I reported the increase in motility and improvement in health a few times on the travis corner, in fact I'm about to share more via private message, I also posted about a suspicious pineapple fast which cures all disease and clears the gallbladder. I had found this after noticing that it had the ability to trigger something in what felt like the gallbladder, followed by BM. The pineapple + coffee in the morning is great to get the digestion going. I also feel like pineapples can be the real safe fiber salad that Ray always wanted (but carrot don't work for me and other things seem to irritate digestion, I didn't try the ground mushrooms), other fruits ain't the same. Perhaps brobro and the rest prevent fermentation and have a cleaning effect.
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"When A Turk's Bowels Move Less Than Three Times A Day, He Consults A Physician."
- Thread starter Amazoniac
- Start date
griesburner
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does pineapple juice from a store work the same as eating fresh sliced whole pineapple? i prefer the juice tastewise and its ready to use instantly. i hate to preper a whole pineapple everyday and its more difficult to find a quality fresh fruit during the whole year.
I'm not you can compare the two unfortunately as I don't know what's left in it (bromelain, vit C, manganese etc..) nor what was there in the first place (fruit ripeness). You can always try, I'd be wary of acidity.
griesburner
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yes i am currently trying it and after a big glas had a bowel movement^^ but that could sure be coincidence
https://raypeatforum.com/community/threads/the-travis-corner.21611/page-68#post-356294yes i am currently trying it and after a big glas had a bowel movement^^ but that could sure be coincidence
Travis
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"When A Turk's Bowels Move Less Than Three Times A Day, He Consults A Physician." stops going to the bathhouse."
ImprovingDaily
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I can attest to this. Eating pineapple, most of the time, makes me wanna go #2. Feels like it stimulates bile flow as well, or maybe just softens the stools for easier evacuation.
ImprovingDaily
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This might be a reason Travis, great observation.
OP
Amazoniac
Member
Antimicrobial effects of crude bromelain extracted from pineapple fruit (Ananas comosus (Linn.) Merr.)
When bromelaid is ingested during constipation, you're left with two choices: allow it to dissolve the body or evacuate it.
ImprovingDaily
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Ha! That's hilarious. I find that after not eating pineapple for a good week, then eating them again, tends to leave my bottom with a "burned " feeling. The body must compensate for all of that proteolytic activity somehow, because that burned feeling goes away after a day or 2 of eating pineapples.
Travis
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Thanks. Since opiate peptides, and all μ-opiates in general, lower dopamine output: bromelain could perhaps induce a roundabout dopaminergic effect in this manner. Many scientists who'd investigated the thrombolytic effects of bromelain often explain this it as due to proteolysis, which seems the most plausible explanation because protein hydrolysis is bromelain's essential function. Castell had actually proved that bromelain can be absorbed whole, with full activity, which perhaps isn't surprising considering its similarity to pepsin: Another acid-stable endogenous proteolytic enzyme that survives stomach conditions. Although there is little evidence for bromelain preventing stroke in clinical trials, it does seem plausible based on in vitro fibrinolytic activity. Epidemiological evidence having state-by-state comparisons place Hawaii curiously-low in stoke incidence per capita, a feather in the hat for Dole™ and pineapples in general. [Though it can be argued, and quite convincingly I might add, that the macadamia nut is truly Hawaii's best export.]
OP
Amazoniac
Member
Travo, is it true that one of your Patreon rewards is going to be a signed pineapple? Should you now be thinking: "Travasoniac, that's actually a greaHold on a second. Re-what? I'm the one who is gifting humanity!"
And @LifeGivingStore, is it true that you're going to sell powdered 'freeze-dried pineapples'* of the variety that the shaman above recommends, for those that just can't get good ones?
*Search for images.
And @LifeGivingStore, is it true that you're going to sell powdered 'freeze-dried pineapples'* of the variety that the shaman above recommends, for those that just can't get good ones?
*Search for images.
Travis
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I really need to finish that first article. The problem is that I like to use so many angles that the content appears infinite and the end never in-sight. I also have peculiar adherence to typography and consider the cadence of conjoined words. You'd think that writing paragraphs in a way that'd sound fluent when spoken would promote their fluent reading, yet omitting the proper scientific modifiers can dilute the acuity of a statement.
Last edited:
OP
Amazoniac
Member
Pineapfel.
@Travis: your dear bromelaid in action.
--
Fruits that might help the digesta:
Solidifying Science: Why Can Certain Fruits Ruin Your Gelatin Dessert?
"The proteases bromelain and papain (which come from pineapples and papayas, respectively) are often used in meat tenderizers. There are several other fruit proteases, however, such as actinidin (from kiwi fruit), ficin (figs) and zingibain (ginger)."
@Travis: your dear bromelaid in action.
--
Fruits that might help the digesta:
Solidifying Science: Why Can Certain Fruits Ruin Your Gelatin Dessert?
"The proteases bromelain and papain (which come from pineapples and papayas, respectively) are often used in meat tenderizers. There are several other fruit proteases, however, such as actinidin (from kiwi fruit), ficin (figs) and zingibain (ginger)."
Last edited:
Travis
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Gelatin is very similar to damaged collagen, perhaps why its used in dermatology. And surprisingly, this enzyme actually improves the healing rate. Bromalein seems completely incapable of proteolyzing tightly-coiled collagen.
mujuro
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Re the thing about maintaining an alkaline colon via lactic acid forming bacteria. Whenever I eat the high protein low fat Chobani yogurt, my sweat during training has a strong odor that resembles ammonia.
