The Pufferfish Keepers' Guide to Thiaminase
- Macauley Sykes
- Feb 3
- 19 min read
Updated: Feb 4
If you keep pufferfish, chances are you have come across the word thiaminase in discussions about diet. It appears frequently in care guides, forum posts, and feeding advice, often accompanied by poorly explained or contradictory warnings.
Thiaminase has long been a concern in other corners of animal husbandry. Keepers of piscivorous birds, reptiles, and even marine mammals have had to reckon with it for decades because of the role it plays in vitamin B1 (thiamine) deficiency. In the fishkeeping arena, and particularly among pufferfish keepers, the significance of this anti-nutrient has been slower to emerge.
As a result, thiaminase remains one of the most commonly mentioned and least clearly understood aspects of pufferfish nutrition. Advice often collapses into rigid food lists or dismissive reassurances, neither of which helps keepers make informed, long-term decisions.
Why This Article Exists
This article exists because, for several years, I could not make sense of what I was seeing.
Although I have kept fish for well over twenty years, it was not until around eight years ago that I became active in aquarium groups on social media. Until then, most of my learning had been book-based. As I began assisting with administrative teams and later established my own platforms, I was exposed to a far wider range of real-world cases than I had encountered before.
It was around this time that I began to notice recurring reports of pufferfish developing serious and often fatal health problems. Some fish stopped eating. Others developed digestive issues, constipation, or abdominal swelling. Many showed neurological impairment, loss of balance, difficulty swimming, immune suppression, or a gradual loss of body mass and condition.
Initially, many of these cases were dismissed as bad luck. Over time, however, the frequency of unexplained illness and death became increasingly difficult to ignore. On the surface, the cases appeared unrelated. No single pathogen, parasite, or environmental factor could explain what was happening. Despite this, I became convinced that they were connected. Something important was being missed.
As more reports emerged, I began comparing notes with private keepers and professionals from multiple countries. I gathered data from forum posts, social media groups, and private conversations, and began a slow process of elimination.
The investigation started with the most obvious factors. Water parameters were scrutinised first. Exposure to toxic levels of ammonia, nitrite, and nitrate was ruled out early on. Water hardness was considered next, but this line of enquiry also failed to account for the pattern. One by one, potential causes were explored and discarded.
When I began comparing the foods these fish had been eating, patterns finally started to emerge. The diets varied widely. Different brands, different formulations, different fish species. Yet a shared nutritional thread kept appearing. Thiaminase surfaced repeatedly in the data. At the time, I noted it, but did not appreciate its significance. It seemed too indirect, too subtle, to account for the severity and diversity of symptoms.
The realisation came from outside fishkeeping altogether.
One weekend, while trying to deal with a persistent weed growing between my patio slabs, I began researching ways to eliminate it. The plant was Horsetail (Equisetum arvense), a prehistoric perennial native to the UK. While reading about control methods, I came across information on its well-documented role in causing a Vitamin B1 deficiency in horses through thiaminase activity. There was that word I had kept seeing in diets: thiaminase.
Signs typically appear after a horse consumes a diet containing 20% or more horsetail for 2–5 weeks.
The parallel was impossible to ignore. The symptoms, the mechanism, the progression. In that moment, the entire pattern snapped into focus. These fish were not dying from a mysterious disease. They were dying from an induced Vitamin B1 deficiency.
All of it made sense once thiaminase was recognised not as a footnote, but as the central mechanism. This article exists to explain that mechanism clearly, to show why thiaminase-related deficiency is so often missed, and to help pufferfish keepers approach feeding in a way that supports long-term health without fear or guesswork.
What is Vitamin B1 (thiamine)?
Before we can understand thiaminase, it helps to first understand thiamine itself.
Vitamin B1, also known as thiamine, is an essential nutrient for almost all animals, including fish. It plays a central role in energy metabolism by allowing the body to release usable energy from carbohydrates. In practical terms, vitamin B1 is required for cells to convert food into the energy that powers movement, digestion, growth, and immune function. It is also critical for the normal function of the nervous system, muscles, and internal organs.
When vitamin B1 is in short supply, energy production begins to fail at a cellular level. Tissues with high energy demands, particularly the brain, nerves, digestive system, and immune system, are affected first. This is why vitamin B1 deficiency can present in such a wide variety of ways, ranging from neurological impairment and digestive dysfunction to immune suppression and wasting.
Unlike some vitamins, vitamin B1 cannot be synthesised by the body and cannot be stored in meaningful quantities. Any excess is quickly excreted, which means a regular dietary supply is essential. Even short interruptions in intake can have consequences, especially in animals with fast metabolisms.
