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The Science Behind Zobria®-T

Zobria-T is a new breakthrough vitamin formulation specifically designed for alcoholics seeking recovery from their addiction to alcohol. 

It is well known that chronic alcohol abuse is responsible for vitamin B1 (thiamine) deficiency.  In fact, vitamin B1 deficiency is an epidemic among alcoholics.  Studies show that up to 80% of alcoholics are vitamin B1 deficient.  This occurs because the impact of long-term use of alcohol causes inadequate nutritional intake of vitamin B1, decreased absorption of vitamin B1 from the gastrointestinal tract, and impaired vitamin B1 utilization in the cells. Click here (http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm) to learn more about the extremely damaging effects of vitamin B1 deficiency in alcoholics.

Adequate vitamin B1 levels are essential for the brain to function properly.  Deficiency in vitamin B1 causes the brain to have decreased control over compulsive and destructive behavior, such as controlling excessive alcohol consumption.  Decreased vitamin B1 levels are also associated with feelings of depression.

In its extreme form vitamin B1 deficiency in alcoholics can be fatal or cause permanent brain damage.  The medical term for this condition is Wernicke Korsakoff Syndrome.  Its street name is “Wet Brain”. 

In a less extreme form vitamin B1 deficiency causes the brain to have decreased ability to moderate and refrain from excessive alcohol consumption.  How do we know this?  Click here (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550087/)

and here (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3818307/)

to learn about the elegant studies by Dr. Ann Manzardo, et al., from the Department of Psychiatry & Behavioral Sciences, University of Kansas Medical Center on the positive effects on the behavior of alcoholics achieved by using the key ingredient in Zobria-T, benfotiamine.   The scientists were able to safely and rapidly decrease alcohol consumption and improve behavior control in people addicted to alcohol by giving them this specialized bioactive form of vitamin B1.

These studies showed that reversing vitamin B1 deficiency in alcoholics with the key ingredient in Zobria-T caused a rapid reduction in alcohol consumption and increased feelings of well being.

The science clearly indicates that the vitamin B1 deficiency commonly experienced by alcoholics can cause them to become prisoner of a vicious cycle: excessive alcohol consumption causes thiamine deficiency and thiamine deficiency promotes excessive alcohol consumption.  In time this vicious cycle can cause damage to the brain as it becomes more and more starved of the very nutrient it needs to control the urge to drink excessively. 

Zobria-T breaks this vicious cycle.  It supplies the brain with a safe highly bioactive form of vitamin B1 that rapidly reverses the deficiency suffered by alcoholics.  Zobria-T restores vitamin B1 levels in the brain allowing for better functioning, better control of destructive behavior and improved ability to moderate alcohol consumption.

See the following for more on science related to how Zobria-T helps to improve the functioning of the brain in chronic alcoholics:

Scientific Research Papers

Double-blind, randomized placebo-controlled clinical trial of benfotiamine for severe alcohol dependence.

Manzardo AM, He J, Poje A, Penick EC, Campbell J, Butler MG.


Alcohol dependence is associated with severe nutritional and vitamin deficiency. Vitamin B1 (thiamine) deficiency erodes neurological pathways that may influence the ability to drink in moderation. The present study examines tolerability of supplementation using the high-potency thiamine analog, benfotiamine (BF), and BF's effects on alcohol consumption in severely affected, self-identified, alcohol dependent subjects. A randomized, double-blind, placebo-controlled trial was conducted on 120 non-treatment seeking, actively drinking, alcohol dependent men and women volunteers (mean age=47 years) from the Kansas City area who met DSM-IV-TR criteria for current alcohol dependence. Subjects were randomized to receive 600 mg benfotiamine or placebo (PL) once daily by mouth for 24 weeks with 6 follow-up assessments scheduled at 4 week intervals. Side effects and daily alcohol consumption were recorded. Seventy (58%) subjects completed 24 weeks of study (N=21 women; N=49 men) with overall completion rates of 55% (N=33) for PL and 63% (N=37) for BF groups. No significant adverse events were noted and alcohol consumption decreased significantly for both treatment groups. Alcohol consumption decreased from baseline levels for 9 of 10 BF treated women after 1 month of treatment compared with 2 of 11 on PL. Reductions in total alcohol consumption over 6 months were significantly greater for BF treated women (BF: N=10, -611 ± 380 standard drinks; PL: N=11, -159 ± 562 standard drinks, p-value=0.02). BF supplementation of actively drinking alcohol dependent men and women was well-tolerated and may discourage alcohol consumption among women. The results do support expanded studies of BF treatment in alcoholism.

Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. Drug Alcohol Depend. 2013 Dec 1;133(2):562-70.


Change in psychiatric symptomatology after benfotiamine treatment in males is related to lifetime alcoholism severity.

Manzardo AM, Pendleton T, Penick EC, Butler MG.



Severe alcoholism can be associated with significant nutritional and vitamin deficiency, especially vitamin B1 (thiamine) which is associated with neurological deficits impacting mood and cognition. Alcohol consumption was reduced among female but not male alcoholics after supplementation with the high potency thiamine analog benfotiamine (BF). We examined the relationship between lifetime alcoholism severity, psychiatric symptoms and response to BF among the alcohol dependent men from this cohort.