Runenight201
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Lol not going to lie I too have tried eating like Travis, and found that most raw cruciferous vegetables too be revolting (too bitter), and too much fruit makes my hyper excited and urinating frequently.
Eating potatoes hands down lets me have 3-4 bowel movements a day. Before I knew much about Peat, my brother and I would joke about how we loved potatoes but they made us defecate so frequently (which we said in a negative manner, now I'm seeing it as a positive thing!). I'm finding that for me, proper health is a balancing act with food. Too much starch and there's too much bulk in my stomach, and I won't be able to eat more but I'll still need more energy. Too much fruit and I'm hyper excited and urinating frequently. Too much milk....never want to go back there, very weird physiological and psychological states. Too much meat/fat and I'll feel nauseous.
However, when I get it all right, with the proper ratio of meat/potatoes/veggies in a meal, with sufficient fruit for dessert, I feel well-fed, not too heavy, and overall very good.
I think Ayurveda focuses heavily on this balancing act of food, and I wouldn't be surprised if what they recommend I'm intuitively doing, something to look into for sure.
raypeatclips
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How much potatoes do you eat per day?
Runenight201
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I don’t count or anything but if I had to estimate I’d guess around 400-500 calories of potatoes a day. Too many and I get bloated and stuffed with insufficient calories. Perhaps it’s not just the potatoes, but the starch/fruit/coffee combo, because usually after those 3 I’m sure to have a bowel movement.
In fact even today as I just finished up my meal, I had to leave some potatoes on my plate because if I ate more I could tell I’d be too bloated. Yet i was still hungry after consuming all my meat and broccoli and oj, but some cucumbers, lettuce, and pineapples fixed that. This leaves me wondering if perhaps I need to up my meat ration per meal to ~.5 lbs per lunch/dinner or perhaps include more lighter, watery veggies and solid fruits to complete the meal. Too much meat and I’ll also notice increased sebum production, so I’ll prob up the veggies/fruit instead.
I think it’s all so individual and may depend on weight, stomach size, muscle mass, stomach acid quantity, etc... as I’m eating I try and pay as much attention to what foods are creating what sensations and adjust accordingly.
In fact even today as I just finished up my meal, I had to leave some potatoes on my plate because if I ate more I could tell I’d be too bloated. Yet i was still hungry after consuming all my meat and broccoli and oj, but some cucumbers, lettuce, and pineapples fixed that. This leaves me wondering if perhaps I need to up my meat ration per meal to ~.5 lbs per lunch/dinner or perhaps include more lighter, watery veggies and solid fruits to complete the meal. Too much meat and I’ll also notice increased sebum production, so I’ll prob up the veggies/fruit instead.
I think it’s all so individual and may depend on weight, stomach size, muscle mass, stomach acid quantity, etc... as I’m eating I try and pay as much attention to what foods are creating what sensations and adjust accordingly.
OP
Amazoniac
Member
Diet, Microbiota, and Metabolic Health: Trade-Off Between Saccharolytic and Proteolytic Fermentation
"The human host produces only 17 carbohydrate-active enzymes, whereas some bacterial species in the gut have more than 200 carbohydrate-active enzymes (Cantarel et al. 2012). Indeed, one of the most prominent tasks of the gut microbiota is aiding the host with the digestion of food. Healthy Western individuals have been reported to obtain 2.8 kcal/g of fiber via microbial fermentation (Behall & Howe 1996), yielding up to 10% of a person’s daily calories (McNeil 1984). This figure is likely much greater in individuals consuming traditional diets rich in complex plant polysaccharides from fruits, vegetables, legumes, tubers, and whole grains. In pigs, which have a similar gut morphology to humans, the proportion of energy obtained from microbial fermentation is more than 20% (Yen et al. 1991)."
"Acetate, propionate, and butyrate are the most abundantly produced SCFAs and are present at approximately a 60:20:20 ratio in the human colon (Cummings et al. 1987). SCFAs are actively absorbed into the gut epithelium and partly utilized by colonocytes (Cummings et al. 1987). Acetate produced in the gut eventually enters the liver and can be used for cholesterol synthesis; however, a large fraction passes the liver and becomes available to peripheral tissues as an energy source (Wolever et al. 1991). Propionate is used for gluconeogenesis in the liver and inhibits cholesterol synthesis from acetate (Wolever et al. 1991). Propionate thus represents a source of glucose for the host. Most of the butyrate that is absorbed is utilized by colonocytes (Cummings et al. 1987), as butyrate represents their main energy source. Relatively little butyrate reaches the circulatory system (Cummings et al. 1987)."
"All Gram-negative bacteria produce the endotoxin lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall. However, the form of LPS produced by members of Proteobacteria is more inflammatory than that produced by members of Bacteroidetes (Vatanen et al. 2016). Thus, although their abundance is normally low, members of Proteobacteria can potentially have a strong impact on the host via their powerful immunogenicity."
"Akkermansia muciniphila is the only gut-associated member of the phylum Verrucomicrobia and has a special role in the gut ecosystem (reviewed in Derrien et al. 2017). Rather than relying on dietary substrates, Akkermansia grows in the mucus layer, degrading host-derived mucins and producing propionate and acetate, which can be further utilized by other bacteria (Derrien et al. 2017). Mucus is a constantly available substrate in the gut, whereas the supply of dietary components may vary, and an organism capable of unlocking this abundant source of carbohydrates and nitrogen likely has a key role in maintaining gut homeostasis (Derrien et al. 2017). Indeed, Akkermansia adheres to enterocytes and stimulates the gut barrier mechanism (Reunanen et al. 2015), protecting the host during excessive calorie consumption from diet-induced metabolic dysfunction (Everard et al. 2013). Akkermansia thus appears to be a keystone species in the gut ecosystem, enabling the microbiota and the host to withstand alternating periods of food scarcity and abundance."
