Note: Public Live Draft Notice. 

This first part (of two) serves as “introduction” to the problems I’m having for many year/s – the (often unexplained) bloating and distensions during fasting both standard (20:4) and prolonged (40+). Revisiting back Dr Bernstein’s lengthy articles also prompted me interest to revisit this topic. 

This first or Part One –  necessitates surface reading on the basics (as well as not so basics).  Gastroparesis, its symptoms and other associated conditions. Extrinsic and intrinsic possible factors.  Before then also – the Questions / food-for-thoughts which I will continue these on Part Two.

I should warn, for those who cling onto the idea that fibre is the holy grail ~ be forewarned this isn’t a writing that fully nods with conventional narrative. But neither is this feature write-up to dismiss them as unhelpful either.

Reading and/or “hoarding” papers, journals and research reviews means far less, comparatively so I’d dare may say ~ against how you implement, experiment and introspect. Hence, how others may opininonate this feature article as simply that – “my opinion piece” ~ be forewarned this appeals to my concern and nuance only.

Consequently writing this in and of itself, doesn’t imply finality nor that I have known all the answers. I truly don’t. There are practitioners, “influencers”, in guest podcasts  ~  far more versed than me in these topics yet still having problems.

On top of it all, this is a Live Public Draft.  I have real obligations overlapping dusk to nights . Often leaving only one or two hours in the early mornings. My channel is not about information frequency, but sincerity on my own limitations*.

 Mistakes, errors and what-not – are all for honesty display. And no, I do not “employ” third party proof checkers. Nor do I use / fully endorse – automation / artificial intelligence.

With all that being said, let’s begin.

The problem(s)

Bloating, distension, ballooning. Almost certainly, every one has had these moments. The traffic jam.

Despite all fluid intakes (that which I don’t necessarily subscribe to general narrative  as my recent experience suggested as otherwise not being good) ~ I don’t know how long exactly – but many years of encumbrance would be my correct guess.

Some days I felt completely fine, but most are riddled with puzzles and question marks.

Therefore, I suspect several things. Although keeping in mind much of this feature writing has been condensed (that which adds further difficulty of writing this in a timely manner).

1. One ~ I may have a slower than usual gut transit.
   Things associated include delayed hunger and appetite though I’m still not convinced this to be “bad”, as I will get to cover this more in the next part.
2. Or two – I’m just getting old.
   Things are just getting more sensitive. Sensitive as in volatile – how I must pay attention any or all potential triggers. As well – reconciling on the topic on gastro’s once again. 

The anatomy. Gas. General causality – extrinsic and intrinsic.

So what is distension? Apparently it is simply gas or “Flatus”, given the technical name for fart that ejects out (as we know it). CO2, Hydrogen, Sulfur and to lesser extent, Methane.

“Gases that are trapped by peristaltic colon exert pressure on the walls, causing the abdominal pain experienced by patients.” Ho KS et al (2012)

Gas, inside the tract, is where the “Trapped wind” got its name  (and the outcome,  aptly so). Literally – the walls of the tract had to keep stretching and expanding while the bubbles kept building up and up. Upon which there is only one inevitability – lots of nagging pain.

So what causes these gas to build up in the first place?  I tend to group these into two listings ~ what I can somewhat control (Extrinsic)  and those I cannot (Intrinsic). 

Extrinsic ~ things I can somewhat control.

• When to break the fast. Sounds obvious, but the duration and/or length have been an interesting finding of mine lately.
• Fibre intake.
• FODMAPs.
• (Too little or too much?) ~ stomach acidity.  I still am adamant to the view that too little (or “dyspepsia”) is far worse than than too much. A decade+ worth ruminating on this topic is enough, at least in my case.
• Swallowing too much “air” ( as “Aerophagia”). That one’s interesting as I tend to (subconsciously) prefer breathing through mouth during exercise.
• Too much fizzy drinks (as after all it’s bubbling in there), but this isn’t clear cut and dry…
• SIBO – small intestinal bacterial overgrowth.
• (Too much) food combining.

Then, the Intrinsic factors. Things I am far less able to control.

• Temperature / environmental / seasonal transitions.
  Technically speaking we “could” control this. Ideally we’d be living in a climate that is consistent as in neither too hot nor cold. Alas, this obviously requires you to ably move / vacate to another environment elsewhere. Unless if you are the “nomad” millionaire owning multiple properties around the globe, we all remain, alas – mere mortals  (or “Normies” ~ as they call it). 
• ANS / The Autonomic nervous system (Parasympathetic Rest/Digest vs Sympathetic Fight/Flight)
  between the brain to all bodily organs; regulating all sensory information and hormonal secretions. Certainly complex yet also susceptible from damage overtime from aging, illness, or injury.
• Ageing.
  Pretty much unavoidable. Which pretty much cascades everything downwards as follows.
  • Nerve Damage (whole lot of complicated topics here, but so it goes) ~ Diabetic neuropathy
  • Inflammation, injury or degradation of the nerve signalling. Mainly concerning the vagus nerve — that runs along the spine responsible for ANS / Autonomic nervous system. 

