Transit time is the new pre and probiotic.

Transit time determines which bacterial species dominate, and which don’t. It determines your neurotransmitters, mood, oxidative stress, inflammation, neurological health, and just your health in general.

Transit time is positively related to fecal pH and tends to be related to methanogen counts (R).

Keep in mind, just because you have a bowel movement each morning doesn’t mean you have a fast transit time. Take 1 tsp charcoal one day and see how long (hours or days) it takes to come out. Complete digestion takes place within 8 hours, so if it takes more than 24 hours, your transit time is on the slow end and could benefit from an increase.

Intestinal pH, transit time & bacterial growth

Intestinal pathogens and putrefactive bacteria prefer a neutral pH, so reducing the pH with SCFA may contribute to the reduction of these bacteria. Fecal pH is markedly increased in patients with severe systemic inflammatory response syndrome (R).

However, when the pH level is increased or decreased by one, the incidence of bacteremia more than triples, and mortality more than doubles (R). 

Regardless, slightly acidic is preferable as it may create a more favorable environment for the growth of beneficial bacteria as opposed to pathogens as well as the stimulation of gut-associated lymphoid tissue. And faster transit time can help with that. Because impaired intestinal motility, by decreasing intestinal clearance, might promote the development of unfavorable habitat for physiological gut microflora and the invasion of small bowel lumen by colonic bacteria.

Transit time & SCFAs

Slowing down transit time reduces the fermentation efficacy of complex carbohydrates and leads to diminished production of the short-chain fatty acids (SCFAs), acetic acid, propionic acid and butyric acid. Slow transit time also reduces hydrogen producers and increases methane producers as mentioned above.

On the other hand, accelerating transit increases SCFA production. This study found that approximately twice as much butyric acid was produced in the fast-transit compared with that in the slow-transit group. The ratio between acetic acid and propionic acid was also roughly two times higher in the slow-transit group. An elevated ratio of acetate:propionate may increase serum lipids and, therefore, possibly cardiovascular disease risk (R).

A recent study involving ~29,000 patients with chronic constipation and >86,000 controls reported that chronic constipation is associated with a significantly higher prevalence and incidence of colorectal cancer and benign colorectal neoplasms compared with those in matched chronic constipation-free individuals (R).

In this study, the participants with low bowel movement frequency at baseline survey had a higher risk for Parkinson’s disease diagnosis in the subsequent 10 years on average (R).

Slow transit time & degeneration

Slow transit time is shown to lead to lower production of SCFAs, such as butyrate. Buyrate is the major energy source of the colonocytes which help to prevent leaky gut and assist with peristalsis. As a side note, if the colonocytes are inflammed, they cannot properly utilize the butyrate.

Energy deficiency in colonocytes leads to a decrease in cellular oxidative phosphorylation (energy production) and an increase in oxidative stress, inflammation, leaky gut, gut dysbiosis, etc.

Butyrate increases ATP and CO₂ which diminishes autophagy and oxidative stress.

Slow transit time leads to an increase in bacteria that create toxic byproducts. The slow transit time also prolongs the duration these byproducts can produce inflammation in the gut and also allows great absorption of these byproducts by the body.

Constipation is associated with increased oxidative stress and inflammation in the gut. The increased creation and absorption of these toxic byproducts cause neurological damage, which then further damages gut function.

Enteric neuron damage may also be caused by bacterial lipopolysaccharide (found in IBS-PI) and the presence of pro-inflammatory agents, which divert tryptophan (the main serotonin precursor) into the kynurenine pathway, leading to high pro-oxidant agent synthesis [31]. In this manner, with both enteric neuron apoptosis and oxidation-promoted mast cell mutation, a vicious cycle involving an aberrant inflammatory response and gut-brain axis impairment leads to high levels of motilin and serotonin and also extremely high levels of somatostatin [25], which are the main factors regulating bowel motility, therefore resulting in diarrhea.

…

Moreover, [50] described a possible pathway of neuroinflammation involved in enteric nerve system impairment that would lead to hyper-excitability followed by impaired intestinal motility. Thus, immune cells such as mast cells or enterochromaffin cells tend to overreact in the colonic mucosa, signaling inflammation to the ENS and further triggering the release of serotonin and several cytokines that mediate local ROS production.

Reference

Gut inflammation doesn’t just cause diarrhhea, but can also lead to slow transit time.