"Vegetarians have a higher abundance of butyrate producers than omnivores (Hippe et al. 2011) but only if they consume more fiber than omnivores (Kabeerdoss et al. 2012). This indicates that it is the amount of fermentable carbohydrates rather than the absence of meat in the diet that is important for the butyrate producers."
"[..]starch has been shown to be the most butyrogenic carbohydrate (Englyst et al. 1987)."
For those consuming casein with a tendency towards constipation or without enough fermentable carbs:
"As the fermentation continues [throughout the gut], the amount of carbohydrates declines toward the distal colon. This decline depends on the amount of fermentable carbohydrates in the diet and on the transit time: Fast transit and a high abundance of dietary fiber and results in more carbohydrates reaching the distal colon. In a typical low-fiber Western diet, gut transit is slow, the amount of carbohydrates reaching the colon is small, and the carbohydrates are thus increasingly depleted. The overall fermentation and organic acid production slow down along the length of the colon, and the pH increases, allowing the acid-sensitive Bacteroides and Proteobacteria to increase in abundance (Duncan et al. 2009, Walker et al. 2005). Indeed, vegans and vegetarians, with higher carbohydrate intake and lower fecal pH, have low fecal abundance of Bacteroides and Proteobacteria (Zimmer et al. 2012)."
"There appears to be a major trade-off between saccharolytic and proteolytic fermentation in the human colon, which is reflected in the taxonomic and functional profiles and is dependent on diet (Figure 1). Colonic bacteria favor carbohydrate fermentation over protein fermentation, and consequently protein fermentation occurs mostly in the distal colon (Macfarlane et al. 1992), where the fermentable carbohydrates are depleted and the pH is close to neutral. Both carbohydrate availability and low pH reduce protein fermentation in vitro (Smith & Macfarlane 1996)."
"The activity of protein fermentation in the colon depends on diet more strongly than the production of SCFAs does (Salonen et al. 2014), indicating that dietary modulation can be an effective way to affect protein fermentation. Plant-based diets reduce bacterial protein fermentation products in feces (David et al. 2014, Ling & Hanninen 1992) and blood (Wu et al. 2016). A recent mouse study demonstrates that the amount of carbohydrates and protein in the diet has a decisive impact on the gut microbiota composition by selecting which bacteria are able to thrive: Low-protein diets select for microbiota able to utilize endogenous nitrogen obtained from host-derived substrates, such as mucus (Holmes et al. 2017)."
"Dietary fat is normally absorbed in the small intestine, and only small amounts reach the colon. Fat is not a primary energy source for colonic microbiota, and in mice it has a minor impact on the microbiota compared to the effects of carbohydrates and protein (Holmes et al. 2017). Nevertheless, the effects of even modest microbiota changes on the host may be significant. A fat-supplementation study in humans showed an increase in the Gram-negative Enterobacteriaceae, Parabacteroides, and Prevotella, as well as in a member of Erysipelotrichia, in response to monounsaturated fat, but not to polyunsaturated fat, indicating that different fatty acids may have varying effects on the gut microbiota (Pu et al. 2016). Polyunsaturated fatty acids (PUFAs) have antimicrobial effects (De Weirdt et al. 2017). Gut bacteria metabolize dietary PUFAs, producing conjugated and saturated fatty acids (De Weirdt et al. 2017). Such PUFA metabolism is identified in several butyrate producers, including members of Lachnospiraceae (De Weirdt et al. 2017), and, indeed, Lachnospiraceae increased in response to PUFA supplementation in a dietary intervention (Pu et al. 2016). Furthermore, the microbiota of individuals with high n-3 PUFA intake have a reduced propensity for protein fermentation (Yang & Rose 2014), suggesting that specific fatty acids may influence the microbial metabolism of other dietary components."
"Rodent studies support the beneficial effect of n-3 PUFAs, showing that they prevent the antibiotic-induced increase in inflammatory Proteobacteria and the decrease in bifidobacteria, resulting in improved gut barrier function and inhibition of endotoxemia (Kaliannan et al. 2016). Intriguingly, n-6 PUFAs have the opposite, inflammatory effect (Kaliannan et al. 2015). The effects are not direct but are mediated via intestinal alkaline phosphatase, which is upregulated by n-3 PUFAs and downregulated by n-6 PUFAs in host tissues (Kaliannan et al. 2015)."
"Dietary fat can influence the microbiota indirectly via the stimulation of bile secretion by the host (Devkota et al. 2012, Islam et al. 2011). Bile acids are toxic to many bacteria, and bile production is considered an important mechanism by which the host reduces the bacterial load in the small intestine. Most of the bile acids are absorbed in the small intestine, but a small fraction passes on to the colon and can influence the colonic microbiota (Islam et al. 2011). The amount of bile acids present in the colon is dependent on dietary fat: High-fat diets increase the amount of bile secreted and consequently the amount of bile acids present in the colon (Cummings et al. 1978)."
"Sugar intake likely mostly affects the small intestinal community, as little dietary sugar normally reaches the colon, although amounts exceeding the digestive capacity of the small intestine lead to rapid sugar fermentation in the colon, often producing uncomfortable gastrointestinal symptoms (Fedewa & Rao 2014). Simple sugars can be present in large amounts in the small intestine. Owing to the pulsatile nature of substrate supply and the fast transit, the microbiota of the small intestine consist of fast-growing bacteria efficiently utilizing simple sugars and amino acids (Zoetendal et al. 2012)."
