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 - contradicted
Falling estrogen levels in women cause a reduction in gut microbial diversity.
"as estrogen levels start to fall and progesterone levels start to fall, but mostly estrogen, you start to see a reduction in microbial diversity within the gut microbiome. And this has been shown across the board with women." (said at 0:02:09)
A systematic review and meta-analysis comparing hypoestrogenic women (postmenopausal or with premature ovarian insufficiency, n=1,267) to euestrogenic premenopausal controls (n=463) found no significant difference in gut microbial alpha-diversity (Shannon index, p=0.990) or major bacterial phyla. While some individual observational studies have reported modest shifts in specific bacterial taxa or non-significant trends, there is no consistent evidence 'across the board' that falling estrogen levels cause a decrease in gut microbial diversity.
- contradicts: Age-Related Changes, Influencing Factors, and Crosstalk Between Vaginal and Gut Microbiota… (Journal of women's health (2002) 2022) · cited 28x in the literature
"The compositions of the vaginal microbiota were significantly different in pre- and postmenopausal women. However, such differences were not noticeable in the gut microbiota." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: The impact of estrogen status on the gut microbiome: a systematic review and meta-analysis… (Frontiers in endocrinology 2026) · cited 4x in the literature
"Out of 1092 studies screened, 7 met the inclusion criteria (n = 45 women with POI, n = 1222 post-menopausal women, n = 463 eustrogenic controls). No significant differences were observed in α-diversity (p=0.990), Bacteroidetes (p=0.440), or Firmicutes abundance (p=0.110) between hypoestrogenic and euestrogenic groups, irrespective of POI or postmenopause." (abstract, results)
pubmedfull study (doi)
Elevated lipopolysaccharide (LPS) can reduce testosterone production in women.
"LPS as LPS increases as that lipopolysaccharide increases, it actually can reduce testosterone production even in women" (said at 0:07:15)
The claim states that elevated lipopolysaccharide (LPS) reduces testosterone production in women, which inverts the observed biological relationship. While chronic endotoxemia suppresses testicular steroidogenesis and lowers testosterone in males, in females LPS exposure stimulates ovarian androgen production. In clinical studies, circulating LPS and endotoxemia markers correlate positively with testosterone levels and hyperandrogenic symptoms in women (such as in polycystic ovary syndrome).
In the 9-year Netherlands Study on Anxiety and Depression, serum LPS was the only biomarker associated with 100% of anxiety and depression cases and predicted symptom severity.
"there was a 9-year long study called the Netherlands Study on Anxiety and Depression, where they were looking at a number of biomarkers in people that were suffering from anxiety and depression, and then they followed them for 9 years to look at the best associated biomarkers with the condition. They found only one biomarker was associated with 100% of the cases of anxiety and depression, and the level of that biomarker could predict how severe their anxiety and depression was. And in fact, in that 9-year follow-up, for any individuals who that biomarker went away, anxiety and depression went away as well. And that one biomarker was LPS, with serum LPS levels." (said at 0:12:35)
The claim significantly mischaracterizes the methodology and findings of the Netherlands Study of Depression and Anxiety (NESDA). NESDA did not measure circulating serum LPS (endotoxin) levels as a biomarker. Instead, researchers used LPS in vitro as an ex vivo laboratory reagent to stimulate blood samples and assess immune cell cytokine production capacity (such as IL-6, IL-8, and TNF-alpha). Furthermore, no biomarker in NESDA was associated with 100% of anxiety or depression cases, nor did symptoms resolve in 100% of individuals whose inflammatory markers normalized. The actual published NESDA analyses demonstrated small effect sizes (such as standardized beta coefficients up to ~0.14) connecting basal and LPS-stimulated cytokine production capacity with anxiety and depressive symptom persistence over 9 years, much of which was attenuated after controlling for health and lifestyle factors.
- contradicts: Cytokine production capacity in depression and anxiety. (Translational psychiatry 2016) · cited 199x in the literature
"Few studies examined the expression of cytokines in response to ex vivo stimulation of blood by lipopolysaccharide (LPS) to study the innate production capacity of cytokines in depression and anxiety. To investigate this, baseline data from the Netherlands Study of Depression and Anxiety (NESDA) were used" (abstract, background, passage verified)
pubmedfull study (doi) - contradicts: Basal and LPS-stimulated inflammatory markers and the course of anxiety symptoms. (Brain, behavior, and immunity 2021) · cited 31x in the literature
"In conclusion, we found that participants with high levels of inflammatory markers have on average high levels of anxiety consisting of physical arousal and agoraphobia, which tended to persist over a period of nine years, albeit with small effect sizes." (abstract, conclusions, passage verified)
pubmedfull study (doi)
Lipopolysaccharide (LPS) induces bone inflammation that promotes osteoclast-mediated bone resorption over osteoblast activity, driving osteoporosis.
"LPS also drives inflammation in the bone. Inflammation in the bone changes these uh cells called osteoclastic cells, which build bone into Sorry, osteoblastic cells, which build bone into osteoclastic cells, which actually reabsorb reabsorb bone and and uh makes makes bone weaker. Um so it drives osteoporosis as well, right?" (said at 0:14:34)
While lipopolysaccharide (LPS) and chronic inflammation promote bone resorption by stimulating osteoclast differentiation and suppressing osteoblast-mediated bone formation, osteoblasts do not transform into osteoclasts. Osteoblasts and osteoclasts arise from two completely distinct cell lineages: osteoblasts develop from mesenchymal stem cells (mesenchymal lineage), whereas osteoclasts differentiate from hematopoietic stem cells and monocyte/macrophage precursors (hematopoietic lineage). In LPS-induced inflammatory bone loss, LPS stimulates Toll-like receptor 4 (TLR4) on osteoblasts and immune cells to upregulate inflammatory mediators, prostaglandins, and receptor activator of nuclear factor-kappa B ligand (RANKL), which recruit and differentiate macrophage/monocyte precursors into active osteoclasts rather than transdifferentiating osteoblasts.
- context: Roles of Toll-like Receptor Signaling in Inflammatory Bone Resorption. (Biology 2024) · cited 38x in the literature
"The ligands for TLR2/1, TLR2/6, TLR3, and TLR5, as well as TLR4, induce osteoclast differentiation associated with the production of PGE2 and the receptor activator of nuclear factor-kappa B ligand (RANKL), an inevitable inducer of osteoclast differentiation in osteoblasts." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Early Growth Response 1 Plays an Essential Role in Proinflammatory and Osteoclastogenic Ac… (FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2025) · cited 3x in the literature
"LPS induces osteoblasts to express proinflammatory cytokines, chemokines, and prostaglandins, as well as macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL), which directly activate adjacent osteoclasts toward bone resorption." (abstract, results)
pubmedfull study (doi) - contradicts: Cibotii Rhizoma Extract Mitigates LPS-Induced Inflammatory Bone Loss by Inhibiting the RAN… (Advanced biology 2026)
"CR suppressed receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived monocyte/macrophage (BMM) cultures by downregulating NFATc1, c-Src, and TRAF6, thereby inhibiting osteoclast formation, podosomal actin ring assembly, and cell fusion." (abstract, results, passage verified)
pubmedfull study (doi)
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