Many commercial pet diet manufacturers follow these nutritional recommendations when formulating pet diets. However, unconventional diets such as unbalanced foods, raw foods and homemade diets are not nutritionally adequate to meet the dietary thiamine recommendations, which in turn increases the risk of developing thiamine malnutrition.

Sweet Potato Diet on a Maltese Terrier

An owner fed a diet of boiled sweet potato for 4 weeks on his 5‐year‐old neutered male Maltese Terrier dog and this nutritionally incomplete diet eventually led to the suboptimal thiamine status of the body. The sweet potatoes fed to the dog were well‐boiled before feeding, and this heating procedure for cooking would have led to a sufficient amount of thiamine loss in sweet potatoes. Because of the low thiamine content in boiled sweet potato (0.09 mg per 100 g of boiled sweet potato), a large quantity of sweet potatoes is needed to be significant to supply adequate amounts of thiamine. Furthermore, intake of dietary carbohydrates has been known to increase the dietary requirements for thiamine based on data from previous human studies. Boiled sweet potatoes are not only low in thiamine, but rich in carbohydrates (approximately 80% of the dry matter in sweet potatoes). Given this background, the consumption of boiled sweet potatoes may further increase the metabolic demand for thiamine and may precipitate thiamine deficiency in a short period.

Symptoms

The Maltese Terrier dog was presented to a referring veterinarian with a 3‐day history of:

• Depression
• Anorexia
• Vomiting
• Seizure clustering
• Generalized ataxia

The owner noticed a progressive deterioration of the neurologic signs over the preceding 3 days. Symptomatic treatment before the presentation with phenobarbital (2 mg/kg twice a day orally) failed to alleviate the seizures.

The dog had been generally healthy until the occurrence of acute seizure episodes. He had been fully vaccinated and dewormed, with no history of trauma or exposure to toxins. Further medical enquiry with the owner revealed that the dog had been fed an almost exclusive diet of boiled sweet potato (Ipomoea batatas) as a primary diet source for 4 weeks with an average consumption of approximately 100–150 g (about one to one and a half small whole sweet potatoes) per day due to his picky eating behaviours (chronic food refusal). Furthermore, this food refusal had gradually worsened over time.

Neurological examination identified generalized ataxia with dysmetric movement and an inability to bear full weight on the hind limbs.

There was no cytological CSF evidence of relatively well‐recognized CNS disorders (e.g. inflammatory, neoplastic and infectious causes). Therefore, based on the inadequate diet history, the hyperlactatemic condition (Type B hyperlactatemia) and the abnormalities seen on MRI, a presumptive diagnosis of thiamine deficiency was established in this patient.

To confirm the presumptive diagnosis of thiamine deficiency, the whole blood sample was submitted to evaluate the blood thiamine concentration. Thiamine content was measured by the high‐pressure liquid chromatography (HPLC) method with the assistance of a commercial laboratory (Neodin Vetlab, Seoul, Korea). The HPLC is a preferable and reliable method of thiamine analysis in humans and animal studies, which helps by directly measuring the phosphorylated form of thiamine (thiamine pyrophosphate, TPP) within RBCs.

Treatment

Following the MRI scan and the blood sampling, a therapeutic trial using thiamine supplementation with dietary intervention was performed on the same day to evaluate the associated response and to rapidly recover the clinical signs.

Sweet potato supplementation was immediately stopped prior to starting the treatment.

Thiamine supplementation was started with oral vitamin B complex  at a total thiamine dose of 45 mg once a day for a month.

Furthermore, the dog’s diet was temporarily changed to a good‐quality prescribed dog food containing high levels of protein and fat.

Recovery

A rapid improvement in neurological signs was seen with the initiation of thiamine supplementation and diet change. There were no additional seizures after being discharged from the hospital. Furthermore, the symptoms of anorexia improved along with the normalization of previous metabolic derangement with the treatment, which consequently accelerated the recovery rate of the remaining neurological abnormalities. Finally, no residual neurological deficits were observed at 3 days after continuous management.

Two weeks after starting thiamine supplementation and dietary intervention, there were no abnormalities on physical and neurological examination. Repeated blood examination showed that the previously observed biochemical abnormalities had entirely normalized.

Conclusion

Thiamine deficiency causes metabolic encephalopathy that can be reversed with early diagnosis and appropriate treatment. Obtaining a comprehensive dietary history is extremely important in suspected cases of thiamine deficiency or in sick animals and urges prompt intervention for nutrition. Measuring blood TPP concentration by HPLC is the most reliable and intuitive method to confirm the diagnosis of thiamine deficiency. MR imaging and blood lactate levels can also provide clinically meaningful insights into the thiamine status. Clinicians should be aware that diet composition can markedly influence the thiamine requirements of dogs. Dietary changes based on dietary composition as well as a complete and well‐balanced diet might be helpful in the rapid recovery of thiamine deficiency.

Source – Veterinary Medicine and Science | First published: 23 September 2020

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1942 – Mild Thiamine deficiency in 11 Women

Williams, Mason, Smith, and Wilder, at the Mayo Clinic in 1942 induced thiamine deficiency, placed 11 women on diets which provided 0.22 mg. of thiamine for each 1000 calories.¹

This allowance was five and a half times greater than that given during their earlier studies and was selected to produce a milder type of deficiency compared to that which might be encountered more frequently in the general population.

Caloric intakes were adapted to the requirements of each subject and moderate activity was permitted.The periods of low thiamine allowance mere continued for 89 to 196 days.

Symptoms

• During this time all subjects showed definite changes of personality.
• Irritable
• Depressed
• Quarrelsome and uncooperative
• Two threatened suicide.
• All became inefficient in their work
• Forgetful
• Lost manual dexterity.
• Their hands and feet frequently felt numb.
• Headaches
• Backaches
• Sleeplessness
• Sensitivity to noises were noted
• The subjects fatigued easily.
• Constipation was the rule, but no impairment.
• Anorexia
• Nausea
• Vomiting
• Epigastric distress were frequently observed.
• Low blood pressure and vasomotor instability mere present in all patients.
• At rest, pulse rates were low (55 to 6O per minute) but tachycardia followed moderate exertion.
• Fasting blood sugar was often abnormally high.

Recovery Notes

When additions of thiamine were made to the diet, the above manifestations disappeared gradually and a sense of well-being returned. Apparent improvement, however, was not so rapid as it had been with the more severe degrees of thiamine deficiency studied.

Conclusion

This gives a really interesting overview on how many symptoms manifest even in a mild thiamine deficient state and also how easily it was induced, considering how alcohol and refined carbohydrate sources can accelerate the use of thiamine, its highly important to pay attention to symptoms that manifest.

Books That Discuss This Subject

Sources

The post Inducing Mild Thiamine deficiency in 11 Women appeared first on Understanding B1 Deficiency.