In the wild, fish meet this requirement through diverse and changing diets. Seasonal variation, prey diversity, and natural feeding behaviours provide a steady supply of micronutrients, including vitamin B1, without the need for conscious balance. In aquaria, the responsibility to provide that balance and variety shifts entirely to the keeper.
When diets are limited, repetitive, or unknowingly disruptive to vitamin B1 availability, deficiency can develop quietly and progressively. Understanding vitamin B1 itself is therefore the first step in understanding how thiaminase becomes a problem.
What is thiaminase?
Now that we understand what vitamin B1 is and why it matters, we can turn to the enzyme that threatens it: thiaminase.
Thiaminases are enzymes found in a surprisingly wide range of organisms and food sources. Their action is simple but destructive. They break down the vitamin B1 molecule into components that the body can no longer use. Once vitamin B1 has been destroyed in this way, it cannot be repaired or recycled. The result is a gradual but persistent depletion of vitamin B1 in the body, which, over time, undermines multiple vital systems.
This is what makes thiaminase so problematic. Deficiency does not appear overnight. Instead, vitamin B1 levels are slowly eroded with each feeding, until the body can no longer compensate.
Researchers recognise two main types of thiaminase:
Thiaminase I This is the most common and the most relevant form for aquarists. Thiaminase I is found in many organisms, including certain fish, shellfish, plants, and bacteria. Crucially, it occurs in several foods that are routinely fed to captive fish. Thiaminase I is responsible for the majority of dietary vitamin B1 loss observed in both wild and captive animals.
Thiaminase II This form is produced primarily by certain bacteria. While it is important in microbiological research, it plays a much smaller role in the diets of aquarium fish and is of limited practical concern for most keepers.
For a long time, thiaminase was largely absent from mainstream aquarium discussion. It was considered a niche problem, relevant to wildlife biologists studying fish declines in the Great Lakes, or to zoo professionals managing the diets of piscivorous birds, reptiles, and marine mammals. In those contexts, its effects were dramatic and well documented.
Only more recently has the relevance to fishkeeping become clear. The same enzyme responsible for population-level crashes in wild fish, or for severe neurological disease in captive predators, can also affect pufferfish when their diets are built around inappropriate or unbalanced food sources.
Symptoms of a Vitamin B1 Deficiency
A deficiency of vitamin B1 does not produce one or two distinctive symptoms. Instead, it can affect multiple systems at once and, if left uncorrected, can ultimately be fatal.
What makes vitamin B1 deficiency particularly difficult for keepers to recognise is the way it presents. The signs are often subtle at first and highly variable. Many overlap closely with symptoms associated with poor water quality, internal parasites, stress, bacterial infection, or age-related decline. A fish that is losing weight, swimming poorly, or refusing food could plausibly be suffering from any number of problems. Vitamin B1 deficiency is rarely the first explanation considered.
Among pufferfish keepers, the following signs are most commonly reported in fish later suspected or confirmed to be vitamin B1-deficient. Growth and condition
Poor growth
Progressive weight loss
General weakness
Muscle wasting (atrophy)
Digestive and abdominal signs
Loss of appetite
Constipation or digestive issues
Abdominal swelling
Abdominal haemorrhage
Neurological and sensory signs
Loss of equilibrium and difficulty swimming
Convulsions and seizures
Blindness
Paralysis
Other neurological impairments
Nerve damage
Organ and systemic signs
Damage to, or outright failure of, internal organs
Reduced immunity (immunosuppression)
Reproductive problems, including the inability to spawn
The sheer diversity of these symptoms is why vitamin B1 deficiency is often described as a “great imitator”. It does not present as a single, recognisable syndrome, but as a patchwork of issues that appear unrelated when viewed in isolation.
This is also why shared experiences within the community have been so important. One keeper reports neurological problems. Another sees appetite loss and wasting. A third struggles with unexplained reproductive failure. Individually, these reports are easy to dismiss as separate problems. When viewed together, patterns begin to emerge, and the role of vitamin B1 becomes far harder to ignore.
Understanding this symptom fragmentation is key. It explains why thiaminase-related deficiency went unrecognised for so long, and why it continues to be overlooked when diets are not examined critically.
Foods that contain thiaminase
Thiaminase occurs in many of the foods that pufferfish keepers commonly use. This is one of the main reasons vitamin B1 deficiency remains such a persistent and confusing issue in the hobby.