"Fructose, in particular, has been shown to influence the gut microbiota in mice, with potentially detrimental effects on host health (Bergheim et al. 2008). In various species, including mice, monkeys, and humans, excessive fructose consumption induces endotoxemia and systemic inflammation (Bergheim et al. 2008, Jin et al. 2014, Kavanagh et al. 2013). The effect is caused by a weakened gut barrier, leading to the leakage of LPS into the circulatory system, and can be prevented by continuous antibiotic treatment targeting the Gram-negative LPS-producing bacteria (Bergheim et al. 2008). Whether fructose directly increases the abundance of the Gram-negative Proteobacteria in humans is currently not clear."
"The microbiota can contribute beneficially to sugar degradation: Supplementation with bifidobacteria has been shown to improve symptoms of lactose intolerance ( Jiang et al. 1996). A recent study showed that genetically lactase-deficient individuals tend to have higher abundances of bifidobacteria than individuals with the genetic capacity to degrade lactose, but no difference was observed in dairy product consumption between the groups (Bonder et al. 2016). Furthermore, the abundance of bifidobacteria was positively associated with dairy product consumption only in the lactase-deficient group. A possible explanation is that bifidobacteria benefit from the presence of lactose and may render genetically lactose-intolerant individuals able to tolerate lactose in their diet. This is supported by the fact that bifidobacteria are absent or reduced in populations that do not consume milk (Obregon-Tito et al. 2015, Schnorr et al. 2014) and are at reduced abundances in vegetarians and vegans (Zimmer et al. 2012)."
"Diets high in fiber reduce the risk of colorectal cancer and improve metabolic health (Aune et al. 2011, Threapleton et al. 2013)."
"Reducing the leakage of LPS by improving the gut barrier via supplementation with fiber (Pendyala et al. 2012), bifidobacteria (Cani et al. 2007b), or Akkermansia (Everard et al. 2013) can effectively promote metabolic health. Conversely, vancomycin treatment, which reduces the abundance of SCFA-producing species and increases the abundance of LPS-producing species in the gut, negatively affects insulin sensitivity (Vrieze et al. 2014). The depletion of bifidobacteria in early life is associated with increased weight gain in later childhood (Korpela et al. 2017), indicating that bifidobacteria, promoted by oligosaccharides in breast milk, are particularly important for healthy metabolic programming in infancy."
"According to a dose-escalation study, more than 35 g of oligofructose per day are required to observe changes in gut hormone levels (Pedersen et al. 2013), indicating that the recommended amount of 25 g of fiber per day may be insufficient for full metabolic benefits."
"Meat-based diets contain both saturated fat and animal protein, which likely influence the gut microbiota and host health synergistically. Protein fermentation results in the production of diverse end products: SCFAs, branched-chain fatty acids (BCFAs), ammonia, amines, and phenolic and indolic compounds (Macfarlane et al. 1992)."
"Butyrate can be produced from the amino acids glutamate and lysine by Fusobacterium and Megasphaera, but unlike the pyruvate-to-butyrate pathway employed by clostridia, this pathway involves the production of ammonia, which may be harmful (Anand et al. 2016). Bacteria use ammonia for amino acid synthesis, and ammonia utilization is increased if peptide availability is low (Walker et al. 2005), indicating that low-protein diets may increase ammonia utilization in the gut."
"The fermentation of sulfur-containing amino acids results in the production of hydrogen sulfide (Devkota et al. 2012). In addition, the heme in red meat induces the production of nitroso compounds (Kuhnle et al. 2007). Many of the protein fermentation products, especially hydrogen sulfide and nitroso compounds, are toxic to intestinal cells and are implicated in the etiology of colorectal cancer (Hughes et al. 2000). Indeed, cancer usually occurs in the distal parts of the intestine, where protein fermentation takes place, and can be attributed to dietary factors such as excessive meat intake and low fiber intake (Aune et al. 2011, Larsson & Wolk 2006). However, it appears that non-meat-derived proteins may not increase the risk of colorectal cancer (Kato et al. 1997, Windey et al. 2012). It is possible the culprit is not protein fermentation per se, but that protein fermentation products act in synergy to induce carcinogenesis in the presence of Nnitroso compounds, hydrogen sulfide, and bile acids, promoted by meat and saturated fat intake."
"Fat intake stimulates bile release, and dietary protein can affect the composition of bile (Hardison 1978). Diet modifies the bile acid pool and the microbiota composition, and, thereby, the microbial metabolism of bile acids. Bile acids are conjugated to glycine or, less commonly in humans, taurine. In humans, the abundance of taurine-conjugated bile acids is dependent on the availability of dietary taurine, which is present in meat and shellfish (Hardison 1978). Glycine- and taurine-conjugated bile acids have decisively different effects on the gut microbiota and the host in mice (Devkota et al. 2012). Taurine is a sulfur-containing amino acid and favors the expansion of sulfite-reducing bacteria, resulting in the production of highly toxic hydrogen sulfide (Devkota et al. 2012). The proportion of taurine-conjugated bile acids thus represents a key determinant of how the microbial metabolism of bile acids affects the host."
