Treat Pets
Differently Treat Pets
Differently

Treat Pets
Differently

Science-backed wellness solutions, developed and analyzed by Canadian veterinary scientists.

Gut Health,
Done Right Gut Health,
Done Right

Gut Health,
Done Right

Pawomics probiotics are formulated specifically for dogs and cats targeted daily gut support based on their unique biology.

Look Deeper.
Care Better Look Deeper.
Care Better

Look Deeper.
Care Better

Your pet can't tell you how they feel but their biology can. At-home DNA and microbiome test kits, developed by Canadian Scientists.

Dog and cat standing side by side against a gray background

Why Your Pet's Microbiome Matters

A balanced gut microbiome supports digestion, skin, and immune health. When it’s disrupted, pets may show signs of allergies, itching, or poor digestion.

LEARN MORE
Close-up of a molecular structure with a light gray background

The Science Behind Pawomics

Every pet's biology is different. Pawomics reads your pet's microbiome and DNA in our Canadian lab, then translates the data into simple steps for better digestion, skin, and long-term health.

EXPLORE THE SCIENCE

The Science Behind

"Bringing our microbiome expertise directly to your pet’s wellness."
Dr. Alissa Cait, PhD
Microbiome Scientist.

A UBC PhD, Dr. Cait transforms complex microbiome research into actionable health solutions.

View Research
Dr. Alissa Cait, PhD portrait, microbiome scientist and UBC PhD researcher focused on turning microbiome science into practical health solutions.

From Research To Real Results

Formulated by Canadian veterinary scientists.
Backed by microbiome research and proven by results.

Two people in white lab coats operating machinery in a sterile environment.

Developed and manufactured in Canada under strict veterinary scientific standards. Pawomics’ research and production take place locally for consistent quality, safety, and traceability.

Formulated by Canadian veterinary scientists specializing in microbiome and genetic research. Each formula is grounded in scientific data, not trends — ensuring species-specific precision.

Built from Pawomics’ proprietary microbiome sequencing and strain identification research. We use real microbiome data to design probiotics that target gut, skin, and immune balance.

Features probiotics such as BL986 and TWK10, supported by published clinical research. Our formulations use evidence-backed strains proven safe and effective for pets.

Non-GMO, preservative-free, and made without unnecessary fillers or artificial additives. We focus on clean, functional ingredients that deliver results without compromise.

Every ingredient and strain is traceable, tested, and genomically verified before release. Transparency is part of our science — we show what’s inside and why it matters.

Non-GMO, preservative-free, and GMP certified for purity and safety. Made in facilities that meet human supplement standards to guarantee clean, safe daily use.

