• Supports memory and learning by inhibiting age related brain volume loss of the hippocampus
  • Maintains verbal skills and comprehension ability
  • Sustains brain cell health by inhibiting beta-amyloid induced neurotoxicity

What makes VIVImind™ the new generation of memory support solutions? Simply, there is no other natural health product with comparable clinical evidence in the marketplace today. It is scientifically supported by over 15 years of rigorous research, including Phase III clinical testing with over 2,000 individuals. It is the first nutraceutical to undergo MRI baseline studies that support its claim for inhibiting atrophy (shrinkage) of the hippocampus by 68% over 18 months. The active ingredient Homotaurine is found in marine red algae. Shrinkage of the hippocampus is caused by formation of a toxic plaque that causes neurons to become damaged or die, which may cause signalling problems to occur in the brain.

Serving Size: 1 Capsule

Homotaurine (3-amino-1-propanesulfonic acid) 50 mg

NPN: 80021111
60 v-caps -Item Number: OVS55006
120 v-caps- Item Number: OVS55007
50 mg
 Gastric Resistant

100% Vegetarian

Recommended Use: Homotaurine has been investigated in phase III clinical studies. VIVImind™ reduces atrophy (shrinking) of the hippocampus, the specific area of the brain involved in memory and learning. Shrinkage can occur with the buildup of a toxic protein called beta-amyloid that causes neurons to malfunction and die. This effect has not been studied in a healthy population. This product is not intended to treat, prevent, or reduce the risk of any specific diseases.

Adult Dose: For Adults 50 years of age or older, take 2 capsules twice daily with a meal, or as directed by a qualified health care professional. May start with 1 capsule at bedtime for one week and then progress to 1 capsule twice daily for an additional week to reduce the chance of nausea. Use for a minimum of 6 months for beneficial effects.

Non-medicinal ingredients: microcrystalline cellulose. Capsule: hypromellose, gellan gum

Cautions: Some people may experience nausea, weight loss, dizziness, or fainting. Do not exceed recommended daily dose as you may experience more of these symptoms. If you experience any weight loss, drowsiness, dizziness, fainting, persistent nausea, vomiting, or diarrhea, consult a health care practitioner. Consumption of homotaurine with alcohol, other medications and/or natural health products with sedative properties is not recommended. Exercise caution if operating heavy machinery, driving a motor vehicle or involved in activities requiring mental alertness. Discontinue use if you experience any confusion or any unexpected memory loss. Do not use if you are diagnosed with stomach ulcers or low blood pressure or if you are pregnant, planning on becoming pregnant, or breastfeeding. Consult a health care practitioner if you have any questions.

  • GMP Manufacturing
  • Independent Testing
  • Quality Assured

Made in Canada
Ovos Natural Health
3900-12th St NE
Calgary, AB
T2E 8H9

  1. VIVImind™- Phase III Clinical Trial Summary – MRI Subgroup Analyses
  2. VIVImind™- Phase III Clinical Trial Summary Investigation of Homotaurine and Alzheimer’s Disease
  3. VIVImind™- Phase III Clinical Trial Summary ADAS-cog Results from the Alphase Study
  4. In Support of VIVImind™

VIVImind™- Phase III Clinical Trial Summary – MRI Subgroup Analyses


Gauthier S. et al. The Effect of Tramiprosate (homotaurine) in Patients with Mild to Moderate Alzheimer’s disease: Exploratory Analyses of the MRI Sub-Group of the Alphase Study. Journal of Nutrition Health & Aging. 2009;13(6):550-557


  • Anti-amyloid therapies have been proposed as a treatment for Alzheimer’s dementia (AD), particularly Tramiprosate (ALZHEMED, homotaurine); in vitro studies have shown that this compound binds to soluble A and inhibits amyloid fibril aggregation and consequently plaque formation.
  • Homotaurine is able to cross the blood-brain barrier and reduce brain amyloid plaque deposition and concentrations, prevent cell death and maintain neural transmission. Further, this compound has also been detected in Cerebral Spinal Fluid (CFS) and has been shown to reduce amyloid beta peptide levels in CSF of AD patients.


  • This study assessed the disease modification resulting from homotaurine supplementation in a subgroup of patients with mild to moderate AD.