"Importantly, bile acids act as hormones, regulating all aspects of metabolism by activating the receptors lk and TGR5, which affect bile production as well as diverse metabolic functions including insulin sensitivity, lipid metabolism, and energy expenditure (reviewed in Wahlström et al. 2016). Bacteria deconjugate and dehydroxylate the host-secreted primary bile acids, altering their affinity to the receptors and thus their impact on host metabolism. However, the interactions between diet, bile acids, and microbiota are complex and poorly characterized in humans. In mice, bile-salt hydrolase activity of the microbiota has been shown to reduce host weight gain, insulin resistance, and blood cholesterol by altering FXR and TGR5 signaling (Joyce et al. 2014, Watanabe et al. 2006). Mice and humans have different bile acid pools, so direct comparison is not possible, but it is likely that bacterial modification of bile acids has significant metabolic consequences in humans as well. An example is the secondary bile acid ursodeoxycholic acid (UDCA), which increases shortly after gastric bypass surgery, and this is suggested to mediate the rapid amelioration of diabetes in these patients (Albaugh et al. 2015). UDCA is a strong agonist of TGR5, which increases energy expenditure and insulin sensitivity (Wahlström et al. 2016)."
"The microbiota of vegetarians and vegans have a significantly reduced capacity to produce TMA, suggesting that the important TMA-producing species are ones that are promoted by meat-based diets (Koeth et al. 2013)."
"[..]shorter studies have shown unfavorable microbiota changes in response to high-protein diets (David et al. 2014, Duncan et al. 2007, O’Keefe et al. 2015, Russell et al. 2011)."
"If consumed chronically, even moderate intake of animal, but not plant, protein is associated with reduced life span (Levine et al. 2014, Solon-Biet et al. 2014), which may be partly explained by the effects of diet on the gut microbiota (Holmes et al. 2017)."
"As humans regulate food intake to meet their protein requirement, a diet deficient in protein leads to overeating (Simpson & Raubenheimer 2005). However, it should be noted that the gut microbiota regulate food intake to meet their carbohydrate requirement, and a diet deficient in fiber leads to overeating as well. A healthy diet must therefore meet the protein requirement of the host and the carbohydrate requirement of the gut microbiota. For sustained metabolic improvement, modifying the quality of dietary carbohydrates may be more effective than replacing them with excess protein and fat. Indeed, successful weight loss can be achieved by ad libitum diets designed to promote a healthy microbiota by supplying a rich variety of fermentable carbohydrates and plant proteins (Xiao et al. 2014)."
"Modulation of the gut microbiota clearly offers opportunities, but dietary interventions often yield varying results. This is not unexpected, as the microbiota composition determines how the dietary components are utilized. All humans have very similar enzymatic capacities for the degradation of dietary compounds, but individuals differ widely in their microbial enzymatic repertoire (Qin et al. 2010). A great part of our individuality is in the gut microbiota, and the individual differences in microbiota composition and gene content may explain individuality in response to dietary change. There is individual variation in the ability of the microbiota to degrade different dietary components (Walker et al. 2011, Yang & Rose 2014), leading to potential differences in the response to dietary substances."
"The availability of dietary nitrogen determines which bacteria win the competition for dietary carbohydrates (Holmes et al. 2017): Low-protein diets select for bacteria that can utilize mucus-derived nitrogen. Thus, differences in habitual protein intake may influence how the microbiota respond to fiber supplementation. This was shown in vitro, where fecal samples from individuals on meat-based diets showed a Bacteroides-dominated response to the added fiber, whereas samples from individuals on plant-based diets showed a butyrogenic response (Yang & Rose 2014)."
"There are examples showing that individuals with a high abundance of Bacteroides spp. and/or low microbiota diversity at baseline fail to respond positively to dietary interventions (Cotillard et al. 2013, Kovatcheva-Datchary et al. 2015, Louis et al. 2016). One possible explanation is that Bacteroides, by adapting flexibly to different dietary components, are able to resist change during short-term dietary interventions. Conversely, individuals with a high abundance of Akkermansia at baseline have been shown to respond positively to weight-loss diets (Dao et al. 2016, Louis et al. 2016). This indicates that in some individuals, with a permissive microbiota, a beneficial response can be elicited rapidly, whereas others may need long-term dietary manipulation to alter the ecological balance in the gut. Indeed, the full effects of a dietary intervention may require microbiota adaptation, a process that may take up to a year (Freeland et al. 2010)."
@Elephanto
"The human host produces only 17 carbohydrate-active enzymes, whereas some bacterial species in the gut have more than 200 carbohydrate-active enzymes (Cantarel et al. 2012). Indeed, one of the most prominent tasks of the gut microbiota is aiding the host with the digestion of food. Healthy Western individuals have been reported to obtain 2.8 kcal/g of fiber via microbial fermentation (Behall & Howe 1996), yielding up to 10% of a person’s daily calories (McNeil 1984). This figure is likely much greater in individuals consuming traditional diets rich in complex plant polysaccharides from fruits, vegetables, legumes, tubers, and whole grains. In pigs, which have a similar gut morphology to humans, the proportion of energy obtained from microbial fermentation is more than 20% (Yen et al. 1991)."
"Acetate, propionate, and butyrate are the most abundantly produced SCFAs and are present at approximately a 60:20:20 ratio in the human colon (Cummings et al. 1987). SCFAs are actively absorbed into the gut epithelium and partly utilized by colonocytes (Cummings et al. 1987). Acetate produced in the gut eventually enters the liver and can be used for cholesterol synthesis; however, a large fraction passes the liver and becomes available to peripheral tissues as an energy source (Wolever et al. 1991). Propionate is used for gluconeogenesis in the liver and inhibits cholesterol synthesis from acetate (Wolever et al. 1991). Propionate thus represents a source of glucose for the host. Most of the butyrate that is absorbed is utilized by colonocytes (Cummings et al. 1987), as butyrate represents their main energy source. Relatively little butyrate reaches the circulatory system (Cummings et al. 1987)."
