HoldsUp

Kiran Krishnan

Microbiome Labs

Kiran Krishnan is a researcher in the field of gut health and the microbiome. His published work focuses on the effects of spore-based probiotics, particularly Bacillus strains, prebiotics, and synbiotics on gut microbiota composition and metabolic activity. His research also investigates the use of dietary and nutritional supplements in models of antibiotic-induced dysbiosis and conditions such as inflammatory bowel disease and hepatic encephalopathy.

36 claims checked on air: 1 context 4 contradicted 14 overstated 12 supported 5 unverified

What they said on air - supported

0:03:09supportedmoderateGLP1s & Your Gut in Menopause: What Women Need to Know

Approximately 40% to 50% of the microbes in the human gut are made up of gram-negative bacteria.

"and a lot of people have around 40-50% of the microbes in their gut made up of gram-negative bacteria." (said at 0:03:09)

The human intestinal microbiota is predominantly composed of two major bacterial phyla: Firmicutes (primarily Gram-positive) and Bacteroidetes (Gram-negative), alongside other groups such as Proteobacteria. Depending on individual variation, enterotype, and the analytical technique used (e.g., electron microscopy, classical Gram staining, or 16S rRNA sequencing), Gram-negative bacteria frequently constitute between 30% and 50% (or more) of the microbial community in many individuals.

0:07:45supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

Estrogen increases glycogen production in the vaginal canal, which feeds Lactobacilli that produce lactic acid to maintain vaginal pH.

"estrogen acts as a metabolite for microbes in the lining of the vaginal canal that increases something called glycogen production. And that glycogen production feeds the lactobacilli that are in the vaginal canal, which then create lactic acid and maintain a healthy vaginal canal." (said at 0:07:45)

Published gynecologic and microbiological literature well establishes that estrogen stimulates the proliferation and maturation of vaginal epithelial cells and the accumulation of glycogen in the vaginal epithelium. This glycogen serves as a primary substrate that is metabolized by vaginal Lactobacillus species to produce lactic acid, which acidifies the vaginal microenvironment (typically maintaining a pH between 3.8 and 4.5) and protects against pathogenic infections.

0:34:40supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

Approximately 80% of vagus nerve fibers are afferent (transmitting signals from gut to brain), while only 20% are efferent (transmitting from brain to gut).

"if you look at the nerve um you know, structure of of that of the vagus nerve itself, it's 80% of the nerves are what we call afferent nerves, which means 80% of the information is actually going from the gut to the brain. And only 20% coming from the brain down to the gut" (said at 0:34:40)

Extensive anatomical and physiological literature confirms that the vagus nerve is a mixed nerve predominantly composed of sensory (afferent) fibers. Approximately 80% of vagal nerve fibers transmit sensory signals from visceral organs (including the gastrointestinal tract) to the central nervous system, while approximately 20% are motor/secretory (efferent) fibers transmitting signals from the brain to visceral targets.

0:39:01supportedvery lowGLP1s & Your Gut in Menopause: What Women Need to Know

Gut microbes metabolize cortisol into byproducts that alter renal potassium-sodium ratios, increasing fluid retention and raising blood pressure.

"there are microbes in the gut that can actually metabolize cortisol, and the metabolic byproducts of that go to the kidneys, and they shift the the solute and solvent ratios in the kidneys. So, the potassium-sodium ratios, which then increases the amount of water that is going back into circulation. So, then the kidneys actually press more water back into circulation in order to increase blood pressure." (said at 0:39:01)

The speaker accurately describes a recognized pathophysiological mechanism known as the glycyrrhetinic acid-like factor (GALF) pathway. Published biochemical and preclinical evidence demonstrates that certain gut microbiota metabolize endogenous glucocorticoids such as cortisol into steroid byproducts. These microbial metabolites enter the circulation and can act as inhibitors of renal 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). When 11β-HSD2 is inhibited, unmetabolized cortisol binds to and activates renal mineralocorticoid receptors, altering renal electrolyte handling (promoting sodium retention and potassium excretion), which increases water reabsorption into the circulation and elevates blood pressure. Because this mechanism is established primarily through in vitro assays, animal models, and mechanistic reviews, the overall certainty of evidence in clinical populations is very low.

0:40:20supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

Interleukin-6 (IL-6) can directly re-trigger the hypothalamic-pituitary-adrenal (HPA) axis without the presence of an external stressor.

"LPS also increases IL-6, which we mentioned before. But one of the things we didn't mention is that IL-6 can actually re-trigger the HPA axis. Even though you don't have another stimulus" (said at 0:40:20)

Interleukin-6 (IL-6) is an established activator of the hypothalamic-pituitary-adrenal (HPA) axis. Controlled clinical trials administering recombinant human IL-6 to healthy human volunteers have demonstrated that IL-6 alone triggers marked, dose-dependent increases in adrenocorticotropic hormone (ACTH) and cortisol secretion without requiring an external psychological or physical stressor.

0:41:55supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

Certain pathogenic bacteria express virulence factors and increase toxin production in response to host stress hormones like epinephrine, norepinephrine, and cortisol.

