Épisodes

  • My wrinkly flatmate

    My wrinkly flatmate
    Jul 29 2026
    Show notesTitle: My Wrinkly Flatmate: Shar Pei Fever, Genes and GriefLength: 18:20In this special, more personal episode of Barks and Biomes, Helen reflects on the first anniversary of her Shar Pei’s passing and on the dog who quietly shaped her path into animal science, microbiome curiosity and science communication. This episode moves between lived experience and veterinary science, exploring Shar Pei fever, SPAID genetics, PRA, heart disease, bloat, instinct and the strange way grief can keep a beloved animal close long after they’re gone.There isn’t a day in the year when he isn’t still felt in some way — in memory, in that imagined huff, in the comfort that some bonds don’t really disappear. That emotional thread sits alongside a deeper look at how extreme breeding, inflammatory disease and comparative medicine connect one wrinkly dog to much bigger One Health questions.In this episode The episode opens with a personal reflection on loss, memory, and why this story matters so much on both emotional and scientific levels. The story goes back to the beginning: moving to a new country alone, choosing a dog, meeting a breeder, and falling fully into the Shar Pei world. The episode explores what people mean by a “primitive‑type” dog and how that showed up in one calm, cat‑like, stubborn, deeply intuitive Shar Pei companion. The focus shifts to breed history: the near‑collapse of the Shar Pei population, the small founder pool, the Matgo Law rescue appeal, and how selection for wrinkles and extreme type helped preserve the breed but also increased disease risk.Helen explains Shar Pei fever and the wider Shar Pei Autoinflammatory Disease (SPAID) complex: recurrent fevers, swollen hocks, inflammation, amyloidosis risk and the lived reality of managing a hereditary periodic fever syndrome.The episode breaks down the genetics in accessible language, including hyaluronic acid/hyaluronan as a sugar‑based glycosaminoglycan found in skin, joints, eyes and the extracellular matrix, and the role of the HAS2 duplication in both wrinkles and inflammatory risk.The conversation widens into comparative medicine, looking at why Shar Pei fever has been discussed alongside Familial Mediterranean Fever in humans, and how similar clinical syndromes can arise through different biological pathways.The episode turns practical: anti‑inflammatory diet, calm environment, early monitoring, infections, allergies, kidneys and the detective work of figuring out what helps a particular dog.The story moves through PRA and MMVD, and into a bigger lesson about not living entirely in fear of the condition you expect most. Helen shares the hardest part of the story: losing him to bloat, the unanswered microbiome questions that linger, and the lesson of learning to trust instinct when you know your dog deeply. The episode ends by bringing the science up to date, covering modern SPAID genetic risk testing, including HAS2‑linked and MTBP‑linked tests, and what they can and cannot tell owners and breeders. The closing returns to grief, gratitude and the idea that behind every diagnosis there is still a relationship, a life and a whole ecosystem of biology and love.Why this mattersShar Pei fever is no longer just seen as “bad luck in a wrinkly dog.” Research has linked the condition to regulatory changes near HAS2, which increase hyaluronan production and help explain why the same biology that creates the breed’s signature skin folds can also contribute to autoinflammatory disease. Clinical resources now describe SPAID as a broader syndrome that can include fever, arthritis, skin disease, otitis and systemic amyloidosis, and newer work has added associated markers such as MTBP to the picture.This makes the Shar Pei an important example of the trade‑offs that can emerge when extreme physical traits are selected within a restricted gene pool. It also makes the breed relevant far beyond dog breeding, because Shar Pei fever has been discussed as a comparative model for human periodic fever syndromes and amyloid‑linked inflammatory disease.Links and resourcesCornell Animal Health Diagnostic Centre – Shar-Pei Autoinflammatory Disease (SPAID): Cornell SPAID pagevet.cornellCornell announcement on SPAID testing: AHDC now offering new test for SPAIDvet.cornellPLoS Genetics paper on the HAS2 duplication: Olsson et al. 2011journals.plosPubMed entry for the HAS2 study: PubMed – HAS2 duplication in Chinese Shar-Pei dogspubmed.ncbi.nlm.nihMSD Veterinary Manual – Shar-Pei Fever: MSD Vet ManualmsdvetmanualShar Pei as a model for human Mediterranean fever: PubMed – Chinese Shar-Pei dogs: a model for human Mediterranean fever?pubmed.ncbi.nlm.nihLabogen SPAID test information: Labogen SPAID testlabogenEmbark overview of Shar-Pei Autoinflammatory Disease: Embark SPAID overviewembarkvetDr Linda Tintle background and Shar Pei health resource: HyVitality / Dr Linda TintlehyvitalityDr Linda Tintle client ...
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    19 min
  • Microplastics in the Pet Bowl: What About Our Animals? Episode 7 Series 1