Eighty-five adult men (mean age=48±8 years) meeting DSM-IV-TR criteria for a current alcohol use disorder who were abstinent <30days participated in a randomized, double-blind, placebo-controlled trial of 600mg BF vs placebo (PL) for 6 months. Psychometric testing included a derived Lifetime Alcoholism Severity Score (AS), Symptom Checklist 90R (SCL-90R), and the Barratt Impulsivity Scale (BIS) at baseline and at 6 months.


Baseline SCL-90-R scale scores for men with high alcoholism severity (AS≥24; N=46 HAS) were significantly greater than for men with low alcoholism severity (AS<24; N=39 LAS), but BIS scores did not differ. MANOVA modeling at follow-up (N=50 completed subjects) identified a significant treatment effect (F=2.5, df=10, p<0.03) and treatment×alcoholism severity level interaction (F=2.5, dfnum=10, dfden=30, p<0.03) indicating reduced SCL-90-R scores among BF treated, HAS males. Above normal plasma thiamine levels at follow-up predicted reduced depression scores in a BF-treated subset (F=3.2, p<0.09, N=26).


BF appears to reduce psychiatric distress and may facilitate recovery in severely affected males with a lifetime alcohol use disorder and should be considered for adjuvant therapy in alcohol rehabilitation.


#NCT00680121 High Dose Vitamin B1 to Reduce Abusive Alcohol Use.

Drug Alcohol Depend. 2015 Jul 1;152:257-63.


The role of thiamine deficiency in alcoholic brain disease.

Martin PR, Singleton CK, Hiller-Sturmhöfel S.


A deficiency in the essential nutrient thiamine resulting from chronic alcohol consumption is one factor underlying alcohol-induced brain damage. Thiamine is a helper molecule (i.e., a cofactor) required by three enzymes involved in two pathways of carbohydrate metabolism. Because intermediate products of these pathways are needed for the generation of other essential molecules in the cells (e.g., building blocks of proteins and DNA as well as brain chemicals), a reduction in thiamine can interfere with numerous cellular functions, leading to serious brain disorders, including Wernicke-Korsakoff syndrome, which is found predominantly in alcoholics. Chronic alcohol consumption can result in thiamine deficiency by causing inadequate nutritional thiamine intake, decreased absorption of thiamine from the gastrointestinal tract, and impaired thiamine utilization in the cells. People differ in their susceptibility to thiamine deficiency, however, and different brain regions also may be more or less sensitive to this condition.

Alcohol Res Health. 2003;27(2):134-42.


Impairment of thiamine absorption in alcoholism.

Tomasulo PA, Kater RM, Iber FL.

Am J Clin Nutr. 1968 Nov;21(11):1341-4.


The multifaceted therapeutic potential of benfotiamine.

Balakumar P, Rohilla A, Krishan P, Solairaj P, Thangathirupathi A.


Thiamine, known as vitamin B(1), plays an essential role in energy metabolism. Benfotiamine (S-benzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine. Once absorbed, benfotiamine is dephosphorylated by ecto-alkaline phosphatase to lipid-soluble S-benzoylthiamine. Transketolase is an enzyme that directs the precursors of advanced glycation end products (AGEs) to pentose phosphate pathway. Benfotiamine administration increases the levels of intracellular thiamine diphosphate, a cofactor necessary for the activation transketolase, resulting in the reduction of tissue level of AGEs. The elevated level of AGEs has been implicated in the induction and progression of diabetes-associated complications. Chronic hyperglycemia accelerates the reaction between glucose and proteins leading to the formation of AGEs, which form irreversible cross-links with many macromolecules such as collagen. In diabetes, AGEs accumulate in tissues at an accelerated rate. Experimental studies have elucidated that binding of AGEs to their specific receptors (RAGE) activates mainly monocytes and endothelial cells and consequently induces various inflammatory events. Moreover, AGEs exaggerate the status of oxidative stress in diabetes that may additionally contribute to functional changes in vascular tone control observed in diabetes. The anti-AGE property of benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Interestingly, few recent studies demonstrated additional non-AGE-dependent pharmacological actions of benfotiamine. The present review critically analyzed the multifaceted therapeutic potential of benfotiamine.

Pharmacol Res. 2010 Jun;61(6):482-8.


Benfotiamine in Treatment of Alcoholic Polyneuropathy: an 8-Week Randomized Controlled Study (BAP I Study)



A three-armed, randomized, multicentre, placebo-controlled double-blind
to examine the efficacy of benfotiamine vs a combination containing benfotiamine and
B,2 in out-patients with severe symptoms of alcoholic polyneuropathy (Benfotiamine
Alcoholic Polyneuropathy. BAP I). The study period was 8 weeks and 84 patients
prerequisite criteria and completed the study as planned. Benfotiamine led to significant improvement in alcoholic polyneuropathy. Vibration perception (measured at the tip of the great toe) significantly improved in the course of the study, as did motor function, and the overall score reflecting the entire range of symptoms of alcoholic polyneuropathy. A tendency toward improvement was evident for pain and co-ordination, no therapy-specific adverse effects were seen.

Alcohol & Alcoholism Vol. 33. No. 6. pp. 631-638. 1998