"some pathogens have learned that when the host is under stress and they're actually measuring your stress hormones like your epinephrine, norepinephrine, cortisol, and so on. When those stress hormones are elevated, that's when they they express their virulence factors and their toxin production" (said at 0:41:55)

The claim is supported by scientific research in the field of microbial endocrinology. Pathogenic bacteria (such as enterohemorrhagic Escherichia coli and Vibrio cholerae) possess sensor proteins (such as the sensor histidine kinase QseC) that recognize mammalian stress hormones, including epinephrine and norepinephrine. Exposure to these host catecholamine stress hormones directly triggers signaling cascades that increase bacterial growth, motility, expression of virulence factors, and toxin production (such as Shiga toxins stx1 and stx2 in E. coli).

0:49:06supportedmoderateGLP1s & Your Gut in Menopause: What Women Need to Know

Normal physiological human gastric pH ranges from 1.2 to 1.3, which is the third or fourth lowest stomach pH among animal species.

"The pH is very low in in normal physiological pH, it could be 1.2, 1.3. That's a very, very acidic environment. In fact, humans have I think the third or the fourth lowest pH in the animal kingdom, only next to like vultures" (said at 0:49:06)

A systematic review compiling vertebrate gastric acidity data found that normal human baseline gastric pH is exceptionally acidic (typically measured around 1.2 to 1.5). In comparative analyses across mammal and bird taxa, human stomach acidity ranks among the most acidic vertebrates, clustering with obligate and facultative scavengers (such as vultures) rather than generalist primates or herbivores.

0:58:37supportedmoderateGLP1s & Your Gut in Menopause: What Women Need to Know

Activation of bitter taste receptors stimulates L cells to secrete GLP-1, CCK, GIP, and PYY, and activates AMPK.

"Aren't bitter taste receptors what signal the L cells of the gut to kick up, too? And that's what The L cells are what secrete GLP-1. GUEST1: That's exactly right, yeah... It kicks up, you know, CCK, GLP-1s, GIPs. It kicks up the PYY, yep. And AMPK as well" (said at 0:58:37)

Activation of bitter taste receptors (TAS2Rs/T2Rs) expressed on enteroendocrine cells in the gut stimulates the secretion of satiety and incretin hormones, including GLP-1, PYY, and CCK, and triggers downstream activation of AMP-activated protein kinase (AMPK) signaling. While classical histology attributes CCK primarily to I cells and GIP to K cells (whereas GLP-1 and PYY are secreted by L cells), colonic and intestinal enteroendocrine cells expressing bitter taste receptors colocalize with and secrete these peptides upon bitter agonist stimulation.

1:01:08supportedmoderateGLP1s & Your Gut in Menopause: What Women Need to Know

Excessive accumulation of secondary bile salts, produced when gut microbes convert primary bile, can cause inflammation in the large intestine.

"there are microbes in your gut that'll convert that bile into what we call secondary bile salts. And those secondary bile salts can be very useful and helpful, but if you do too much of it, it can actually create inflammation in the large bowel." (said at 1:01:08)

The speaker's statement accurately reflects the physiology and pathophysiology of bile acid metabolism. Primary bile acids synthesized by the liver are metabolized by colonic bacteria into secondary bile acids (such as deoxycholic acid and lithocholic acid). While physiological concentrations contribute to homeostatic signaling, excessive levels or detergent activity can disrupt mucosal integrity, promote bacterial translocation, and trigger colonic epithelial inflammation.

1:05:35supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

One of the primary biological functions of bitter taste perception in the mouth is to detect potential dietary poisons.

"one of the most important aspects of the bitters for the mouth is to detect potential poisons." (said at 1:05:35)

The scientific consensus in evolutionary biology and gustatory physiology establishes that bitter taste perception evolved primarily as a protective mechanism to detect and deter the ingestion of naturally occurring toxic substances, such as plant alkaloids and poisons.

1:05:50supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

The cephalic phase response increases salivation and gastric secretions to prepare the digestive system for incoming food.

"The cephalic response is just your brain getting ready for food, right? So, it starts increasing salivation. It starts increasing some gastric secretions. Gets your body ready for food coming in" (said at 1:05:50)

The cephalic phase response is an established physiological reflex mediated by the central and autonomic nervous systems (primarily via the vagus nerve) triggered by sensory cues such as the sight, smell, or taste of food. It stimulates salivation, gastric acid and enzyme secretion, and pancreatic secretions in anticipation of nutrient ingestion to prepare the gastrointestinal tract for digestion.

1:06:15supportedhighGLP1s & Your Gut in Menopause: What Women Need to Know

Smelling and seeing food triggers the cephalic phase response.

"you can actually increase the cephalic response just by smelling food and seeing food. And we all have done that, right? You smell bacon, for example, and you're like, "Ah." Your mouth starts watering, right? That's a cephalic response." (said at 1:06:15)

The claim is supported by established human physiological research. Cephalic phase responses—including anticipatory salivation, digestive enzyme secretion, and hormonal shifts—are rapid preabsorptive physiological reactions triggered by sensory cues such as the sight, smell, taste, and texture of food.

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