One of the challenges in addressing thiaminase is that there is no definitive list of which species do and do not contain it. The available science is incomplete, uneven across regions, and sometimes contradictory. Even within a single species, thiaminase activity can vary considerably depending on season, location, age, or which tissues are examined. In many organisms, the viscera show far higher activity than the muscle tissue, which further complicates interpretation.
What we can say with confidence is that thiaminase has been documented across a broad range of prey groups that feature heavily in captive diets. Prey Groups Known to Contain Thiaminase:
Fish: especially members of the carp and minnow family (Cyprinidae), along with alewife, smelt, and other small forage fishes.
Bivalves: clams, mussels, and scallops (though oysters appear to lack thiaminase).
Gastropods: some snails and limpets.
Cephalopods: including squid and octopus.
Crustaceans: crabs, lobsters, crayfish, prawns, shrimp, krill, and barnacles.
Among the foods most frequently offered to pufferfish that are known or strongly suspected to contain thiaminase are the following.
Common Thiaminase-Positive Foods in Pufferfish Diets:
Fish from the family Cyprinidae, including carps, minnows, barbs, and barbels
Certain prawns, including caramote prawn (Melicertus kerathurus)
Various shrimp species, including Macrobrachium rosenbergii and species within the genus Penaeus
Mussels, particularly zebra mussel (Dreissena polymorpha) and quagga mussel (Dreissena bugensis)
Various clams, including members of the family Veneridae
Species-level insights
Mussels
Dreissenid mussels: Zebra (D. polymorpha) and quagga (D. bugensis) mussels consistently show very high thiaminase activity, in some cases 5–100 times higher than forage fish like alewife. Levels vary by season (highest in spring), location, and depth.
Blue mussel (Mytilus edulis): Activity has been detected, but results are inconsistent: some studies find thiaminase, others do not. This may reflect differences in methodology or which tissues were tested.
Clams
Hard clams: tested in mid-20th-century feeding studies showed significant thiaminase activity, enough to destroy measurable amounts of dietary thiamine.
Shrimp
In the aquarium world, shrimp (particularly Penaeus spp., such as tiger shrimp) are widely assumed to be thiaminase-positive. However, peer-reviewed, species-specific assays are lacking. The available evidence is anecdotal or generalised across crustaceans, rather than conclusive.
Why Thiaminase-Rich Foods Became Hobby Staples
It is reasonable to ask why foods known to contain thiaminase, such as clams, mussels, prawns, shrimp, and small feeder fish, remain so common in pufferfish diets. The answer has less to do with what puffers actually require and more to do with how the aquarium hobby has evolved.
Misunderstandings of natural diets
For many years, pufferfish, particularly larger species, have been broadly described as molluscivores. Once established, that label shaped feeding advice across the hobby. Many keepers began constructing diets heavily, and sometimes exclusively, around clams and mussels.
In reality, wild pufferfish diets are far more varied. Some species are primarily insectivorous. Others are opportunistic generalists. Even large riverine puffers consume a wide range of prey types, including insects, crustaceans, worms, and plant material alongside molluscs. The oversimplification of “puffers eat snails and shellfish” has unintentionally pushed many captive diets towards foods with a high thiaminase burden.
Price and availability
Mussels, clams, prawns, and shrimp are inexpensive and widely available through supermarkets and fishmongers. They can be purchased in bulk, frozen easily, and portioned with minimal effort. By contrast, many foods that better reflect natural diets, such as insects or a wider range of invertebrates, are harder to source and often more expensive.
For keepers working within a budget, the convenience and affordability of supermarket seafood are difficult to ignore, even when those foods come with nutritional drawbacks.
Keeper convenience
Beyond cost, thiaminase-rich foods are convenient. Frozen shellfish and shrimp require little preparation, do not need to be cultured or collected, and fit neatly into a routine feeding schedule. A single bag can last weeks and feed multiple fish.
By comparison, sourcing or maintaining live foods or assembling a more varied diet tailored to a species requires more time, planning, and often additional knowledge. For new keepers in particular, simplicity tends to take priority over nuance.
Tradition and habit
Once certain foods became established as standard, they were repeated in care sheets, books, and forum advice as the correct way to feed pufferfish. Over time, these recommendations became self-reinforcing. Diets built around clams, mussels, and shrimp were normalised, even as evidence accumulated that they were a poor substitute for the diverse diets most puffers consume in the wild.