    Microplastics in the Pet Bowl: What About Our Animals? Episode 7 Series 1
    Jul 17 2026
    Show Notes: Microplastics in the Pet BowlThis episode explores how microplastics move from the wider environment into livestock systems and pet food, and why that matters for animal health, food systems, and the One Health conversation.[1][2][3] It focuses on what is known, what is still uncertain, and how listeners can think about the issue without drifting into panic or overstatement.[2][3][4]Episode overviewMicroplastics are plastic particles smaller than 5 mm, while nanoplastics are even smaller fragments that may cross biological barriers more easily.[1][5] Research now shows that these particles are present across agricultural systems, including livestock feed, faeces, milk, meat, blood, and commercially available pet foods.[6][7][8][9][2][10]A 2026 UK study of 38 pet food products found microplastics in 76% of products and across 84% of brands tested.[2][10] The same work reported higher contamination in cheaper “value” products and found that pet foods often contained higher concentrations than many human foods studied so far.[2][10] Key points from the episode- Microplastics in animal diets may come from multiple sources, including contaminated raw ingredients, processing equipment, food-contact materials, and packaging.[11][2][3]- The current evidence does not show that packaging is the only source of contamination in pet food, and the 2026 study could not assign contamination to one stage of production.[2][3][4]- Reviews of livestock and poultry systems report microplastics in feed, with some studies finding 36–300 particles per kilogram of feed in certain settings.[7][9][12]- Plastic particles have also been detected in livestock faeces, suggesting ingestion and excretion are occurring routinely in production systems.[9][12]- A Dutch pilot study detected plastic particles in livestock feed, milk, meat, and blood, suggesting that at least some particles or associated compounds may move beyond the gut.[8] New research worth notingRecent rumen research from a team including scientists at the University of Helsinki found that tested microplastics did not remain inert in the rumen.[13][14][15] Instead, they interacted with the microbial ecosystem, altered fermentation patterns, and appeared to be partially broken down into smaller fragments by rumen microbes.[13][14][15]A 2026 study using polystyrene microplastics in dairy cow feed similarly reported reduced gas production and altered volatile fatty acid profiles, again pointing to disrupted rumen fermentation.[16] The same work suggested rumen microbes were capable of partially degrading polystyrene into smaller chemical components.[16]At the cellular level, recent experimental work has reported nanoplastic uptake in farm-animal cells associated with reproduction and muscle growth, raising early questions about potential impacts on fertility, development, and food production.[17][18] These are early-warning findings from experimental systems rather than proof of real-world damage on farms.[17][18] What remains uncertainThe health significance of microplastics in pet food is still not clear.[3][4] The UK Pet Food industry body has noted that the 2026 pet food study identified contamination but did not assess health outcomes, while regulators such as the US FDA say available evidence does not yet demonstrate clear harm at typical exposure levels in food.[3][4]That uncertainty matters because media narratives around microplastics can shape public anxiety as much as scientific evidence does.[19][20] A careful interpretation is that the contamination signal is real, but the dose-response relationships, long-term health outcomes, and most important contamination routes still need better study.[2][3][4]Practical listener takeaways- Avoid panic; the research points to a real contamination issue, but not to a simple instruction to stop feeding commercial pet food.[3][4]- Think about total plastic contact in a pet’s environment, including bowls, toys, packaging, and storage conditions.[3]- Replace visibly damaged plastic bowls and toys when practical.- Store pet food in cool, dry conditions and avoid exposing bags or trays to excessive heat for long periods.[3]- Watch for future research that separates ingredient contamination from packaging and processing effects.[11][2][3]- “According to a 2026 University of Sussex and University of Exeter study, microplastics were found in about three-quarters of the pet foods tested.”[2][10]- “Very recent rumen work involving the University of Helsinki suggests microplastics are not inert in the rumen and can disrupt fermentation.”[13][14]- “Regulators say the evidence does not yet prove harm at typical food exposure levels, but they also accept this is an emerging field.”[3][4] Source links- [University of Sussex summary of the 2026 pet food study](https://www.sussex.ac.uk/broadcast/read/70901)[2]- [Environmental Toxicology and Chemistry: Microplastic prevalence in commercially available ...
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    14 min