  • Design: Multi-centered, randomized, double blind placebo-controlled parallel-design study
  • 1052 patients were screened at 67 study centers across US, EU and Canada over an 18-month period.
  • Patient criteria met for study inclusion: Men and women (50 years and older) with a diagnosis of AD by standard criteria. Stable doses of the following medications were permitted in the study: anxiolytics, sedatives, hypnotics, antidepressants, antipsychotics, anticonvulsants, estrogens, statins, Vitamin E (
  • Exclusion criteria: Px with other causes of dementia (PHx, physical or neurological examination.) BMI: 28. Life expectancy of < 2 years. Any clinically significant, uncontrolled disease.
  • Intervention: Groups: 1:1:1 ratio of 100mg BID (n=352) of tramiprosate, 150 mg BID of tramiprosate (347), Placebo BID (353). Length of study: 8 week titration period, 70 consecutive weeks of administration and testing.
  • Primary screening: ADAS-cog, CDR-SB, and .5 Tesla vMRI scan of hippocampus. A clinical assessment conducted at: Baseline, Weeks 13, 26, 39, 52, 65, and 78.
  • Analysis for Covariance (ANCOVA) studies were conducted to compare the psychometric values (ADAS-cog data, and CDR-SB data) with vMRI data- testing for“main effects for groups and visit, as well as for groups by visit interactions.”


  • The final statistical model which considered covariates revealed a statically significant difference between the two groups for the 150mg group at weeks 26 and 52, with marginally significant difference at week 13 and 39.
  • The slope analysis (more sensitive in detecting significance between group differences in ADAS-cog scores) indicated that the rate of decline for ADAS-cog was decreased (P=0.05 for 100mg Vs. Placebo) and (P=0.130 for 150mg Vs. Placebo) or (P=0.051 combined 100/150mg groups Vs. Placebo) Statistical Significance was defined as a (P < 0.15).
  • Overall“the final modeling analyses of ADAS-cog revealed between-group differences and trends in favour of homotaurine.”
  • No changes were found in the CDR-SB results in any of the groups in either statistical model.

Key Observations

  • 68% difference between 100mg BID and placebo groups (P=0.035).
  • A 120% difference between 150mg BID group and placebo group (P=0.009).
  • At Week 78, there was an overall correlation between changes in HV and in ADAS-Cog scores Vs. Placebo (P=0.18)

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VIVImind™- Phase III Clinical Trial Summary Investigation of Homotaurine and Alzheimer’s Disease


Saumier D. et al. Lessons Learned in the Use of Volumetric MRI in Therapeutic Trials in Alzheimer’s disease: The AlzhemedTM (Tramiprosate) Experience. Journal of Nutrition Health & Aging. 2009:13(4); 370-372


  • Several studies in AD have suggested that Magnetic Resonance Imaging (vMRI) measures may be valid markers of disease progression, in particular to detect lower statistical measurement variance than clinical measures and because they may have greater sensitivity to detect treatment effects in anti-amyloid drug trials.
  • Anti-amyloid therapies have been proposed as a treatment for Alzheimers dementia (AD) particularly Tramiprosate (ALZHEMED, homotaurine).
  • As this therapy appears quite promising it is imperative to ensure the appropriate assessment is conducted.


  • To determine the “feasibility, sensitivity and clinical relevance”of the neuroimaging biomarker: volumetric Magnetic Resonance Imaging (vMRI) to measure the effects of anti-amyloid therapies.


  • Design: Multi-centered, randomized, double blind, 18 month placebo-controlled study.
  • 1052 patients screened using MMSE for mild to moderate AD. All were on cholinesterase inhibitors (with/without memantine) for ≥4 months prior to screening.
  • Intervention: 100mg BID of tramiprosate, 150 mg BID of tramiprosate, Placebo BID.
  • Primary screening: ADAS-cog, CDR-SB, and .5 Tesla vMRI scan of hippocampus.
  • Clinical assessment conducted at: Baseline, Weeks 13, 26, 39, 52, 65, and 78.
  • A MRI sub study was conducted; 508 patients were studied at 51 ACR-NEMA approved MRI sites.
  • 4 MRI scanners were used: GE-Signa, Siemens-vision, Siemens-Symphony, and Philips Gyroscan.
  • Centralized assessment of hippocampus volume (HV) derived from a 1.5Tesla weighted 3D volumetric sequence.
  • ANCOVA model was used to derive MRI data by comparing treatment groups with respect to change from baseline for HV, using baseline HV, site and duration of MRI follow up.
  • 388 scan pairs were submitted for volume analysis; 312 were of adequate quality to assess the HV change, including 109 placebo group scan pairs.