Preventing a Vitamin B1 Deficiency: Feeding with Ecology in Mind
Preventing vitamin B1 deficiency is always preferable to trying to correct it once a pufferfish is already unwell. When a fish is fed a diet built largely, or entirely, around thiaminase-containing foods, deficiency becomes likely over time. This is not a matter of opinion. It is a straightforward biochemical process. Thiaminase destroys vitamin B1 faster than the animal can replace it.
As reserves are gradually depleted, subtle health problems emerge and, if nothing changes, they can progress to serious, sometimes irreversible, damage.
Some aquarists attempt to manage this risk by setting numerical limits, such as restricting thiaminase-positive foods to no more than 20% of the overall diet. While this guideline is widely circulated, it should be treated with caution. As we have discussed, thiaminase activity varies enormously between species, between populations of the same species, by season, and even between different tissues of the same prey animal. The viscera of a small fish may carry far higher activity than its muscle. A bivalve collected at one time of year may present a very different thiaminase load than the same species collected at another. What appears safe in one context may be unsafe in another.
Because of this uncertainty, micromanaging percentages rarely provides the protection keepers expect.
A far more reliable approach is also the simplest one. Feed pufferfish in a way that closely replicates what they actually eat in the wild.
Thiaminase becomes a problem in captivity largely because puffers are so often maintained on narrow, repetitive, and ecologically inappropriate diets. Raw clams, mussels, endless cubes of prawn, or feeder fish are frequently offered as staples, sometimes to the near exclusion of everything else. Wild pufferfish do not eat this way. They are opportunistic feeders with broad, flexible diets shaped by habitat, season, and life stage. They rarely subsist on the kind of monotonous, thiaminase-heavy diets that cause problems in aquaria.
When we replicate natural feeding ecology, thiaminase risk largely resolves itself.
This principle applies across species. By studying what puffers actually consume in the wild, and by selecting captive foods that reflect that ecology, we naturally reduce reliance on high thiaminase items without having to obsess over lists or percentages. Variety increases. Nutritional balance improves. Vitamin B1 intake stabilises.
At Pufferfish Enthusiasts Worldwide, this philosophy underpins our care guidance. Our species-specific feeding recommendations are based on field studies, gut content analyses, and long-term observations by experienced keepers. Fish raised under this approach consistently show better growth, stronger immune function, more natural behaviour, and far fewer unexplained health issues.
The Amazon puffer, Sphoeroides asellus, is a good example. In the hobby, it is often described as a molluscivore.
In reality, gut content studies of wild populations show that they are primarily insectivorous, feeding heavily on aquatic insects and larvae. Insects carry little to no thiaminase burden.
When Amazon puffers are fed accordingly, using a mix of insects, worms, and insect-based prepared foods, vitamin B1 deficiency is rarely encountered.
The Pea Puffer, Carinotetraodon travancoricus, shows a similar pattern, thriving in nature on insect larvae and small invertebrates rather than on shellfish.
Even the large African species challenge common assumptions. The Fahaka, Tetraodon lineatus, undergoes an ontogenetic dietary shift. Juveniles feed primarily on insects, crustaceans, worms, and small soft prey. Only as adults do they increasingly exploit hard-shelled molluscs.
The Mbu, Tetraodon mbu, is a benthic opportunist, feeding on snails, freshwater crabs, crayfish, worms, insects, and occasional fish across the Congo basin and Lake Tanganyika. In both cases, molluscs form part of a broader, varied diet, not the foundation of it.
In captivity, these same fish are often restricted to mussels, clams, and prawns. This narrows their dietary intake, increases thiaminase exposure, and deprives them of the diversity to which they are adapted. By offering a rotating mix of snails, crustaceans, worms, insects, and insect-based foods, keepers can better replicate natural diets while still providing the hard-shelled prey needed to manage beak growth.
When feeding is guided by ecology rather than convenience, vitamin B1 deficiency is no longer a persistent threat. The solution is not restriction, but alignment. Not fear, but understanding.
Following nature does more than prevent a problem. It produces healthier fish, longer-lived fish, and fish that display the full range of behaviours that make pufferfish so compelling to keep. Just as importantly, it encourages keepers to think critically, share findings, and refine husbandry collectively. In that sense, preventing vitamin B1 deficiency is not simply about avoiding harm. It is about raising the standard of pufferfish care as a whole.
Treating a Thiamin Deficiency
The encouraging news is that vitamin B1 deficiency can often be reversed if it is recognised and addressed early. Because vitamin B1 is used rapidly by the body and not stored in significant reserves, restoring it through diet can sometimes lead to noticeable improvements within days. Appetite may return, activity levels may increase, and in young fish, growth can resume.