Neurotransmitters involved in transit time

Acetylcholine, serotonin, motilin and prostaglandins promote transit time, whereas somatostatin and PYY reduce transit time.

Inflammation in the gut, caused by slow transit time, oxidative stress, the absorption of endotoxins, promote neurological inflammation and dysfunction of the neurons involved in gut health and transit time. So even after the inflammation has been resolved, someone might still have gut issues, due to damaged neurons (R). Focusing on regenerating neurological health should then be the main focus. More on that in just a bit.

Inflammation leads to the downregulation of the serotonin transporter (SERT; which “deactivates” the effect of serotonin), which in turn makes serotonin more effective. Inflammation also causes the numbers of enterochromaffin cells to increase, which presumably leads to still more serotonin secretion (R).

Serotonin is inflammatory and contributes to IBS and other gut disorders.

But far more important than neurotransmitters is the energy status of the intestine.

This study found (in old mice) that NAD⁺ reduces with age. As NAD⁺ declines, so does bowel function and transit time, stool quality and stool weight (R). Interestingly, they also found significantly upregulated colonic tryptophan hydroxylases (TPH) expression (the enzyme that creates serotonin), serotonin release and expression of colon-predominant type IV serotonin receptor. Increased TPH1 activity, enterochromaffin cell serotonin content and serotonin have also been found in humans with chronic constipation (R).

So how can serotonin be elevated in constipation if it promotes transit time? It’s because the energy status is much more important that the neurotransmitters.

So despite significantly elevated serotonin, they still had reduced transit time and bowel health. And it’s all because of low NAD⁺.

The reason for the low NAD⁺ and subsequent colonic degeneration is because of reduced key NAD⁺-generating enzyme expression as well as increased NAD⁺ catabolizing enzymes.

So the true feature of gastrointestinal health is energy levels and a high NAD:NADH ratio.

Here’s how to increase transit time speed

#1 Increase the NAD:NADH ratio

From the same mouse study above, increasing the NAD:NADH ratio with the administration of beta nicotinamide mononucleotide, an NAD⁺ precursor, elevated colonic NAD⁺ levels and improved defecation (R).

Niacin, niacinamide and nicotinamide ribose (NR) are also very effective at increasing NAD+.

Methylene blue, inosine, vitamin K2 (MK-4), and other quinones, such as beta-lapachone, emodin, CoQ10, etc., are all very effective at increasing the NAD:NADH ratio.

Aloe (containing emodin) has been frequently used in treating constipation-predominant IBS (R). Emodin can enhance the function of small intestinal peristalsis of mice by mechanisms of promoting secretion of motilin, lowering the content of somatostatin and inhibiting Na⁺–K⁺-ATPase activity of small intestinal mucosa (R).

#2 Probiotics

Lactobacillus Rhamnosus

This study found that 5 different strains of L. rhamnosus relieved constipation with different aspects of the GI tract, including gastrointestinal regulatory peptides, neurotransmitters, neurotrophic factors, and gut microbiota (R).

L. rhamnosus FHeNJZ7-1 and FFJND15-L2 led to a significant increase in the concentration of serotonin in the colon, so they would be best avoided if you have some kind of intestinal inflammation as serotonin is inflammatory and implicated in IBS.

L. rhamnosus CCFM1068, FHeNJZ7-1, and FTJDG11-1 reduced the PYY concentrations in the serum of constipation model mice and alleviated the inhibitory effect of this peptide on GI transit and motility (R).

Both L. rhamnosus FHeNJZ7-1 and FZJHZ11-7 administration led to significant increases in the expression of BDNF content in the colon. Patients with constipation often present with abnormal enteric nervous system functions, and previous reports on constipation have described reduced numbers of colonic neurons and damage to this cell population. BDNF plays key roles in the development and maturation of neurons and promotes the regeneration of intestinal neurons and can also accelerate colonic peristalsis and increase the frequency of defecation.

L. rhamnosus FZJHZ11-7 is shown to increase the abundance of Coprobacillus, which is low in people with obesity and constipation (R).

So if I had to pick, I’d go with FHeNJZ7-1 and FZJHZ11-7 as they can lower PYY and increase BDNF and Coprobacillus, which should help with bowel health and transit time and constipation.

Other probiotics

Other probiotics, such as Lactobacillus Plantarum (R, R, R), Lactobacillus paracasei subsp. paracasei  NTU 101 (R) and Lactobacillus reuteri Shirota (R) can also be helpful at lower endotoxin, improving gut function and increasing transit time.