The pathophysiologies.

So here are the outcomes, if left unchecked, we’ve known so far. Starting with common then not so common.

• Nausea, vomitting, persistent diarrhoea….
• Functional dyspepsia..
• Functional bloating..
• IBS (not to be confused with IBD despite both concerning the bowels apparently the latter is far more serious).
• A whole series of inflammatory conditions (here goes a list once again, as accordingly to Cleveland clinic):

• • Appendicitis.
  • Pancreatitis.
  • Peritonitis.
  • Gastroenteritis.
  • Cholecystitis.
  • Diverticulitis.
  • Neonatal necrotizing enterocolitis.
  • Inflammatory bowel diseases.
  • Botulism.
  • Sepsis.

Certainly there’s more I’d wager, as I’m certainly no gastroenterologist.

Gastroparesis, Bezoars, lack of peristalsis.

Firstly, why do I think these being the prime suspects? Simply put I have been experiencing some, though not all of the symptoms associated quite regularly. Often with few to little explanation.

• Early satiety.
• Bloating during next day fasting and;
• Early fullness.

All these During or after / post ingestion of meals usually solids.

Usually my movements started around 3PM onwards the next day. However this obviously depends on how much I ate during calorie surplus / carb allowance days. Depending on obviously also – general stress and environmental / seasonal conditions. This is with enough fluid intake (2-3L at least, including coffees and teas).

What is Gastroparesis?

“Gastroparesis” is itself quite literally means a pause of stomach emptying. It is multi-faceted in its etiology. Meaning ~ multiple causes.

I am thankful, that I am yet / never that is, throughout my years of Keto, IF and now CKD+IF ~to experience nausea and vomitting. Only one or two  instances where diarrhoea were involved ~  this typically resolves within two days, at most. That also thankfully – occurred during weekends.

What is Perilstaylsis?

Perilstaylsis refer to motility, transit or simply – movement.  The lack of movement is where “bolus” (pre-digested mix of food with most enyzymes mixed ~ amylase,  proteases, lipase, HCLs and bicarbonates) does not move at all. According to gastroenterologist terms, “peristaltic ileus” is where movement becomes slow to a halt.

If left unchecked, there’s possibility of Bezoars formation. Not much explanation (I hope here is needed). But if food simply “sit there” for days, then potentially ~ the tiny opening to the pylorus / the small intestine becomes blocked. Thereby preventing digestion altogether.

What are Bezoars?

Bezoars are clumped, undigested matter that piles up and up that apparently takes months if not, years to form. Although I have seen some references proclaiming they can form much sooner.

So far documented to have five types (Galan DM & Rabat RL 2024). Most common is Phytobezoars made up of cellulose and/or other non digestible fibres. Then there’s Pharmacobezoars — refer to the indigestible fillers, additives excipients or carrier molecules upon which drugs are delivered. Polybezoars are matter(s) from totally non-food source – think metals, and plastics (one may argue microplastics as included)*. There’s also Lactobezoards deriving from milk (breast milk interestingly enough) – but are considered very rare (as in only “ninety six” (96) known cases recorded going back from the 1950s).

*TRIVIA. Apparently there’s a study in UAE (United Arab Emirates)  examining mortality correlation between camels and presence of plastics in their digestive tract .  This was apparently ~ the very first Google® search results upon entering the keyword “Polybezoars” originates.

Finally, there are two more types that are interesting.

“Diospirobezoar” ~ seems to be caused only by eating persimmons and from excess tannins (which that includes tea). “Trichobezoar”~ involves evidence of eating human hair ~ which that apparently is a known psychiatric illness (commonly in women) called “Trichotillomania and Trichophagia.

I am glad to say I am not the latter. Though I empathize the very small however percentage of readers reading this, who may, under exceptional circumstances – be diagnosed or suspected of such a condition. That – I’d wager, is where psychiatry intervention or counselling might be warranted.

Now questions meet (more) questions.

And so it begins my food for thoughts section.

Obviously due to this Part One’s already lengthy reading, I can only cap to three (3) questions, the rest will follow on in Part Two. 

So how does Fasting affect all of this?

“During fasting, multiple physiological adaptations occur to conserve energy during the fasting period. For instance, GE is slowed in both animal models [46] and healthy individuals during fasting periods [47]. “ (Abdulrasak M et al 2025).

Firstly, onto the research.

• The widely popular mainstream amusement that “fasting shrinks the organs and stomach” do somewhat holds some truth.
  • “Intestinal atrophy” or in other words, shrinkage of the intestinal overall mass has been reported extensively in animal studies (Ducarmon QR et al. 2023).
• This study looked at 14 subjects upon 12 and 24 hours of fasting (RB Jones et al. 2012). 12 of them were found with slowed gastric emptying.
• Ramadan fasting (12-16 hours, from dawn then break at sunset) appears to be mixed in terms of gastroparetic symptoms; where they appear more prevalent among the diabetics (Abdulrasak M et al 2025).
  • For context – dates (considered high FODMAPs), followed by legumes ~ (chickpeas) hummus, lentils (though eggs and chicken, obviously no pork allowed) are usually considered the “general” principles.    
• Low stomach acid (again, coinciding with my conviction on betaine HCL’s importance) ~ is implicated during the fasting state. 

