of bioscience and bioengineering (2013)

'Since FK-OS2 [lipophilic vinegar fraction] contains the LPS described above, we consider it likely that the TLR4 ligands in kurozu are LPS. At a concentration of 10 mg/ml, FK-OS2 induced TNF-α production in murine spleen calls, whereas it only slightly induced IFN-γ production at concentrations of up to 1 mg/ml .' ―Hashimoto

'The yield and AC₅₀ data obtained in the above experiment demonstrated that Fukuyama kurozu is at least 2.5-fold more immunostimulatory than brand B kurozu.' ―Hashimoto

'We detected ladder patterns in the SDS-PAGE profiles of FK-OS2, which was found to contain 3-hydroxy fatty acids, suggesting that LPS are present in these fractions.' ―Hashimoto​

On the small metabolite front: you might suspect ochratoxin, gliatoxin, and aflatoxin to be present in anything inoculated with Aspergillus—intentionally or not. Gliatoxin enhances the invasiveness of Aspergillus in humans and is quite dangerous, yet since it has a redox-labile disulfide bond this would be too unstable to persist. Ochratoxin will concentrate and the kidneys and is responsible for cancer in Baltic grain-eaters, yet aflatoxin is indisputably the more dangerous and potent metabolite. Aflatoxin will induce liver cancer in nanomole concentrations, yet it is also claimed to be 'not produced by Aspergillus oryzae.'

'Aflatoxin is not! produced by shoyu Koji mold (Aspergillus oryzae), and green tea very good for prostate.' ―Official Slogan of Japanese Biochemical Society​

I would be weary of rice vinegar, yet trace concentrations of mold fragments could help keep a person's immune system on red alert against Aspergillus species, spores of which are inhaled daily by the dozens due to their unusually small nature. Aspergillus species are considered 'the weeds of the culture room,' so much that its presence in human biopsy samples is routinely ignored as 'artefact.' This practice confounds the accurate apprehension of its prevalence, yet it has been found in arthritic joints. Aspergillus is also responsible for more respiratory infections than any other and for these reasons I'd assume it rather common. Aspergillus also secretes an 18 kDa ribotoxin that binds host ribosomes, thereby eliciting autoantibody formation against nucosome–ribotoxin fragments subsequent of cell lysis. These antibodies can then cross-react with the host's nuclear proteins, inducing symptoms indistinguishable from lupus.

 

[Inaut]

thanks for the quick and extremely informative post---once again