Browse the Blog

Can You Clone a Dog? Why DNA Is Only Part of the Story
BLOG

Can You Clone a Dog? Why DNA Is Only Part of the Story

Short Answer Yes, a dog can be cloned at the level of nuclear DNA, but cloning cannot recreate the same dog. Appearance, personality, epigenetic regulation, mitochondrial DNA, microbiome, early development, and lived experience all vary. A cloned dog may be genetically very close to the original, but it is not the same biological individual. Key takeaway: Cloning transfers nuclear DNA with high fidelity and very little else. In 2001, a team at Texas A&M produced the world's first cloned cat. They named her CC, for Carbon Copy. Her genetic donor was a calico named Rainbow. CC was born tabby-and-white. The two cats shared essentially identical nuclear DNA and looked noticeably different anyway. That outcome, which surprised some people at the time, follows directly from the biology. It's a useful starting point for understanding what pet cloning does and doesn't copy. What Cloning Actually Does Pet cloning uses a technique called somatic cell nuclear transfer (SCNT). A skin cell is taken from the donor animal, and its nucleus (containing the nuclear DNA) is inserted into an egg cell that has had its own nucleus removed. An electrical pulse triggers development, the resulting embryo is transferred into a surrogate dam, and roughly two months later, a puppy is born. The critical word there is nuclear. SCNT copies the nuclear genome with high fidelity. A 2013 whole-genome comparison of Snuppy (the world's first cloned dog) and his donor Tai found a level of DNA-sequence similarity comparable to human identical twins, confirming that a clone and its donor share almost exactly the same genes. But genes are only part of the story. The Epigenome: What DNA Doesn't Tell You CC's coat is an intuitive example of a broader problem. When a somatic cell nucleus is transferred into an enucleated egg, the reprogramming machinery of the oocyte has to strip away the donor cell's existing epigenetic state and rebuild it from scratch. This process is error-prone. The epigenome, the layer of chemical modifications (DNA methylation, histone marks) that sits on top of the DNA sequence and regulates which genes are switched on or off, is not faithfully reset. Studies in cattle and pigs have shown that cloned embryos carry widespread errors in DNA methylation at imprinted gene regions, specifically the areas where only the maternal or paternal copy of a gene should be active. A 2018 study in mouse SCNT embryos found broad loss of H3K27me3 imprinting that disrupted normal post-implantation development. These errors have measurable consequences: large offspring syndrome, cleft palate, and genitourinary defects occur at elevated rates in cloned animals. One of the more striking examples comes from an analysis of over 1,000 cloned dogs. In several German Shepherd clones, XY males developed with female physical characteristics, an outcome called sex reversal. The gene responsible for triggering male development, SRY, was present and intact in every clone. But it was chemically silenced by hypermethylation, meaning the gene existed in the genome but was effectively switched off. Clones from that donor inherited the same silenced state, and male development never initiated. When researchers chemically stripped the methylation from donor cells before cloning, the rate of sex reversal dropped. The DNA sequence was never the issue; the problem was the layer of instructions written on top of it. Personality: Mostly Built, Not Born The behavioral picture is similar. Dog behaviors are moderately heritable, meaning genetics contributes but explains less than half the variance in most traits. A large-scale study of working-dog candidates found heritability estimates for traits like boldness and environmental reactivity in the range of 0.1 to 0.4, depending on the trait. Research on cloned dogs suggests that broad temperament tendencies, such as boldness or scent drive, can be somewhat reproduced across clones from one donor. But individual personality is shaped by early socialization, formative experiences, and developmental noise that cannot be predicted from DNA. The dog that learned to trust you after a rough start at the shelter, the one with a specific vendetta against one particular park squirrel: none of that is in the genome. The Microbiome: The Part No One Mentions As a microbiome scientist, this is the piece I find most overlooked. Your dog's gut, skin, and oral microbiomes (the communities of bacteria that influence immunity, digestion, inflammation, and even behavior via the gut-brain axis) are not inherited through DNA. They are built from scratch at birth, seeded first by the mother during delivery and nursing, then shaped by diet, environment, household microbes, and the other animals they live with. A cloned puppy is typically delivered by C-section from a different surrogate dam than the original dog ever had. That alone alters the starting microbial community. Research in cloned Göttingen minipigs found that genetically identical clones raised on identical diets showed no reduction in gut microbiota variability compared to non-cloned controls; the clone's microbiome was just as individually variable as any ordinary pig's. A smaller study in three cloned dogs found that while dominant bacterial taxa were shared, the proportional composition differed meaningfully between individuals, including