  • At week 78: the mean changes from baseline for the placebo group in the MRI subset were 7.8 (9.2) and 2.0 (2.6) points for the ADAS-cog and CDR-SB measures. Results were lower than expected with large standard deviation’s (SD) suggesting significant “within and between patient variance.”
  • Changes in HV were -192.2 (223.0) mm3 (volume decrease). CV for HV was 1.16. Closer to estimate values though the SD was higher than anticipated, maybe due to inclusion of more sites than have been previously studied.
  • Correlations between ADAS-cg, CDR-SB and HV at baseline were -0.16 (p=0.11) and -0.25 (p<0.05). Correlations between ADAS-cg, CDR-SB and HV after change were -0.17 (p=0.07) and 0.08 (p=0.43). These results approached statistical significance and support the clinical validity of the vMRI biomarker. However the magnitude of the correlation indicates that these measures“do not entirely quantify similar disease processes.”

Key Observations

  • Supports the utility of vMRI“to provide evidence for disease modification in AD clinical trials.”
  • vMRI may be useful in demonstrating treatment effects earlier in disease as hippocampus atrophy is thought to precede cognitive and clinical decline.

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VIVImind™- Phase III Clinical Trial Summary ADAS-cog Results from the Alphase Study


Saumier D. et al. Domain -Specific Cognitive Effects of Tramiprosate in Patients with Mild to Moderate Alzheimer ’s Disease: ADAS-cog Subscale Results From The Alphase Study. The Journal of Nutrition, Health and Aging. (2009);13 (9):808-812


  • Tramiprosate (Homotaurine, ALZHEMED) is an amyloid β antagonist, found to be neuro-protective against amyloid-mediated neurotoxicity in the brain
  • An 18-month Phase III clinical study performed in mild to moderate Alzheimer’s disease patients showed trends towards cognitive benefits in the Tramiprosate treated patients as measured by ADAS-cog scores
  • ADAS-cog assess changes in global cognition by measuring 11 domain-specific items: 7 performance tests (Word Recall, Object Naming, Commands, Constructional Praxis, Ideational Praxis, Orientation, Word Recognition), and 4 rater based scales (Remembering Test Instructions, Spoken Language Ability, Word Finding Ability, Language Comprehension)
  • Cognitive decline is observed by a positive change from baseline which indicates progressing low scores on cognitive tests


  • The present study observes the analyses performed on scores obtained from the specific ADAS-cog subscales in the Alphase study, in order to determine whether specific types of cognition can be impacted by tramiprosate administration.


  • Analyses: Data from the ADAS-cog reported in the Alphase trial was analyzed according to sub-domain.
  • ANOVA analyses were used to compare the data between each tramiprosate group and Placebo.
  • All analyses were based upon observed cases in the intent- to- treat population as defined by patients who had an ADAS-cog assessment performed at Baseline and a minimum of one follow up visit.


  • Patients in the tramiprosate 100 mg BID group experienced less decline on the Remembering Test Instructions, Following Commands, Language Comprehension, Spoken Language Ability and Object Naming subscales compared to Placebo.
  • Patients in the tramiprosate 150 mg BID group experienced less decline on the Ideational Praxis subscale compared to Placebo.

Key Observations

  • The findings of this analysis revealed statistically significant differences in 6-different cognitive domains in patients treated with tramiprosate compared to Placebo.
  • The following ADAS-cog subscales demonstrated significant improvement: Following Commands, Language Comprehension, Ideational Praxis, Object Naming, Remembering Test Instructions and Spoken Language Ability.
  • Tramiprosate may have benefit on memory, language and praxis skills in mild to moderate Alzheimer’s individuals

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In Support of VIVImind™

VIVImind revisited: Examining the evidence carefully and avoiding the rush of blood to the head and jumping on the naysayer’s bandwagon. Dr. Traj Nibber VIVImind (homotaurine) is a naturally occurring molecule present in a certain type of seaweed; it easily crosses the blood brain barrier and has been shown to prevent the formation of amyloid beta plaques (ABP) in the brain. Ten animal studies have shown that VIVImind prevents the conversion of amyloid beta into its oligomers and fibril forms. These forms have proven to be much more toxic to the nerve cells affecting cognition and act at an accelerated rate beyond that of the normal ageing process. Previous human studies confirmed VIVImind’s safety and its ability to clear ABP from the brain in Alzheimer’s disease (AD) patients. In 2009, VIVImind underwent the final and most expensive phase of a drug testing program called phase III study. This was a gold standard, double-blind placebo controlled randomized study of 1052 mild to moderate AD patients in sixty seven centers across North America. Patients were placed in one of three groups: (i) 200mg of VIVImind per day, (ii) 300mg of VIVImind per day or (iii) untreated (placebo) group for 18 months.