There are, however, clear limits to recovery. Fish that experience deficiency during critical developmental stages may regain weight and general condition, but the growth they missed cannot always be recovered. In these cases, individuals often remain permanently smaller than they otherwise would have been, even after vitamin B1 levels are restored.
When deficiency progresses further, outcomes become more variable. Veterinary intervention, including high-dose supplementation or injectable vitamin B1, can sometimes stabilise fish already showing neurological or systemic signs. Some individuals respond well, regaining normal function and going on to live without obvious impairment. Others show partial improvement, only to be left with lingering weaknesses that resurface under stress. In advanced cases, where nervous tissue or internal organs have already sustained damage, supplementation may slow or halt further decline but cannot reverse what has been lost.
This variability is precisely what makes prevention so important. Once vitamin B1 levels fall too low, the difference between recovery and deterioration often depends on how early the deficiency is identified and how severely the fish has been affected. Timely intervention can mean the difference between a full recovery and a permanent vulnerability that never fully resolves.
For keepers, the lesson is straightforward. Treatment can work, but it is never a substitute for prevention. Feeding in a way that reflects a fish’s natural ecology not only reduces the risk of deficiency but also avoids placing fish in a position where recovery is uncertain and damage may already be irreversible.
Frequently asked questions
Q: Can I just feed thiaminase foods occasionally?
A: Feeding small amounts occasionally is less risky than making them the bulk of the diet. But because thiaminase levels vary by species, season, and tissue type, it’s impossible to set a universal “safe” percentage. Our advice is to minimise or avoid them long-term, and instead focus on replicating your puffer’s natural diet.
Q: Why do so many keepers feed clams, mussels, and shrimp if they can be risky?
A: Mostly because of convenience, cost, and tradition. These foods are cheap, easy to buy, and have long been recommended as “puffer staples.” Unfortunately, this doesn’t reflect the diverse natural diets puffers eat in the wild, and that’s where the problem lies.
Q: Can adding a thiamine (Vitamin B1) supplement to food counteract the thiaminase in that food?
A: Not reliably. Thiaminase acts by breaking down thiamine before the fish can absorb it. If the enzyme is present in a food item, then any thiamine in that food (including what you’ve added as a supplement) can be destroyed before it provides any benefit. In other words, sprinkling or soaking vitamins onto a thiaminase-rich food won’t make that particular item “safe.”
This isn’t just theory. When we reached out to the manufacturers of two of the best-selling aquarium vitamin supplements, they confirmed that their products cannot be relied upon to overcome thiaminase activity in the foods themselves. Supplements have their place, but they are not a free pass for feeding foods that are otherwise unsuitable.
Q: Does cooking destroy thiaminase?
A: Yes, heat will inactivate thiaminase, but the exact time and temperature needed depend on the food item, its size, and how it is prepared. For example, thorough boiling or baking is generally effective, but a quick blanch may not always be enough, especially for larger pieces of fish or shellfish.
It’s also worth noting that thiamine itself is heat-sensitive. Prolonged or very intense cooking can reduce the natural vitamin B1 content of a food, even as the thiaminase enzyme is destroyed. This means cooking can make a risky food safer by eliminating the enzyme, but it doesn’t necessarily make that food a strong source of thiamine on its own.
Q: Is thiaminase only found in saltwater (marine) animals?
A: No. Thiaminase occurs in both freshwater and marine species. It has been documented in a wide range of organisms, from freshwater cyprinids (carps and minnows) and dreissenid mussels (zebra and quagga) to marine fish like anchovy and smelt, as well as various clams, prawns, and other invertebrates.
Because it is so widely distributed, the presence of thiaminase is not linked to whether an animal lives in freshwater or saltwater; it depends on the species itself. This is one of the reasons why clear, species-level data is so important, and why keepers need to look beyond simple “freshwater vs. marine” assumptions when planning diets.
Q: Does freezing food destroy thiaminase?
A: No. Freezing does not inactivate thiaminase. The enzyme remains active in frozen foods and will continue to break down thiamine in that tissue, even while stored. This means that frozen clams, mussels, prawns, or thiaminase-positive fish still carry the same risk as when they were fresh.
It’s also worth remembering that thawing can leach out water-soluble vitamins, including thiamine, further reducing the nutritional value of the food. Freezing is excellent for preservation and convenience, but it does not make thiaminase-rich foods any safer from a vitamin B1 perspective.