one clone whose gut was dominated by a different genus entirely. The gut microbiome your original dog developed over years of shared meals, walks, and household exposure cannot be cloned. It has to be built again, from a different starting point, in a different environment. To understand how microbial communities influence everyday pet health, see Pawomics’ Microbiome Science overview. The Ethics Are Real Too The efficiency numbers for SCNT are also worth sitting with. Published per-embryo success rates remain around 1 to 5% across species, meaning that producing one healthy clone typically requires multiple egg-donor females to undergo hormone stimulation and surgical egg retrieval, and multiple surrogate dogs to carry embryos to term. The ASPCA has called for a moratorium on the research, promotion, and sale of cloned pets specifically because of the burden placed on those animals, whose involvement is never mentioned in the marketing. What You Actually Can't Clone Pet cloning companies sell genetic identity. What they can't sell is biological identity, and the list of things that aren't guaranteed is longer than most people expect. You can't guarantee your clone will look the same. As CC the cat demonstrated, coat color and pattern depend on developmental events that happen independently in every embryo, regardless of shared DNA. Two clones from the same donor can look meaningfully different from each other and from the original. You can't guarantee your clone will behave the same. Broad temperament tendencies have some heritability, but individual personality is built through experience. The clone starts from a different developmental baseline, with a different surrogate, in a different environment. It will have its own history. You can't guarantee the same gut biology. The microbiome your original dog built over years of shared life with you, shaped by your household, your diet, your environment, has to be assembled from scratch by the clone. It will be colonized by different microbes from a different surrogate and shaped by wherever it grows up. That has real downstream consequences for immunity, digestion, and potentially behavior. And in some cases, you can't even guarantee the same sex. Male donors occasionally produced female clones, not due to any change in the DNA sequence, but because the gene responsible for triggering male development was epigenetically silenced in the donor cells and that silencing was inherited by the clone. The honest summary is this: cloning transfers nuclear DNA with high fidelity and very little else. The epigenome is reset during reprogramming. The mitochondrial genome comes from the oocyte donor. The microbiome is seeded by a surrogate and built by a new environment. Whether future cloning technology will close those gaps is an open question. For now, the distance between what SCNT copies and what constitutes an individual animal is large enough that the two should not be confused. Quick Comparison: What Cloning Copies vs. What It Cannot Recreate Part of the dog What cloning can copy What still changes Nuclear DNA Copied with high fidelity Not the full biological identity Appearance Some inherited traits Coat pattern and development can differ Epigenome Not reliably copied Gene activity may be reset incorrectly Personality Broad tendencies may be partly heritable Experience and environment shape the individual Microbiome Not inherited through DNA Seeded by birth, diet, environment, and household exposure Frequently Asked Questions 1. Can you clone a dog exactly? No. Cloning can copy nuclear DNA with high fidelity, but it cannot recreate the same epigenome, microbiome, development, environment, or life history. A cloned dog may be genetically close to the original, but it is not the same individual. 2. Will a cloned dog look the same? Not always. As CC the cat demonstrated, coat color and pattern can depend on developmental events that happen independently in each embryo, even when nuclear DNA is essentially identical. 3. Will a cloned dog have the same personality? Not exactly. Genetics can influence broad temperament tendencies, but individual personality is shaped by early socialization, formative experiences, environment, and developmental noise. 4. Can a dog’s microbiome be cloned? No. A dog’s microbiome is not inherited through DNA. It is seeded at birth and shaped by diet, environment, household microbes, medication history, and the animals and humans the dog lives with. 5. What can DNA testing tell pet owners? DNA testing can provide genetic-level insights, such as breed background, inherited traits, and potential risk markers. Pawomics’ DNA Health Test is designed to help pet owners understand genetic information as one layer of personalized care. Related Pawomics Resources DNA Health Test — for genetic-level insights and inherited traits Gut Microbiome Test — for understanding your pet’s gut microbial community Skin Microbiome Test — for exploring the skin ecosystem Oral Microbiome Test — for oral microbiome and dental-health related insights Veterinary Probiotics-5 — for daily microbiome support References Whole-genome comparison of Snuppy and donor Tai 2018 study on H3K27me3 imprinting in mouse SCNT embryos Analysis of over 1,000 cloned dogs and sex reversal Working-dog candidate heritability study Gut microbiota variability in cloned Göttingen minipigs Gut microbiota composition in cloned dogs ASPCA position statement on pet cloning