"All Gram-negative bacteria produce the endotoxin lipopolysaccharide (LPS), a component of the Gram-negative bacterial cell wall. However, the form of LPS produced by members of Proteobacteria is more inflammatory than that produced by members of Bacteroidetes (Vatanen et al. 2016). Thus, although their abundance is normally low, members of Proteobacteria can potentially have a strong impact on the host via their powerful immunogenicity."
"Akkermansia muciniphila is the only gut-associated member of the phylum Verrucomicrobia and has a special role in the gut ecosystem (reviewed in Derrien et al. 2017). Rather than relying on dietary substrates, Akkermansia grows in the mucus layer, degrading host-derived mucins and producing propionate and acetate, which can be further utilized by other bacteria (Derrien et al. 2017). Mucus is a constantly available substrate in the gut, whereas the supply of dietary components may vary, and an organism capable of unlocking this abundant source of carbohydrates and nitrogen likely has a key role in maintaining gut homeostasis (Derrien et al. 2017). Indeed, Akkermansia adheres to enterocytes and stimulates the gut barrier mechanism (Reunanen et al. 2015), protecting the host during excessive calorie consumption from diet-induced metabolic dysfunction (Everard et al. 2013). Akkermansia thus appears to be a keystone species in the gut ecosystem, enabling the microbiota and the host to withstand alternating periods of food scarcity and abundance."
"Vegetarians have a higher abundance of butyrate producers than omnivores (Hippe et al. 2011) but only if they consume more fiber than omnivores (Kabeerdoss et al. 2012). This indicates that it is the amount of fermentable carbohydrates rather than the absence of meat in the diet that is important for the butyrate producers."
"[..]starch has been shown to be the most butyrogenic carbohydrate (Englyst et al. 1987)."
For those consuming casein with a tendency towards constipation or without enough fermentable carbs:
"As the fermentation continues [throughout the gut], the amount of carbohydrates declines toward the distal colon. This decline depends on the amount of fermentable carbohydrates in the diet and on the transit time: Fast transit and a high abundance of dietary fiber and results in more carbohydrates reaching the distal colon. In a typical low-fiber Western diet, gut transit is slow, the amount of carbohydrates reaching the colon is small, and the carbohydrates are thus increasingly depleted. The overall fermentation and organic acid production slow down along the length of the colon, and the pH increases, allowing the acid-sensitive Bacteroides and Proteobacteria to increase in abundance (Duncan et al. 2009, Walker et al. 2005). Indeed, vegans and vegetarians, with higher carbohydrate intake and lower fecal pH, have low fecal abundance of Bacteroides and Proteobacteria (Zimmer et al. 2012)."
"There appears to be a major trade-off between saccharolytic and proteolytic fermentation in the human colon, which is reflected in the taxonomic and functional profiles and is dependent on diet (Figure 1). Colonic bacteria favor carbohydrate fermentation over protein fermentation, and consequently protein fermentation occurs mostly in the distal colon (Macfarlane et al. 1992), where the fermentable carbohydrates are depleted and the pH is close to neutral. Both carbohydrate availability and low pH reduce protein fermentation in vitro (Smith & Macfarlane 1996)."
"The activity of protein fermentation in the colon depends on diet more strongly than the production of SCFAs does (Salonen et al. 2014), indicating that dietary modulation can be an effective way to affect protein fermentation. Plant-based diets reduce bacterial protein fermentation products in feces (David et al. 2014, Ling & Hanninen 1992) and blood (Wu et al. 2016). A recent mouse study demonstrates that the amount of carbohydrates and protein in the diet has a decisive impact on the gut microbiota composition by selecting which bacteria are able to thrive: Low-protein diets select for microbiota able to utilize endogenous nitrogen obtained from host-derived substrates, such as mucus (Holmes et al. 2017)."
"Dietary fat is normally absorbed in the small intestine, and only small amounts reach the colon. Fat is not a primary energy source for colonic microbiota, and in mice it has a minor impact on the microbiota compared to the effects of carbohydrates and protein (Holmes et al. 2017). Nevertheless, the effects of even modest microbiota changes on the host may be significant. A fat-supplementation study in humans showed an increase in the Gram-negative Enterobacteriaceae, Parabacteroides, and Prevotella, as well as in a member of Erysipelotrichia, in response to monounsaturated fat, but not to polyunsaturated fat, indicating that different fatty acids may have varying effects on the gut microbiota (Pu et al. 2016). Polyunsaturated fatty acids (PUFAs) have antimicrobial effects (De Weirdt et al. 2017). Gut bacteria metabolize dietary PUFAs, producing conjugated and saturated fatty acids (De Weirdt et al. 2017). Such PUFA metabolism is identified in several butyrate producers, including members of Lachnospiraceae (De Weirdt et al. 2017), and, indeed, Lachnospiraceae increased in response to PUFA supplementation in a dietary intervention (Pu et al. 2016). Furthermore, the microbiota of individuals with high n-3 PUFA intake have a reduced propensity for protein fermentation (Yang & Rose 2014), suggesting that specific fatty acids may influence the microbial metabolism of other dietary components."