What happens to the vagus nerve doing amidst prolonged fasting? Sadly the research thus far are too complex for me to derive understandable conclusions. But so far – on what I can gather:

• The vagus nerve appears more active after 48 hour fast (Khasar SG et al 2003).  Unfortunately just an animal study. Because “48 hours of fast” ~ for a rat – translate to a very, very long time comparatively to us human. To illustrate for context a mouse lives up to two years. 
• The ANS / autonomic nervous system appears more primed towards “rest and digest” phase during the fasting window. This, to me seems logical given if there is no incoming calories (except gluconeogenesis).
• This paper, despite complicated and beyond my knowledge on the ANS, suggests that fasting indeed induces “profound” changes  (Schwerdtfeger AR & Rominger C 2024). Interesting here at least it is based on the classic 16/8 formatting. But  / alas ~ the subjects are relatively young (<22 yrs) and entirely new to IF/TRF. 

But what happens during actual starvation?

I should stress that I am not, nor have I ever been ~ in state of true starvation. Infrequent 40+ hours fasting here and there each year is, I’d wager ~ “mild” compared to our ancestors.  

However it’d be interesting to know what happens, or what the literature has to say, when it comes digestive state in a malnutrition state.

The “worst” of all account I have read so far ~ had much reference within war times~ the holocaust and prisoners-of-wars. There is such a thing as “nutritional diarrhoea” where digestive system simply cannot tolerate any caloric input.

“Refeeding Syndrome” also becomes relevant here. This is where sudden jump in calories prompted major stress response should and if (apparently) – electrolyte imbalances are not addressed first and foremost (Sharma-Persaud et al. 2022). This may occur  in as quick as five days of fasting as proclaimed here.   Dr Jason Fung also wrote a good article, citing several prominent individual(s) embarking more than dozens (of days) worth of fasting, and the not-so-good outcomes.

People might think, “sure, that just applies to a small few crazies out there“. I’d stop and question ~ how many anorexics out there, or orthorexics in our midst in general ~ who are obsessed with dieting culture? Chances, more than just a “few”. Malnutrition among anorexics particularly deserves considerate amount of attention and support.

“Liberal feeding with rich foods, such as were supplied with well-meant but mistaken kindness by fighting units when the camp was first uncovered, or even by injudicious dieting in hospital, caused abdominal pain and vomiting, and precipitated or exacerbated diarrhea, sometimes with fatal results.”  (Kelly, P. 2020)

Starvation of experimental animals induces marked loss of intestinal weight, villus surface area, and enterocyte mass (47, 48). Starvation increases intestinal permeability (48, 52), although recent evidence suggests that this may be complex as starvation can also reduce expression of claudin-2 (which increases paracellular ion flux) through autophagy (53). (Kelly, P. 2020)

Worse during winters, less on summers.

Criticise me yet again for being an anecdote, but I felt more susceptible to these distension problems during winters.  Prolonged cold exposures especially during fasting  causes some tension and clenching all muscles ~ readily shivering, simply when it has to. Warmer days – the opposite happens

I think that logically, cold environment = stasis or preservation. Warmth or heat = progress or at least – some ‘activity‘.

This is perhaps why – the old  advocates on gentle walks after heavy meals.  Exercise for instance, does at the very least halts that distension, though only temporarily before returning again on the later evenings (approaching daily 20-21 hours fasts).

I do agree that cold exposure generally obligate higher metabolic stress, as the body compensates to maintain thermal stasis (which presumably, around 37 degrees C). This paper (note: truncated behind paywall for surface reading only) proclaimed 5% “increase” in 24 hour energy metabolism.

But ~ what about  human research on fasting, gut conditions and seasonal transitions? Far and few.

1. This pilot study of ten days of fasting found a shift of gut bacterium (the family) towards “Proteobacteria phylum” whilst Firmicutes and Bacteroidetes families were lowered. But it didn’t (at least from what I can find) discuss anything with temperature or cold exposures.
2. This one on animal models (squirrels) suggested an increase in bacterial balance. But the paper’s writing and its layered prerequisites on technical and gastro terms ~ I admit – are all beyond me and made me unsure of its conclusions, if any to interpret meaningful correlations. Also, in regards to animal->human extrapolations ~  (most of us) don’t hibernate like squirells do, unless perhaps one may say – extremely sedentary, immobile and/or obese.

Conclusion (Part 1)

I should maintain and assert whilst that these problems are highly elusive,  they do come and go. 

As I said, I still do not have all the answers, only signs that I can at least identify. 

In the next part I will cover more questions and other food for thoughts. 

Live-it-Forward,

AW.