Quote from Dr. Garrett Smith on February 4, 2019, 11:32 pm

The first study shows that butyrate increases the production of retinoic acid (the most damaging form of Poison/"Vitamin A":

The SCFA butyrate stimulates the epithelial production of retinoic acid via inhibition of epithelial HDAC.

We conclude that the SCFA butyrate inhibits HDAC3 and thereby supports epithelial RA production.

If you're here, you would be safe in ASSuming that if butyrate increases retinoic acid production, that I would believe that butyrate is NOT a good thing.  Also remember that I'm always after the long-term results in actual living organisms (in vivo), and much less in the short-term petri-dish type studies (in vitro).

Resistant starch is/was a big fad for a while.  One of the supposed benefits of it was that it would be fermented in the gut into short-chain fatty acids like butyrate (butyric acid).  Here's a bit more on it:

Resistant starch is a type of highly-fermentable insoluble fiber. Unlike most starches, resistant starch isn’t fully broken down in your small intestine. It “resists” the action of your digestive enzymes because of its molecular structure; and instead of being a source of slow-burning carbohydrates for you, it becomes food for specific types of bacteria in your colon (which ferment it to produce beneficial short-chain fatty acids like acetic acid, propionic acid, and butyric acid).

For a while, people were ALL about this stuff.  That is, until they started to realize that all the bloating, flatulence, and general poor digestive symptoms that came along with it weren't worth it.  Maybe it wasn't as good for them as the science had told them it would be?  Hey, does that sound sort of like the story of Poison/"Vitamin A" maybe?  Do you remember how I connected these two above?

Potato starch is a common source of resistant starch.  Now, on to the tumor-enhancing effects of resistant starch (and thus butyrate / butyric acid):

Wheat bran suppresses potato starch--potentiated colorectal tumorigenesis at the aberrant crypt stage in a rat model.

METHODS: Three groups of rats received either a low-RS/low-fiber ("basic") diet, the basic diet containing raw potato starch as 20% of carbohydrate content, or the potato starch diet plus 10% of "wheat bran" fiber. Epithelial proliferation, aberrant crypt foci (ACF), and tumors were measured 6 and 20 weeks after a 10-week course of dimethylhydrazine.

RESULTS: Rats on the potato starch diet had tumors more frequently and had larger tumors than rats consuming the wheat bran or basic diets.

Intestinal tumorigenesis in the Apc1638N mouse treated with aspirin and resistant starch for up to 5 months

The Apc1638N mouse model, which carries a targeted mutant allele within the adenomatous polyposis (Apc) gene and develops intestinal tumours spontaneously, predominantly in the small bowel, was used to investigate the effects of two potential chemopreventive agents, aspirin and α-amylase resistant starch (RS). Heterozygous Apc+/Apc1638N mice were fed semi-purified diets rich in animal fat, animal proteins and sucrose and low in dietary fibre (Western style diets) from ~6 weeks up to 6 months of age. Two of the diets contained aspirin (300 mg/kg diet) and two RS (1:1 mixture of raw potato starch: Hylon VII at 200 g/kg diet) in a 2×2 factorial design. A fifth treatment group were fed a conventional rodent chow diet. The mice fed the Western style diets became almost three times as fat as the chow-fed mice but this did not affect tumour yield. Treatment with RS resulted in significantly more intestinal tumours whereas aspirin alone had no effect. However, there was a significant aspirin×RS interaction, which suggests that aspirin could prevent the small intestine tumour-enhancing effects of RS in this Apc-driven tumorigenesis model. The possibility that large amounts of purified forms of resistant starch may have adverse effects within the small bowel is a novel observation that requires further investigation since greater intakes of starchy foods (and of RS) are being encouraged as a public health measure in compensation for reduced dietary fat intake.

Anytime something is either a Poison/"Vitamin A" compound (beta-carotene, isotretinoin aka Accutane) or it raises Poison/"Vitamin A" activity (butyrate from resistant starch), and it is put in a study where the researchers are planning/hoping to see it reduce cancer...they nearly always get the exact OPPOSITE.

Contrasting effects of non-starch polysaccharide and resistant starch-based diets on the disposition and excretion of the food carcinogen, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), in a rat model.

Indeed, carcinogen biovailability was significantly enhanced by resistant starch.

I would include Poison/"Vitamin A" in the carcinogen group. So what about in humans?

Effect of Enzyme-resistant Starch on Formation of 1,N²-Propanodeoxyguanosine Adducts of trans-4-Hydroxy-2-nonenal and Cell Proliferation in the Colonic Mucosa of Healthy Volunteers

There are indications now that enzyme-RS induces oxidative stress that is not correlated with increased cell proliferation. If it is accepted that the formation of DNA adducts reflects oxidative stress, which in turn accelerates the process of carcinogenesis, then certain forms of RS may have a tumor-enhancing effect rather than a tumor-protective effect.

And finally, increased resistant starch intake was associated with an increase in a heart disease risk marker:

Diets high in resistant starch increase plasma levels of trimethylamine-N-oxide, a gut microbiome metabolite associated with CVD risk

Production of trimethylamine-N-oxide (TMAO), a biomarker of CVD risk, is dependent on intestinal microbiota, but little is known of dietary conditions promoting changes in gut microbial communities. Resistant starches (RS) alter the human microbiota. We sought to determine whether diets varying in RS and carbohydrate (CHO) content affect plasma TMAO levels. We also assessed postprandial glucose and insulin responses and plasma lipid changes to diets high and low in RS. In a cross-over trial, fifty-two men and women consumed a 2-week baseline diet (41 percentage of energy (%E) CHO, 40 % fat, 19 % protein), followed by 2-week high- and low-RS diets separated by 2-week washouts. RS diets were assigned at random within the context of higher (51–53 %E) v. lower CHO (39–40 %E) intake. Measurements were obtained in the fasting state and, for glucose and insulin, during a meal test matching the composition of the assigned diet. With lower CHO intake, plasma TMAO, carnitine, betaine and γ-butyrobetaine concentrations were higher after the high- v. low-RS diet (P<0·01 each). These metabolites were not differentially affected by high v. low RS when CHO intake was high. Although the high-RS meal reduced postprandial insulin and glucose responses when CHO intake was low (P<0·01 each), RS did not affect fasting lipids, lipoproteins, glucose or insulin irrespective of dietary CHO content. In conclusion, a lower-CHO diet high in RS was associated with higher plasma TMAO levels. These findings, together with the absence of change in fasting lipids, suggest that short-term high-RS diets do not improve markers of cardiometabolic health.

If it walks like a duck, and talks like a duck, it's probably a duck.  If it increases retinoic acid, makes people farty and bloated, has significant research showing trends towards making more and bigger tumors, and increases markers associated with heart disease...it's probably NOT good for you.  Just another internet-diet-blogger trend that needs to die.