Two end points were selected:

  • Standardized cognitive tests like ADAS-cog and CDR-SB for clinical assessment and,
  • MRI scans of the brain particularly of the hippocampus region of the brain that is associated with learning and memory, as a measure of the rate of disease progression. This test is a sensitive predictor of the pathology of AD.

At the end of the study the statistical significance (or the p value) for the two cognitive tests did not quite reach the magical mark of less than 0.05 which is considered significant, however, the MRI scans were highly significant. Unfortunately, the regulatory authorities denied VIVImind™ an AD reducing claim but instead allowed a claim that VIVImind™ “reduces atrophy (shrinking) of the hippocampus” as a natural health product. As usual, the media got hold of this and over represented the lack of significance of the two cognitive tests as VIVImind™ having failed the study and, claimed VIVImind™ did not have any beneficial cognitive effects. Closer examination of the data however shows that VIVImind™ is highly beneficial and effective against age-associated cognitive decline, and that a number of factors contributed against reaching the significance level: First, this was the first AD study of its type so there was no precedent in the design of the study including factors such as the number of patients to select, type of AD patients to recruit who had either mild, moderate or severe symptoms, and how long to conduct the study. Second, the placebo or the untreated group of AD patients with which VIVImind™ was being compared did not do too poorly; their cognitive test scores were higher than expected and this made VIVImind™’s results look less impressive. Third, because the study was conducted in many different centers, there was a considerable variation within and between the groups which skewed the results considerably. Fourth, given the complex and diverse nature of AD, the difficulty of diagnostic accuracy of mild to moderate AD patients which ranges from 23%-96%, makes testing any therapy for AD difficult to assess by simple statistical analysis. In retrospect, one could argue that the number of patients recruited should have been higher, the duration should have been longer than 18 months, restricted to fewer centers, and tested in more severe AD patients. However, these results do not suggest that VIVImind™ is ineffective; rather when the data is re-evaluated taking into account all of the above, a completely different picture emerges namely that VIVImind™ is highly effective and clinical significance (p< 0.05) was achieved for both treated groups when compared to placebo even as early as 26 and 52 weeks. The reduction in the atrophy of the brain using a new and powerful MRI technique suggests that VIVImind™ is very effective. The rate of atrophy of the brain is a predictor of the progression of AD, and VIVImind™ reduced the shrinking by 68% when a daily dose of 200mg is compared to placebo, and by 120% when 300mg daily dose is compared to placebo! It must be remembered the study looked specifically at the hippocampal volume and the hippocampus is the key learning and memory centre. Finally, the results in a subset of AD patients that had the apoE4 gene, which is an indicator of a more severe and aggressive form of AD, shows a highly significant effect even at 18 months. Various researchers continue to promote the benefits of VIVImind™; a recent 2012 paper by leading Italian researches in AD and key opinion leaders in Montreal both support the benefits of VIVImind™ in cognitive health. back to top

VIVImind Info Sheet (DOWNLOAD PDF)

1. What is VIVImind™?

For an aging population, VIVImind™ represents a breakthrough in one of the key consequences of getting older – memory loss. VIVImind™ is a science-based natural health product that has been scientifically proven to support memory function based on the naturally occurring ingredient, homotaurine, found in seaweed. VIVImind™:

  • Supports the brain structure associated with memory and learning
  • Help to preserve memory
  • Sustains brain cell health
  • Maintains verbal skills and comprehension ability
  • Supports planning and execution skills

2. Is VIVImind™ an extract of the natural form of homotaurine found in seaweed?

No. The active ingredient in VIVImind™ is a synthetic form of homotaurine, which is chemically and biologically identical to the natural compound. Extracts are generally close to 100% pure, which means an extract of homotaurine would contain nothing but homotaurine. The chemically synthesized form of homotaurine is also a 100% pure extract. Think of it as a lock and key concept: homotaurine is the key that will fit the lock, which is a cellular receptor in the hippocampus region of the brain. As long as the key has the same structure, it will fit the lock. Therefore, homotaurine, whether a natural extract or chemically synthesized, it will have the same effect.

3. Is homotaurine the same  as taurine?

No. Homotaurine and taurine are two different compounds that belong to the same chemical family but have different origins and effects. Taurine is a major constituent of digestive fluids produced by the liver (bile). Taurine can be found in small amounts in the tissues of many animals including humans. Homotaurine does not convert into taurine after digestion and vice versa. Homotaurine has shown a protective effect on brain cells, while taurine has no protective effect.