Does Your Cat Need Fiber? What the Research Actually Shows
Gut Health

Does Your Cat Need Fiber? What the Research Actually Shows

Short Answer Yes — but not in the way most pet owners assume. Cats don't digest fiber themselves, but the microbes in their colon do, producing short-chain fatty acids (SCFAs) that have measurable effects on colonic motility, mucosal architecture, and gut health. The right type and dose of cat fiber matters more than whether fiber is present at all. Key Takeaway: Fermentable fiber, at the right dose and of the right type, produces real benefits for feline gut health — but generic advice like "add pumpkin" rarely reaches therapeutic levels. The Carnivore Case Against Fiber Cats are obligate carnivores with short intestines and almost no host-derived carbohydrate-digesting enzymes, evolutionarily adapted to a diet of meat, fat, and not much else. Given that, you might believe fiber is irrelevant for cats. The anatomical case isn't unreasonable. The feline small intestine is roughly 2.5 times body length (compared with approximately 6:1 in dogs and 10:1 in humans), the cecum is a vestigial 2–3 cm blind bud with no saccular capacity, and gastrointestinal transit is fast. There is no obvious structural infrastructure for the kind of prolonged fermentative digestion that characterizes herbivore and even omnivore gut physiology. The physiological picture reinforces this. Salivary and pancreatic amylase activity in cats is low relative to omnivores (Stevens & Hume, 1995), and cats lack several of the enzymatic pathways that allow other species to extract nutritional value from plant-derived carbohydrates in the small intestine. Host-mediated digestion of fiber is, for practical purposes, absent. The evolutionary dietary argument extends this further. Wild felids consume diets composed almost entirely of animal tissue, with plant-derived fiber entering the diet incidentally, primarily through the gut contents of prey. The selective pressure for fiber fermentation capacity is not obvious in a lineage that evolved as obligate carnivores. Taken together, the structural, physiological, and dietary evidence makes a coherent case that fiber is simply not relevant to feline nutrition. The Microbial Counterargument Mammalian fiber utilization does not depend on host enzymatic activity or evolutionary dietary history. It depends on microbial fermentation in the large intestine, a system that operates largely independently of host physiology. The question is therefore not whether cats are built to digest fiber, but whether their gut microbial community can. The feline colon harbors a dense microbial community dominated by Firmicutes, particularly Clostridium clusters I and XIVa, which include characterized butyrate-producing species, alongside Bacteroidetes, Proteobacteria, and Actinobacteria (Ritchie, Steiner & Suchodolski, 2008). These communities demonstrably ferment dietary fiber when it is present, producing short-chain fatty acids at concentrations that are difficult to dismiss (Brosey, Hill & Scott, 2000; Sunvold et al., 1995a, 1995b). Why would a carnivore gut microbiome retain this capacity? One plausible explanation is that it was never primarily selected for fiber fermentation in the first place. The dominant substrate in a carnivore colon is undigested protein, and many of the bacterial taxa and enzymatic pathways involved in amino acid fermentation are sufficiently substrate-flexible to process carbohydrates when they are present. On this interpretation, fiber fermentation in cats is not a paradox requiring explanation. It is a consequence of substrate flexibility in a microbial community shaped by protein. Acetate, propionate, and butyrate are produced from both protein and carbohydrate fermentation across mammalian species; the same end products, via related pathways, from different starting materials. This hypothesis has not been directly tested in cats, but it is consistent with the broader biochemistry of microbial fermentation and with the substrate-nonspecificity of the primary SCFA end products. What Fermentation Actually Produces in Cats Brosey, Hill & Scott (2000) measured volatile fatty acid (VFA) concentrations and pH across gastrointestinal segments in 14 healthy adult cats. Total VFA concentrations in the proximal and distal colon averaged 109 and 131 mmol/L respectively, with individual VFA ratios of approximately 60:25:15 (acetate:propionate:butyrate). Colonic pH ranged from 5.0–6.3 proximally to 4.4–5.7 distally. The authors noted that these concentrations were comparable to values reported for the ruminant forestomach (Bergman, 1990). One caveat concerns total amounts. While colonic VFA concentrations were comparable to the ruminant forestomach, total VFA amounts throughout the gastrointestinal tract were low, consistent with a short, non-voluminous intestinal tract. The authors concluded that VFAs "probably contribute minimal metabolic energy in cats" (Brosey et al., 2000). That conclusion applies specifically to caloric contribution and should not be read as a statement about functional relevance more broadly, as SCFAs exert signaling and structural effects at concentrations well below those required for meaningful energy contribution. A second caveat concerns substrate attribution. The VFAs measured cannot be attributed exclusively to fiber fermentation, nor is this unique to cats. Acetate, propionate, and butyrate are produced by microbial fermentation of both carbohydrate and protein substrates across mammalian species. Undigested protein reaches the large intestine in all animals and is subject to microbial catabolism. Branched-chain fatty