"Rodent studies support the beneficial effect of n-3 PUFAs, showing that they prevent the antibiotic-induced increase in inflammatory Proteobacteria and the decrease in bifidobacteria, resulting in improved gut barrier function and inhibition of endotoxemia (Kaliannan et al. 2016). Intriguingly, n-6 PUFAs have the opposite, inflammatory effect (Kaliannan et al. 2015). The effects are not direct but are mediated via intestinal alkaline phosphatase, which is upregulated by n-3 PUFAs and downregulated by n-6 PUFAs in host tissues (Kaliannan et al. 2015)."
"Dietary fat can influence the microbiota indirectly via the stimulation of bile secretion by the host (Devkota et al. 2012, Islam et al. 2011). Bile acids are toxic to many bacteria, and bile production is considered an important mechanism by which the host reduces the bacterial load in the small intestine. Most of the bile acids are absorbed in the small intestine, but a small fraction passes on to the colon and can influence the colonic microbiota (Islam et al. 2011). The amount of bile acids present in the colon is dependent on dietary fat: High-fat diets increase the amount of bile secreted and consequently the amount of bile acids present in the colon (Cummings et al. 1978)."
"Sugar intake likely mostly affects the small intestinal community, as little dietary sugar normally reaches the colon, although amounts exceeding the digestive capacity of the small intestine lead to rapid sugar fermentation in the colon, often producing uncomfortable gastrointestinal symptoms (Fedewa & Rao 2014). Simple sugars can be present in large amounts in the small intestine. Owing to the pulsatile nature of substrate supply and the fast transit, the microbiota of the small intestine consist of fast-growing bacteria efficiently utilizing simple sugars and amino acids (Zoetendal et al. 2012)."
"Fructose, in particular, has been shown to influence the gut microbiota in mice, with potentially detrimental effects on host health (Bergheim et al. 2008). In various species, including mice, monkeys, and humans, excessive fructose consumption induces endotoxemia and systemic inflammation (Bergheim et al. 2008, Jin et al. 2014, Kavanagh et al. 2013). The effect is caused by a weakened gut barrier, leading to the leakage of LPS into the circulatory system, and can be prevented by continuous antibiotic treatment targeting the Gram-negative LPS-producing bacteria (Bergheim et al. 2008). Whether fructose directly increases the abundance of the Gram-negative Proteobacteria in humans is currently not clear."
"The microbiota can contribute beneficially to sugar degradation: Supplementation with bifidobacteria has been shown to improve symptoms of lactose intolerance ( Jiang et al. 1996). A recent study showed that genetically lactase-deficient individuals tend to have higher abundances of bifidobacteria than individuals with the genetic capacity to degrade lactose, but no difference was observed in dairy product consumption between the groups (Bonder et al. 2016). Furthermore, the abundance of bifidobacteria was positively associated with dairy product consumption only in the lactase-deficient group. A possible explanation is that bifidobacteria benefit from the presence of lactose and may render genetically lactose-intolerant individuals able to tolerate lactose in their diet. This is supported by the fact that bifidobacteria are absent or reduced in populations that do not consume milk (Obregon-Tito et al. 2015, Schnorr et al. 2014) and are at reduced abundances in vegetarians and vegans (Zimmer et al. 2012)."
"Diets high in fiber reduce the risk of colorectal cancer and improve metabolic health (Aune et al. 2011, Threapleton et al. 2013)."
"Reducing the leakage of LPS by improving the gut barrier via supplementation with fiber (Pendyala et al. 2012), bifidobacteria (Cani et al. 2007b), or Akkermansia (Everard et al. 2013) can effectively promote metabolic health. Conversely, vancomycin treatment, which reduces the abundance of SCFA-producing species and increases the abundance of LPS-producing species in the gut, negatively affects insulin sensitivity (Vrieze et al. 2014). The depletion of bifidobacteria in early life is associated with increased weight gain in later childhood (Korpela et al. 2017), indicating that bifidobacteria, promoted by oligosaccharides in breast milk, are particularly important for healthy metabolic programming in infancy."
"According to a dose-escalation study, more than 35 g of oligofructose per day are required to observe changes in gut hormone levels (Pedersen et al. 2013), indicating that the recommended amount of 25 g of fiber per day may be insufficient for full metabolic benefits."
"Meat-based diets contain both saturated fat and animal protein, which likely influence the gut microbiota and host health synergistically. Protein fermentation results in the production of diverse end products: SCFAs, branched-chain fatty acids (BCFAs), ammonia, amines, and phenolic and indolic compounds (Macfarlane et al. 1992)."
"Butyrate can be produced from the amino acids glutamate and lysine by Fusobacterium and Megasphaera, but unlike the pyruvate-to-butyrate pathway employed by clostridia, this pathway involves the production of ammonia, which may be harmful (Anand et al. 2016). Bacteria use ammonia for amino acid synthesis, and ammonia utilization is increased if peptide availability is low (Walker et al. 2005), indicating that low-protein diets may increase ammonia utilization in the gut."
"The fermentation of sulfur-containing amino acids results in the production of hydrogen sulfide (Devkota et al. 2012). In addition, the heme in red meat induces the production of nitroso compounds (Kuhnle et al. 2007). Many of the protein fermentation products, especially hydrogen sulfide and nitroso compounds, are toxic to intestinal cells and are implicated in the etiology of colorectal cancer (Hughes et al. 2000). Indeed, cancer usually occurs in the distal parts of the intestine, where protein fermentation takes place, and can be attributed to dietary factors such as excessive meat intake and low fiber intake (Aune et al. 2011, Larsson & Wolk 2006). However, it appears that non-meat-derived proteins may not increase the risk of colorectal cancer (Kato et al. 1997, Windey et al. 2012). It is possible the culprit is not protein fermentation per se, but that protein fermentation products act in synergy to induce carcinogenesis in the presence of Nnitroso compounds, hydrogen sulfide, and bile acids, promoted by meat and saturated fat intake."
