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Strange but true: bile in your gut produces rockier boners
Constipation is a common issue, yet fortunately the underlying causes have been largely worked out.
The most common cause could be overgrowth of M. smithii in the small intestine leading to excessive methane production, yet dietary opiate peptides — a.k.a. exorphins — certainly also play a role.
Hypothyroidism is also a cause of constipation, and while this can be explained by increased α2‑adrenoceptors there’s also a second mechanism involved.
Hypothyroidism is generally accompanied by cholestasis, or reduced bile flow.
Bile acids have been shown to increase motility through TGR5, a cell membrane receptor shown to influence intestinal muscle tension.
Administration of thyroid hormone has been shown to increase total bile output, especially of chenodeoxycholic acid which’s the stronger TGR5 activator of the two primary bile salts.
“In addition to their role in the digestion and absorption of dietary fat, bile acids control intestinal motility and secretion […]” ―Alemi, 2013
So besides taking iodide to enhance thyroid hormone synthesis and selenium to convert it into the active form (T3), taurine supplementation can also help in increasing bile flow.
Moreover, the taurine‑conjugated bile acids are more potent TGR5 activators than their corresponding glycine‑conjugated analogues.
Taurine also has been shown to prevent gallstones.
Chenodeoxycholic acid itself can also be taken to eliminate constipation, and its taurine conjugate has also been shown to eliminate gallstones.
This was proven in 1983:
This study involved 20 gallstone patients all having constipation.
Although this was an experimental study, the subjects imply an epidemiological relationship between cholestasis and constipation.
They divided the group in two: Ten subjects were given 250 milligrams of chenodeoxycholic acid three times per day, with meals, and the ten remaining served as their controls.
They noted a very strong trend towards increased motility in subjects taking chenodeoxycholic acid.
But a few complained of diarrhea, so it could be better to synthesize our own bile acids using taurine.
In this way, we cannot “overdo it” because bile production is regulated.
Also, increasing endogenous bile production would ensure it’s delivered exactly where it needs to be and when.
Taurine supplementation has been proven to increase:
- Total bile output
- Tauro‑chenodeoxycholate formation
- Enzymes involved in its synthesis
They took a group of hamsters, added taurine to their drinking water, cannulated their biliary duct, and then measured bile output.
After 15 days, they noted a large increase in bile elimination in the taurine group:
They also noted a 30% increase in cholesterol 7α‑hydroxylase activity in the liver.
This is the rate‑limiting enzyme in cholic acid synthesis, and BOTH primary bile acids require the 7α‑hydroxyl group.
Since taurine is a natural metabolite of cysteine within the body, the authors explained the 7α‑hydroxylase increase through glutathione.
Cysteine is needed for glutathione production, and whatever spares the former should increase the latter.
So besides preventing gallstones, increased cysteine and glutathione are another benefit of taking taurine.
Taurine is completely natural and safe. The rats easily tolerated about 3 times the normal dietary intake.
“Taurine-conjugated bile acids are more water-soluble and less toxic than glycol-conjugated bile acids.” ―Bellentani, 1987
Also consistently shown to increase bile output is thyroid hormone.
This finding helps to explain symptoms of cholestasis reported in hypothyroid cases, and also the established link between hypothyroidism and constipation.
And since 70 to 80% of the cholesterol synthesized by the body is excreted as bile acids, low bile output could be why hypothyroidism is often accompanied with hypercholesterolemia.
This study examined the effect of thyroid hormone on bile output using five groups of rats.
One group was made hypothyroid with propylthiouracil, one served as control, and three others were given varying doses of triiodothyronine (T3) — the most active thyroid hormone.
After killing the rats, they determined the total amount of bile acids in their digestive tracts, as well as the proportions of each particular one.
They also injected radioactive [C14]‑cholic and [C14]‑chenodeoxycholic acids into the rats to determine bile acid turnover, and from this they could calculate the daily production rate.
They found a near doubling of the total bile acid pool in the thyroid treated rats, with most of the increase comprised of chenodeoxycholic acid.
“For normal rats, this production was found to have a mean value of 4.9 mg, while all the thyroid hormone-treated rats had mean values of about 8.0 mg.” ―Strand, 1963
This is important because chenodeoxycholic acid was found to be more potent at TGR5 receptors than cholic acid, the other primary bile acid.
And of the two secondary bile acids, i.e. the bacterial metabolites of primary ones, the one derived from chenodeoxycholic acid is more potent than the one derived from cholic acid.
Irrespective of type, the taurine conjugated bile acids are always more potent than the glycine conjugates.
So not only does thyroid hormone increase total bile production, it does it by increasing the more powerful bile acid.
And taking taurine would make it more powerful yet.
“This tendency towards increased total bile acid production in the thyroid hormone-treated rats was mainly due to a 2- to 3-fold increase in the daily synthesis of chenodeoxycholate.” ―Strand, 1963
This same series of potency was observed in classic studies on colonic motility before TGR5 had even been discovered.
Although only three bile acids were tested, logic would imply that lithocholic acid would’ve been the most potent had they used it.