acids — specifically isobutyrate, isovalerate, and 2-methylbutyrate, which derive more specifically from fermentation of branched-chain amino acids (valine, leucine, and isoleucine respectively) — were also present in Brosey's data alongside the straight-chain SCFAs. What distinguishes cats is not the presence of amino acid fermentation products but the proportionally higher contribution of protein to colonic substrate, reflecting their high dietary protein intake and relatively rapid gastrointestinal transit. Rochus et al. (2013) provided direct in vivo evidence of this in cats: guar gum supplementation, by impairing small intestinal protein absorption, increased the proportion of colonic butyrate derived from amino acid fermentation, with elevated plasma 3-hydroxy-butyrylcarnitine confirming that this protein-derived butyrate was absorbed and metabolized. Straight-chain SCFAs, including butyrate, are therefore not reliable markers of carbohydrate fermentation specifically. Brosey's cats were fed a commercial dry diet that the authors themselves described as containing "a relatively large amount of carbohydrate and moderately fermentable fiber compared with most canned commercial diets," alongside a substantial protein load. The measured VFA profile therefore reflects mixed-substrate fermentation from the outset, with fiber and protein both contributing in proportions the study design did not attempt to partition. No published study has directly partitioned fiber-derived versus protein-derived SCFA contributions in the cat colon in vivo. Whether a given SCFA molecule in the feline colon originated from a carbohydrate or an amino acid substrate is, at present, an open question. What is less open is that the compounds are present, that fermentable fiber supplementation demonstrably increases their production (Sunvold et al., 1995a, 1995b), and that their effects do not depend on resolving the substrate question. Demonstrated Effects: Motility, Mucosal Architecture, and Colonocyte Function The most directly demonstrated SCFA effect in cats is colonic motility. Rondeau et al. (2003) applied sodium acetate, propionate, and butyrate (1–100 mM) to colonic smooth muscle strips from seven adult cats and seven kittens. All three SCFAs produced tonic isometric contractions in longitudinal, though not circular, colonic smooth muscle, with a potency ranking of butyrate > propionate >> acetate. Plateau responses were achieved at 50–100 mM, within the in vivo range measured by Brosey. Contractions were abolished by the L-type calcium channel blockers nifedipine and verapamil, identifying the signaling mechanism. This provides a direct, feline-specific mechanistic basis for fermentable fiber's role in colonic motility and, by extension, for its established clinical benefit in feline constipation (Freiche et al., 2011, n=66, 82–93% response rate on psyllium-enriched diet; Keller et al., 2024, n=9 healthy cats). An important caveat: Rondeau's experiment was conducted on excised tissue strips in buffer. The mechanism is demonstrated in feline tissue under controlled conditions, but in vivo confirmation of the full motility pathway in living cats has not been published. Bueno et al. (2000a) examined colonic morphology and colonocyte metabolic activity in 28 cats fed non-fiber control, cellulose, beet pulp, or pectin/gum arabic diets. Per-cell mucosal oxygen consumption ranked pectin/gum arabic > beet pulp > cellulose > control, a gradient that tracks fermentability and is consistent with more fermentable fiber delivering more substrate to fuel colonocyte metabolism. The companion paper (Bueno et al., 2000b) measured what was actually being absorbed across the colonic wall. Beet pulp produced the highest net colonic absorption of acetate and butyrate, alongside beneficial effects on colonic microbial populations (Rochus, Janssens & Hesta, 2015). Pectin/gum arabic, despite generating higher luminal SCFA concentrations, produced lower net absorption alongside loose stools and weight loss at the fiber inclusion levels tested. Both papers confirmed measurable improvements in colonic mucosal cell density and crypt structure in fiber-supplemented cats relative to controls. The synthesis across these two studies is that maximizing fermentation is not the goal. Pectin/gum arabic generates more total fermentation activity, but the rapid fermentation rate causes digestive disruption that limits both tolerance and absorption. Beet pulp generates enough fermentation to meaningfully increase SCFA absorption, support colonocyte metabolic activity, and maintain normal stool quality and food intake. The relevant measure is not luminal SCFA concentration but how much actually crosses the colonic mucosa and what condition the animal is in while it does so. On both counts, a moderately fermentable fiber outperforms a highly fermentable one. Butyrate is frequently described in secondary literature as the primary energy source for colonocytes in cats, extrapolated from Roediger's work in rats and humans (Roediger, 1980, 1982). The preferential oxidation of butyrate by colonocytes is a conserved mammalian cellular mechanism, and there is no known reason to expect feline colonocytes to differ biochemically. However, the total amounts of butyrate produced in the cat colon are lower than in the species where this has been established, and faster gastrointestinal transit reduces cumulative mucosal exposure time. Whether butyrate reaches the mucosal surface in sufficient quantities to serve as the dominant colonocyte fuel in cats, rather than simply one of several substrates, has not been directly measured. The Bueno tissue-level oxygen