"Fat intake stimulates bile release, and dietary protein can affect the composition of bile (Hardison 1978). Diet modifies the bile acid pool and the microbiota composition, and, thereby, the microbial metabolism of bile acids. Bile acids are conjugated to glycine or, less commonly in humans, taurine. In humans, the abundance of taurine-conjugated bile acids is dependent on the availability of dietary taurine, which is present in meat and shellfish (Hardison 1978). Glycine- and taurine-conjugated bile acids have decisively different effects on the gut microbiota and the host in mice (Devkota et al. 2012). Taurine is a sulfur-containing amino acid and favors the expansion of sulfite-reducing bacteria, resulting in the production of highly toxic hydrogen sulfide (Devkota et al. 2012). The proportion of taurine-conjugated bile acids thus represents a key determinant of how the microbial metabolism of bile acids affects the host."
"Importantly, bile acids act as hormones, regulating all aspects of metabolism by activating the receptors lk and TGR5, which affect bile production as well as diverse metabolic functions including insulin sensitivity, lipid metabolism, and energy expenditure (reviewed in Wahlström et al. 2016). Bacteria deconjugate and dehydroxylate the host-secreted primary bile acids, altering their affinity to the receptors and thus their impact on host metabolism. However, the interactions between diet, bile acids, and microbiota are complex and poorly characterized in humans. In mice, bile-salt hydrolase activity of the microbiota has been shown to reduce host weight gain, insulin resistance, and blood cholesterol by altering FXR and TGR5 signaling (Joyce et al. 2014, Watanabe et al. 2006). Mice and humans have different bile acid pools, so direct comparison is not possible, but it is likely that bacterial modification of bile acids has significant metabolic consequences in humans as well. An example is the secondary bile acid ursodeoxycholic acid (UDCA), which increases shortly after gastric bypass surgery, and this is suggested to mediate the rapid amelioration of diabetes in these patients (Albaugh et al. 2015). UDCA is a strong agonist of TGR5, which increases energy expenditure and insulin sensitivity (Wahlström et al. 2016)."
"The microbiota of vegetarians and vegans have a significantly reduced capacity to produce TMA, suggesting that the important TMA-producing species are ones that are promoted by meat-based diets (Koeth et al. 2013)."
"[..]shorter studies have shown unfavorable microbiota changes in response to high-protein diets (David et al. 2014, Duncan et al. 2007, O’Keefe et al. 2015, Russell et al. 2011)."
"If consumed chronically, even moderate intake of animal, but not plant, protein is associated with reduced life span (Levine et al. 2014, Solon-Biet et al. 2014), which may be partly explained by the effects of diet on the gut microbiota (Holmes et al. 2017)."
"As humans regulate food intake to meet their protein requirement, a diet deficient in protein leads to overeating (Simpson & Raubenheimer 2005). However, it should be noted that the gut microbiota regulate food intake to meet their carbohydrate requirement, and a diet deficient in fiber leads to overeating as well. A healthy diet must therefore meet the protein requirement of the host and the carbohydrate requirement of the gut microbiota. For sustained metabolic improvement, modifying the quality of dietary carbohydrates may be more effective than replacing them with excess protein and fat. Indeed, successful weight loss can be achieved by ad libitum diets designed to promote a healthy microbiota by supplying a rich variety of fermentable carbohydrates and plant proteins (Xiao et al. 2014)."
"Modulation of the gut microbiota clearly offers opportunities, but dietary interventions often yield varying results. This is not unexpected, as the microbiota composition determines how the dietary components are utilized. All humans have very similar enzymatic capacities for the degradation of dietary compounds, but individuals differ widely in their microbial enzymatic repertoire (Qin et al. 2010). A great part of our individuality is in the gut microbiota, and the individual differences in microbiota composition and gene content may explain individuality in response to dietary change. There is individual variation in the ability of the microbiota to degrade different dietary components (Walker et al. 2011, Yang & Rose 2014), leading to potential differences in the response to dietary substances."
"The availability of dietary nitrogen determines which bacteria win the competition for dietary carbohydrates (Holmes et al. 2017): Low-protein diets select for bacteria that can utilize mucus-derived nitrogen. Thus, differences in habitual protein intake may influence how the microbiota respond to fiber supplementation. This was shown in vitro, where fecal samples from individuals on meat-based diets showed a Bacteroides-dominated response to the added fiber, whereas samples from individuals on plant-based diets showed a butyrogenic response (Yang & Rose 2014)."
"There are examples showing that individuals with a high abundance of Bacteroides spp. and/or low microbiota diversity at baseline fail to respond positively to dietary interventions (Cotillard et al. 2013, Kovatcheva-Datchary et al. 2015, Louis et al. 2016). One possible explanation is that Bacteroides, by adapting flexibly to different dietary components, are able to resist change during short-term dietary interventions. Conversely, individuals with a high abundance of Akkermansia at baseline have been shown to respond positively to weight-loss diets (Dao et al. 2016, Louis et al. 2016). This indicates that in some individuals, with a permissive microbiota, a beneficial response can be elicited rapidly, whereas others may need long-term dietary manipulation to alter the ecological balance in the gut. Indeed, the full effects of a dietary intervention may require microbiota adaptation, a process that may take up to a year (Freeland et al. 2010)."
@Elephanto
EMF Mitigation - Flush Niacin - Big 5 Minerals
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