A researcher observed a significantly lower abundance of Bifidobacterium and Bacteroides species in the gut microbiota of patients with functional constipation than in normal controls (R).

Supplementing the probiotic VSL#3, increased Lactobacillus, Bifidobacterium and Bacteroides species by many folds in people without constipation, but not in those with constipation. Regardless, mean Bristol scores and complete spontaneous bowel movements (CSBMs)/week increased significantly in those with functional constipation after ingesting VSL#3. Relief of subjective CSBM frequency, stool consistency and abdominal bloating were reported in 70%, 60%, and 47% of patients. After VSL#3 cessation, 44.4% of patients with symptom improvement experienced constipation recurrence mostly within one month (R).

#3 Saturated fat

Saturated fat, such as MCT and stearic acid, can increase transit time speed.

An excess of intracolonic saturated long-chain fatty acids (SLCFAs) was associated with enhanced bowel motility in NMS rats. Heptadecanoic acid (C17:0) and stearic acid (C18:0), as the most abundant odd- and even-numbered carbon SLCFAs in the colon lumen, can promote rat colonic muscle contraction and increase stool frequency. Increase of SLCFAs was positively correlated with elevated abundances of Prevotella, Lactobacillus, and Alistipes.

Reference

Avocado consumption, by increasing Faecalibacterium, Lachnospira, and Alistipes, leads to elevated SCFA and stearic acid levels, which improve gut health and transit time (R). Stearic acid promotes transit time by activating the GPR40 receptor in the gut.

The consumption of animal protein has also been shown to increase Bacteroides and Alistipes (R). When I eat a lot of protein, rich in stearic acid, especially with only honey, my bowel movements are amazing.

If you want to learn more about the benefits of dairy fat, which is a good source of C15 and C17, check out my article on the subject.

#4 Lower Methanobrevibacter

The methane producing bacteria, Methanobrevibacter, are thought to contribute to constipation. Methane slows transit time and makes the stool hard, which in excess, causes constipation.

Reducing Methanobrevibacter with anti-biotics, such as neomycin and/or rifaximin (although they work better together) help against constipation.

Natural compounds that lower methane producers and increase transit time speed are garlic powder and bitter orange and the combo works even better (R). Garlic and cinnamon essential oil has also been shown to be effective (R).

Lastly, the probiotic mixture for PROBA® (PROBA Formula) consisted of 6 species of probiotics (L. plantarum, L. salivarius, L. casei, L. acidophilus, B. animalis subsp. lactis and B. bifidum) reduces Citrobacter, Klebsiella, and Methanobrevibacter which improves gut health and transit time (R).

#5 Use poop promoting (laxative) herbs

An 18-week prospective, randomized, double-blind, placebo-controlled clinical study on 120 subjects documented that Ma Zi Ren Pill increased complete spontaneous bowel movement and decreased straining at evacuation and no serious adverse effects were noted (R).

A randomized, double-dummy, double-blind, and placebo-controlled trial on 120 participants showed that CCH1 was superior to lactulose for promoting spontaneous bowel movements (R).

Other good laxatives include magnesium (Epsom salt, Mg citrate, etc.), high dose vitamin C, prunes, figs (R), cascara sagrada, senna, aloe bitters, Rhubarb, ox bile, UDCA (R) and TUDCA (the laxative properties of bile acids have been recognized since 1868).

#6 Walk regularly

Walking is one of the best ways to stimulate transit time. It’s almost guaranteed that you’d have an amazing bowel movement after a good morning walk.

As a side note, have you ever seen that when dogs smell flowers they can immediately get a bowel movement? Similarly, I feel I get better transit time and bowel movements when I walk in nature vs an area without much greenery.

#7 Optimize vitamin D levels

Vitamin D is essential for gut health and low vitamin D is also associated with constipation (R).

All the more reason to go for the walk each day in the sun.

#8 Eat a diet that helps you

Just because a diet works for someone doesn’t mean it’s going to work for you. For example, there is a threefold difference in mean transit time in men consuming identical diets (R).

So this comes down to experimentation.

If you’re looking for simple guidelines on how to do it, check out my Alpha Energy Nutrition Course.

If you want to learn more about the gut connection and health, check out my other articles:

• The gut-testosterone connection
• The gut-brain connection
• The gut-thyroid connection
• The gut-hair loss connection