consumption data are consistent with butyrate playing a significant colonocyte-fuel role, but the primary fuel claim should be held with some reservation given the quantitative differences in colonic butyrate availability between cats and the species from which the claim originates. Comparison: Generic Fiber Advice vs. a Microbiome-Informed Approach Most popular advice treats "cat fiber" as a single category. The research tells a more specific story. Feature Generic Fiber Advice(e.g. "add pumpkin") Microbiome-Informed Approach(Pawomics) Focus Adding "some fiber" Matching fiber type and dose to the cat's microbiome Typical dose ~0.5 g fiber per tbsp pumpkin 8–28% dietary fiber (therapeutic range) Fiber type Mostly non-fermentable cellulose Moderately fermentable (e.g. beet pulp) or targeted psyllium Evidence Anecdotal Cat-specific peer-reviewed research Output Uncertain effect Measurable improvements in motility and mucosal health Fiber Type, Dose, and the Limits of Home Supplementation The fermentability spectrum has direct practical implications: Non-fermentable fibers (cellulose): Add fecal bulk, useful for glycemic management and weight control, but produce no fermentation-derived benefits. Highly fermentable fibers (FOS, inulin, pectin): Drive SCFA production, but at inclusion levels above ~3–5% cause loose stools and reduce apparent protein digestibility (Hesta et al., 2001), limiting practical dose in cats. Highly viscous fibers (guar gum): Viscosity itself impairs small intestinal protein digestion and amino acid absorption, pushing undigested amino acids into the colon where they are fermented — a consequence of physical properties rather than fermentability per se (Rochus et al., 2013). Moderately fermentable mixed fibers (beet pulp): Produce SCFA profiles and colonic morphology outcomes that are consistently favorable across the available cat-specific literature (Sunvold et al., 1995a; Bueno et al., 2000a, 2000b). Psyllium: A separate useful niche — high solubility with low fermentability, producing gel-forming effects that increase fecal moisture and bulk without the digestive side effects of rapidly fermentable fibers. Strong clinical evidence for constipation management (Freiche et al., 2011; Keller et al., 2024). The dose question is where much popular advice breaks down. One tablespoon of canned pumpkin provides approximately 0.5 g of total dietary fiber (Freeman, 2017). Therapeutic high-fiber diets for cats typically contain 8–28% total dietary fiber on a dry matter basis. Pumpkin is not harmful at typical supplementation doses, but its fiber content is insufficient to drive the fermentation-based effects described in the experimental literature, and the fiber type it provides — predominantly insoluble and low-fermentability cellulose and hemicellulose — is not the type most relevant to those effects. Casual fiber supplementation with home foods rarely approaches therapeutic concentrations, and the type of fiber matters as much as the amount. A Practical Approach: Test, Treat, Track Rather than guessing which cat fiber food or supplement might help, a more targeted approach starts with understanding the cat's microbiome. Test the ecosystem. Start with an at-home Cat Gut Microbiome Test to map the bacterial community actually present in your cat's gut. The report identifies imbalances, overgrowths, and missing fermenters. Treat with precision. Based on the results, match fiber type to the cat's microbial profile — moderately fermentable fiber for fermentation-derived benefits, psyllium for constipation-dominant cases, or targeted Probiotics-5 to seed the missing SCFA-producing strains. Track the response. Reassess stool quality, motility, and coat condition over 4–8 weeks. A follow-up test confirms whether the intervention actually shifted the microbial community. What Remains Uncertain Several claims that appear with confidence in secondary literature deserve more careful qualification. Whether butyrate reaches the feline colonic mucosa in sufficient quantities to serve as the dominant colonocyte fuel, rather than one of several substrates, has not been directly measured. The lysine-to-butyrate fermentation pathway, characterized in specific human gut microbiota, has not been documented in the feline microbiome. Large pathogen-suppression effects attributed to prebiotics in cats — sometimes citing dramatic reductions in Clostridium perfringens — rest largely on a single older study (Sparkes et al., 1998) using culture-based techniques now understood to underestimate microbial diversity. More recent molecular studies show variable and generally more modest microbiome shifts. More broadly, most feline fiber research involves small numbers of healthy adult colony cats assessed over short periods. Whether findings generalize to pet cats of diverse ages, breeds, health statuses, and dietary backgrounds is unknown. Optimal fiber doses for specific clinical conditions have not been systematically established. And the fermentation of animal-derived substrates — including collagen, cartilage, and connective tissue — by the feline gut microbiome remains almost entirely unstudied, despite being arguably the most evolutionarily relevant fiber-analog for an obligate carnivore. Conclusion The carnivore case against fiber is coherent and anatomically well-grounded. But the microbial evidence consistently complicates that picture. The feline colonic microbiome can ferment fiber, produces SCFAs at significant concentrations, and those compounds have measurable effects on colonic motility and mucosal architecture that have been directly demonstrated in cat-specific studies. The full scope of