The TGR5 receptor is truly a bile acid receptor and affects motility in real time.
Yet unlike intestinal 5‑HT4 and acetylcholine receptors which always respond the same way, the TGR5 receptor exerts effects which vary by region.
It’s almost as if the TGR5 receptor evolved to orchestrate the digestive process by sensing bile salts and their secondary metabolites.
By activating this membrane receptor, bile acids stimulate the proximal colon while causing a relaxation of the distal colon.
“Luminal bile acids exert region-specific actions in the intestine.” ―Alemi, 2013
They also slow transit of the small intestine to allow for efficient absorption, yet their net effect is to promote motility.
This has been proven clinically in the past many times, and again only recently by using genetically engineered mice:
They used three different types of mice.
One group was normal, one was genetically engineered to overexpress TGR5, and one was genetically modified to lack it.
This manipulation was successful, and the TGR5 knock‑out mice did not respond in the slightest to bile acids.
The TGR5 knock‑out translated into 1.4‑fold slower intestinal transit as compared to normal mice.
Conversely, rats overexpressing TGR5 receptors had 2.2‑fold FASTER transit compared to the normal wild‑type mice.
The main effect on muscle appears dependent on serotonin and CGRP release, as inhibitors of these blunted the response.
The inhibitor of calcitonin gene‑related peptide (CGRP) was more effective than the serotonin inhibitor, implying that the former is more involved in mediating response to bile acids.
Moreover, immunolocalization showed a near perfect relationship between the two.
When colored images of CGRP and TGR5 are superimposed, the result is essentially one color with little trace of the others:
In other words: the TGR5 receptor is always found in close proximity to CGRP, a neurotransmitter that it releases.
The fit between TGR5 and CGRP is better than that between TGR5 and serotonin, entirely consistent with the inhibitor study.
The genetic elimination of TGR5 also decreased water content by 35%, an effect that surely led to constipation.
“In keeping with the prokinetic actions of bile acids and TGR5, deletion of TGR5 delays gastrointestinal transit whereas overexpression of TGR5 accelerates colonic transit.” ―Alemi, 2013
Yet water loss can be an effect of constipation and not a cause due to prolonged absorption time, making this finding somewhat ambiguous on its own.
This water‑loss effect has been studied in detail however, and the results suggest that bile acids actively influence aquaporin expression:
Aquaporins are water channels found in many body areas, including the kidneys, blood-brain barrier, and intestines.
In the intestines, aquaporins control the direction of water flow and have been found relevant to motility.
It’s been estimated that the colon absorbs between 1.5 to 2 liters of water per day.
A difference of a few pints in either direction, obtainable through aquaporin expression, can result in either diarrhea or constipation.
This study fed cholic acid to rats for three days and examined aquaporin expression in their digestive tracts.
They noticed an increase in aquaporin‑7 and ‑8, with a decrease in aquaporin‑3.
Aquaporins can either be secretory or absorptive, yet seeing as the change was accompanied by an increased water content, you’d think AQP3 is of the latter type.
And aquaporin‑7 and ‑8 should be secretory types, or those which act to transfer water from the body out into the digestive tract.
This is the trend they found…
After a statistical analysis, aquaporin‑3 was the only subtype negatively correlated with intestinal water content (r = −.798).
Conversely, aquaporin‑7 (r = .748) and aquaporin‑8 (r = .668) were found to be positively correlated.
So bile salts act in two ways to increase motility:
- By controlling muscle contraction/relaxation via CGRP release
- And also by increasing water content through aquaporin expression
Bile acids have very complex and coordinated actions, so much so that other constipation remedies seem primitive by comparison.
Secondary bile acids are more potent agonists of TGR5 receptors than are primary ones.
This could be seen as an evolutionary device to sense completeness of digestion, a timing mechanism, and could perhaps be another indication of their complex role.
Iodide and selenium can be used to increase bile production through thyroid hormone synthesis.
Bile output can be increased further by supplementing with taurine, which is also needed to synthesize the most effective type (taurochenodeoxycholic acid).
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Bazzoli, F. "Treatment of constipation with chenodeoxycholic acid." Journal of International Medical Research (1983) https://journals.sagepub.com/doi/abs/10.1177/030006058301100211
Bellentani, S. "Taurine increases bile acid pool size and reduces bile saturation index in the hamster." Journal of lipid research (1987) http://www.jlr.org/content/28/9/1021.full.pdf
Strand, Ove. "Effects of ᴅ-and ʟ-triiodothyronine and of propylthiouracil on the production of bile acids in the rat." Journal of lipid research (1963) http://www.jlr.org/content/4/3/305.full.pdf
Alemi, Farzad. "The receptor TGR5 mediates the prokinetic actions of intestinal bile acids and is required for normal defecation in mice." Gastroenterology (2013) https://www.sciencedirect.com/science/article/pii/S0016508512014564
Yde, Jonathan. "Characterization of AQPs in mouse, rat, and human colon and their selective regulation by bile acids." Frontiers in nutrition (2016) https://www.frontiersin.org/articles/10.3389/fnut.2016.00046/full