Q: If my fish shows symptoms, can thiamine deficiency be treated?
A: Early cases can often be reversed by removing thiaminase-rich foods and restoring a balanced diet. In severe cases, veterinary intervention with concentrated thiamine supplements may be needed. However, nerve and organ damage caused by long-term deficiency is usually permanent. Prevention is always the safer path.
Q: What should I feed instead?
A: The best guide is nature itself. Different puffers have different diets; some are insectivores, some are opportunists, some mix crustaceans and molluscs. Our individual care guides provide species-specific food suggestions based on both wild ecology and long-term keeper experience. By following nature, you avoid the thiaminase trap and give your puffers the balanced nutrition they need.
Where Critics Sometimes Miss the Point
A common response to the recommendations in this article is:
“There’s no controlled study proving this in aquarium pufferfish.”
That is true. It is also not a strong rebuttal.
In niche areas of animal care, particularly those involving uncommon species or specialised husbandry, controlled trials are rare, expensive, and often ethically or practically unfeasible. Their absence does not imply safety, nor does it invalidate risks demonstrated through other lines of evidence.
In these fields, progress typically comes from converging evidence rather than perfect experiments.
Absence of a controlled trial does not equal absence of risk.
Nutritional and welfare standards often advance through biochemical understanding, field ecology, cross-taxa comparisons, and long-term outcome tracking.
Preventative husbandry is, by necessity, probabilistic rather than absolute.
The argument presented here follows that model. It is not a claim of certainty, but a case for caution informed by biochemistry, ecology, veterinary literature, and repeated real-world outcomes. Waiting for a species-specific controlled trial before adjusting husbandry practices would mean accepting avoidable losses in the meantime.
Responsible care evolves by reducing known risks where possible, especially when the proposed solutions align closely with natural biology and carry minimal downside.
That is the framework within which this article operates.
Author’s Note
This article was not written to alarm, nor to prescribe rigid rules. It grew out of years of unease, observation, and pattern recognition, and from the realisation that some of the most serious problems in fishkeeping are not caused by obvious mistakes, but by assumptions that go unchallenged for too long.
If there is one takeaway, it is this: when in doubt, look to nature. Wild diets are rarely perfect, but they are rarely narrow, repetitive, or static. Replicating that diversity in captivity solves more problems than it creates.
Thiaminase taught me an important lesson. When symptoms refuse to fit neatly into diagnostic boxes, it is often because we are looking in the wrong place. Nutrition, ecology, and long-term feeding patterns matter just as much as water quality and disease management, yet they are far easier to overlook.
The approaches described here are not theoretical. They are based on outcomes observed over many years, across many keepers, and across a wide range of species. Fish raised with these principles in mind consistently fare better. They grow more steadily, behave more naturally, and avoid many of the slow, unexplained declines that prompted this investigation in the first place.
Disclaimer
This article is intended for educational and informational purposes only. While it draws on scientific literature, field studies, and long-term husbandry outcomes, it is not a substitute for professional veterinary diagnosis or treatment.
Fish health is influenced by many variables, including species, age, environment, water chemistry, genetics, and husbandry practices. Symptoms described here may have multiple possible causes, and not every case of illness or decline will be related to vitamin B1 deficiency or thiaminase exposure.
Where fish are severely unwell, deteriorating rapidly, or showing advanced neurological or systemic signs, consultation with a qualified aquatic veterinarian is strongly recommended. Therapeutic interventions, such as injectable vitamin supplementation, should be undertaken only with appropriate professional guidance.
The feeding recommendations discussed in this article are based on current knowledge and best practices, but nutritional science is an evolving field. Keepers are encouraged to remain curious, continue learning, and adapt their approach as new evidence emerges.
Ultimately, responsibility for animal care rests with the keeper. The aim of this article is not to dictate rigid rules, but to provide context, understanding, and a framework for making informed, thoughtful decisions in the best interests of the fish.
References
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US Geological Survey (2019) Thiamine (Vitamin B1) Deficiency in Fish and Wildlife. Columbia Environmental Research Center. Available at:https://www.usgs.gov/centers/columbia-environmental-research-center/science/thiamine-vitamin-b1-deficiency-fish-and(Accessed: [insert date]).
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Renjithkumar, C.R., Roshni, K. and Ranjeet, K. (2020) ‘Feeding ecology of the freshwater pufferfish Carinotetraodon travancoricus in the Western Ghats, India’, International Journal of Aquatic Biology, 8(5), pp. 300–310. https://doi.org/10.22034/ijab.v8i5.922
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