their effects, within the gut and beyond, remains incompletely understood. What is clearer is that fermentable fiber, at appropriate doses and of appropriate types, produces favorable gut health outcomes in cats, and that the optimal fiber sources are specific rather than generic. Dose matters in ways popular advice often fails to capture. Understanding the microbial community that does this work — its composition, its functional capacity, and its current state of balance — is the most direct route to understanding whether and how fiber intervention is likely to help a given cat. Frequently Asked Questions Q: Does my cat really need fiber if cats are obligate carnivores?A: Cats don't digest fiber themselves, but the microbes in their colon ferment it into short-chain fatty acids that support motility and mucosal health. So while cats don't need fiber the way humans or dogs do, fermentable fiber at the right dose produces measurable gut health benefits. Q: Is pumpkin a good cat fiber food?A: Pumpkin is safe but rarely reaches therapeutic fiber doses. A tablespoon provides roughly 0.5 g of fiber — mostly non-fermentable cellulose — whereas therapeutic high-fiber cat diets contain 8–28% fiber on a dry matter basis. For occasional stool firming it's fine; for fermentation-driven benefits, it's not the right tool. Q: What's the best cat fiber supplement?A: It depends on the goal. Beet pulp (a moderately fermentable fiber) has the strongest evidence for supporting SCFA production and colonic health. Psyllium has the strongest evidence for constipation relief. Highly fermentable fibers like inulin can cause loose stools above ~3–5% inclusion. The "best" supplement is the one matched to the individual cat's microbiome and symptoms. Q: Can fiber help my cat's constipation?A: Yes — psyllium in particular has strong clinical evidence, with one study showing an 82–93% response rate in constipated cats (Freiche et al., 2011). Fermentable fibers like beet pulp also support colonic motility through SCFA signaling. Chronic constipation warrants a veterinary workup, but dietary fiber is a well-supported first-line intervention. Q: How do I know which type of fiber my cat needs?A: A gut microbiome test identifies which bacterial communities are present, which are missing, and what substrates they're best equipped to ferment. That's the most direct way to move from generic fiber advice to a supplement choice grounded in your cat's actual biology. References Bergman EN (1990). Energy contributions of volatile fatty acids from the gastrointestinal tracts in various species. Physiological Reviews, 70(2), 567–590. Brosey BP, Hill RC & Scott KC (2000). Gastrointestinal volatile fatty acid concentrations and pH in cats. American Journal of Veterinary Research, 61(4), 359–361. Bueno AR, Cappel TG, Sunvold GD et al. (2000a). Feline colonic morphology and mucosal tissue energetics as influenced via the source of dietary fibre. Nutrition Research, 20(7), 985–993. Bueno AR, Cappel TG, Sunvold GD et al. (2000b). Feline colonic microbes and fatty acid transport: effects of feeding cellulose, beet pulp and pectin/gum arabic fibres. Nutrition Research, 20(9), 1319–1328. Freeman LM (2017). The problem with pumpkin. Tufts Cummings School of Veterinary Medicine Clinical Nutrition Service. Freiche V, Houston D, Weese H et al. (2011). Uncontrolled study assessing the impact of a psyllium-enriched extruded dry diet on faecal consistency in cats with constipation. Journal of Feline Medicine and Surgery, 13(12), 903–911. Hesta M, Janssens GPJ & Debraekeleer J et al. (2001). The effect of oligofructose and inulin on faecal characteristics and nutrient digestibility in healthy cats. Journal of Animal Physiology and Animal Nutrition, 85(3–4), 135–141. Keller E et al. (2024). Psyllium husk powder increases defecation frequency and faecal score, bulk and moisture in healthy cats. Journal of Feline Medicine and Surgery, 26(4). Ritchie LE, Steiner JM & Suchodolski JS (2008). Assessment of microbial diversity along the feline intestinal tract using 16S rRNA gene analysis. FEMS Microbiology Ecology, 66(3), 590–598. Rochus K, Janssens GPJ & Van de Velde H et al. (2013). Highly viscous guar gum shifts dietary amino acids from metabolic use to fermentation substrate in domestic cats. British Journal of Nutrition, 109(6), 1022–1030. Rochus K, Janssens GPJ & Hesta M (2015). Dietary fibre and the importance of the gut microbiota in feline nutrition: a review. Nutrition Research Reviews, 27(2), 295–307. Roediger WEW (1980). Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut, 21(9), 793–798. Rondeau MP, Meltzer K, Michel KE, McManus CM & Washabau RJ (2003). Short chain fatty acids stimulate feline colonic smooth muscle contraction. Journal of Feline Medicine and Surgery, 5(3), 167–173. Sparkes AH, Papasouliotis K, Sunvold G et al. (1998). Effect of dietary supplementation with fructooligosaccharides on faecal flora of healthy cats. American Journal of Veterinary Research, 59(4), 436–440. Stevens CE & Hume ID (1995). Comparative Physiology of the Vertebrate Digestive System (2nd ed.). Cambridge University Press. Sunvold GD, Fahey GC, Merchen NR et al. (1995a). Dietary fiber for cats: in vitro fermentation of selected fiber sources by cat fecal inoculum and in vivo utilization of diets containing selected fiber sources and their blends. Journal of Animal Science, 73(8), 2329–2339. Sunvold GD, Hussein HS, Fahey GC et al. (1995b). In vitro fermentation of cellulose, beet pulp, citrus pulp, and citrus pectin using fecal inoculum from cats, dogs, horses, humans, and pigs and ruminal fluid from cattle. Journal of Animal Science, 73(12), 3639–3648.