4. How does VIVImind™  work?

As we age, certain brain regions start to shrink. This shrinkage reflects loss of brain cells. One brain region in which brain cell loss occurs is the hippocampus, a region responsible for learning, memory and spatial navigation. Shrinkage of the hippocampus has been associated with learning and memory problems2. Why does the loss of brain cells in the hippocampal region occur? Scientific research indicates that the buildup of certain toxic proteins3-4 called beta-amyloid (or A-beta) is detrimental to the brain. When these proteins reach excessive levels, they cause neurons (brain cells) within the brain to malfunction and die. When neurons are damaged or die, signaling problems occur in the brain that ultimately effects memory and learning abilities3. Research has shown that VIVImind™ protects brain cells by two mechanisms: it reduces the accumulation of toxic Aβ proteins, which can deposit as plaques in the brain. VIVImind™ also protects brain cells from the toxic effects of the Aβ proteins and thus reduces brain cell toxicity, damage and death, in part through activation of brain cell receptors, called GABAa receptors, in an area of the brain associated with learning and memory (the hippocampus). VIVImind™ is a patented product based on the naturally occurring ingredient homotaurine, which binds to A-beta proteins and reduces the deposition and toxic effects of these proteins in the brain4. In a groundbreaking study performed in Canada and the United States using brain scans (Magnetic Resonance Imaging  -MRI), VIVImind™ was shown to significantly reduce the loss of brain volume in the hippocampus. In fact, VIVImind™ was proven to preserve 68% more brain volume versus placebo (like a sugar pill)5. Individuals taking VIVImind™ also performed better on memory and thinking tests compared with individuals taking placebo. VIVImind™ was found to improve cognitive performance (verbal skills, memory, comprehension ability, planning and execution skills) by 33% versus placebo5.

VIVImind™ has been shown to:

Protect the brain structure associated with memory and learning.

The hippocampus is a brain region associated with learning and memory. VIVImind™ can help reduce the loss of volume of this very important region through the aging process.

Support  memory

You know how you can be introduced to someone and forget their name two minutes later? VIVImind™ can support you in maintaining your ability to remember things like people’s names.

Sustain brain cell health

With age, it is normal to lose brain cells. VIVImind™ can help protect your brain cells during the normal course of aging.

Maintain verbal skills and comprehension ability

VIVImind™ can help you maintain your level of verbal comprehension and your overall quality of speech. So when you are telling a story or making a presentation, VIVImind™ can help you retain your train of thought.

Support planning and execution skills

You have just arrived at your vacation destination and you suddenly realize that you forgot to cancel your newspaper subscription. VIVImind™ can help you maintain your ability to go from the initial planning to remember everything you need to make it a trip you will never forget.

5. What is the recommended dosage for VIVImind™ ?

Each capsule of VIVImind™ contains 50 mg of homotaurine. VIVImind™ capsules should be taken daily and should be swallowed whole (not crushed, blended or mixed). The recommended adult dose is 2 capsules twice daily with a meal, or as directed by a qualified health care professional. To reduce the possibility of nausea, it is recommended to start with 1 capsule at bedtime for one week and then progress to 1 capsule twice daily for an additional week. If you miss a dose, simply start again the next day at your regular time. Do not double the dose to make up for the missed dose.

6. What result should I expect to see, or experience after taking VIVImind™ ?

VIVImind™ is a long term use product. It is effective for both improving current cognitive health as well as preventing future decline. Individuals who are concerned about their memory, or want to proactively protect their cognitive health can use VIVImind at a younger age, before cognitive concerns arise. It is important to remember that the brain is a highly complex organ and brain cell deterioration takes nearly 50 years before symptoms arise. Clearing this toxic plaque also takes time. Therefore, using VIVImind™ is a long term commitment to your future health and quality of life.

7. Is VIVImind™ safe?

After hundreds of millions of dollars invested and 15 years of rigorous scientific research, including clinical testing with over 2,000 individuals1 in 68 European, 50 U.S. and 17 Canadian medical centres, VIVImind™ is now available for consumers. The product has been shown to be safe and generally well tolerated at the recommended daily dose. Some people may experience symptoms such as nausea, weight loss, dizziness or fainting. The recommended dose should not be exceeded, since people may experience more of these symptoms. It should be noted that from what we have seen in the scientific data to date, certain symptoms such as nausea, are generally transient and normally subside by themselves with consistent use. If they persist, contact your health care practitioner.

8. Can VIVImind™ be used with other natural products or medications?

Metabolism studies suggest that interactions between VIVImind™ and other products are not likely to occur6. No specific interaction studies were conducted with other products. For further information, contact your healthcare professional.