Can You Get Sick From Dog Kisses? The Scientific Truth About Shared Bacteria
BLOG

Can You Get Sick From Dog Kisses? The Scientific Truth About Shared Bacteria

  The Short Answer That smell coming from your dog's mouth isn't just "normal dog breath." In most cases, it's an early sign of bacterial imbalance in the mouth — and a peer-reviewed study found that some of those bacteria can be shared between dogs and their owners through everyday contact like licking and close proximity. Key Takeaway Understanding your dog's oral health is one of the most overlooked aspects of preventive care — for them, and potentially for you. Why Does My Dog's Breath Smell So Bad? You've probably noticed it. That unmistakable smell when your dog yawns, pants, or goes in for a kiss. Most pet owners chalk it up to "just being a dog thing." But it's worth taking a closer look. Bad breath in dogs is almost always a sign of bacterial activity in the mouth. And dogs are far more prone to oral disease than most people realize: 95–100% of dogs develop gingivitis (early-stage gum inflammation) at some point in their lives. 50–70% progress to periodontitis — advanced gum disease that damages the tissue and bone holding teeth in place. By age three, most dogs already show early signs of periodontal disease, according to the American Veterinary Medical Association (AVMA). The smell isn't random. It's the byproduct of bacteria breaking down tissue in the mouth. Generally, the stronger the smell, the more advanced the bacterial activity tends to be. What Actually Lives in Your Dog's Mouth? A dog's mouth contains hundreds of bacterial species — most of them completely harmless. But a peer-reviewed study published in Archives of Oral Biology took a closer look at the specific bacteria linked to gum disease, and the numbers are striking. Researchers collected dental plaque samples from 66 dogs and 81 owners across 64 families and tested for 11 periodontopathic (gum disease–associated) bacteria using DNA analysis. Here's what they found in the dogs: 77% carried Tannerella forsythia: A bacteria that breaks down gum tissue. 71% carried Porphyromonas gulae: Closely related to a pathogen known to cause gum disease in humans. 67% carried Campylobacter rectus: Linked to inflammation and bone loss around teeth. These aren't exotic pathogens. They're bacteria that live quietly in your dog's mouth every day. Most healthy dogs show no obvious symptoms — which is exactly why regular oral health monitoring matters. Can You Catch Something from Your Dog Licking You? This is the question most pet owners Google at some point — usually right after their dog licks their face. The honest answer is: it's possible, but it's not common, and it's not a reason to panic. The same 2012 study found a notable pattern: every owner who tested positive for Porphyromonas gulae also had a dog that tested positive for the same bacteria. The researchers concluded that some periodontopathic bacteria "could be transmitted between humans and their companion dogs" through routine close contact. That contact includes: Your dog licking your face or hands Sharing utensils or cups (yes, some people do this) Close sleeping proximity It's worth noting that a dog's overall oral microbiome is quite different from a human's — researchers at the Forsyth Institute found that only about 16% of canine oral bacteria overlap with human oral bacteria (Dewhirst et al., 2012). Most of what lives in your dog's mouth stays in your dog's mouth. But for the specific bacteria associated with gum disease? The overlap is more relevant — and worth being aware of, especially if you or someone in your household is immunocompromised. The CDC also notes that Capnocytophaga, another bacteria found in dog saliva, can occasionally cause serious illness in people with weakened immune systems. What Most Dog Owners Think vs. What Science Says What most owners assume What the research shows "Bad breath is just normal for dogs" It's usually a sign of bacterial imbalance or gum disease. "Dog kisses are totally harmless" Some gum disease–associated bacteria may be shared through contact. "Dental care can wait until it's a real problem" Most dogs show signs of gum disease by age 3; silent damage starts early. "It's a mouth issue, not a health issue" Periodontal disease is linked to changes in kidney, liver, and heart tissue. Research has found that dogs with greater periodontal disease burden showed higher rates of pathological changes in the heart, liver, and kidneys (Pavlica et al., 2008). A more recent review confirmed that treating periodontal disease actually reduces those systemic markers — supporting a real, not just coincidental, connection. So What Can You Actually Do About It? You don't need to stop kissing your dog. You just need to pay closer attention to what their mouth is telling you. Here is a practical starting point: Look for early signs: Red or swollen gums, visible tartar buildup, or persistent bad breath are all worth noting — and worth mentioning at your next vet visit. Start a routine: Even a few brushing sessions per week can meaningfully reduce bacterial buildup. Dental chews and water additives can support — but not replace — mechanical cleaning. Get a professional cleaning: Many dogs need a veterinary dental cleaning under anesthesia at some point. This isn't optional grooming — it's preventive medicine. Understand what's actually happening: Bad breath is a symptom, not just an inconvenience. Knowing the bacterial picture behind it allows for more targeted care. Understanding your dog's oral microbiome is part of understanding their overall health. At Pawomics, our tests give you a clearer picture of the bacterial balance in your dog's mouth — so care decisions are based on data, not guesswork. Frequently Asked Questions Why does my dog's breath suddenly smell worse than usual? A sudden change — especially if it's strong, sweet-smelling, or has a urine-like quality — can signal something beyond normal gum disease. Kidney disease, diabetes, and gastrointestinal issues can all affect breath. If the change is dramatic, see a vet promptly. Is dog saliva cleaner than human saliva? This is a persistent myth. Dog and human saliva contain different bacteria — neither is inherently "cleaner." Dogs' mouths contain hundreds of bacterial species, most harmless to humans, but some that are relevant to oral health in both species. Can my dog's bad breath affect my health? For healthy adults, the risk is low. For people who are immunocompromised, elderly, or have open wounds, more caution is reasonable. The 2012 Yamasaki study suggests that gum disease–associated bacteria can move between dogs and their owners. How often should I have my dog's teeth professionally cleaned? The AVMA recommends annual veterinary dental exams as a baseline. The frequency of professional cleanings varies by breed, age, and individual health status — your vet is the right person to guide that decision. Do small dogs have worse dental health than large dogs? Generally, yes. Smaller and brachycephalic (flat-faced) breeds tend to have more crowded teeth, which creates more surfaces for bacteria to accumulate. They often need more frequent dental attention. Stop Guessing, Start Knowing. Your dog's oral microbiome holds the key to their systemic health. Get the data-driven blueprint you need to protect their smile and their future. Explore Microbiome Test Scientific References:1. Yamasaki Y, et al. Archives of Oral Biology. 2012;57(9):1183–1188.2. Dewhirst FE, et al. PLOS ONE. 2012. Forsyth Institute.3. Pavlica Z, et al. Journal of Veterinary Dentistry. 2008.4. Harvey CE. Veterinary Clinics of North America: Small Animal Practice. 2022.