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Liver Protection & Antioxidant Support


60 Tablets 3000mcg Vitamin A

  • Protects and supports the liver
  • Used in Herbal Medicine as an alterative to remove waste
  • Stimulates digestion
  • Increases bile flow
  • Antioxidant support & Promotes sleep


• Protects and supports the liver
• Used in Herbal Medicine as an alterative to remove waste
• Stimulates digestion
• Increases bile flow
• Antioxidant support
• Promotes sleep
LiverCalm is one half of our specialized formulations designed to help with detoxification, to maintain liver health and support liver functions.  The main function of the liver is to filter the blood coming from the digestive tract before it is passed to the rest of the body. It is also responsible for detoxifying chemicals and secrete bile that will further breakdown food. Milk thistle (silymarin) is a flowering herb that is native to Mediterranean countries and is used as a natural treatment for liver problems such as cirrhosis, jaundice, hepatitis and gallbladder disorders. Other ingredients found in this formulation include turmeric, burdock D-L-alpha lipoic acid, chamomile, etc. These ingredients are also present to support healthy liver functions and health but they are also used as a diuretic, help remove waste products via the kidneys and skin, increase bile flow, aid digestion, relieve mild digestive upset and inflammatory conditions of the gastrointestinal tract. For a more complete liver care and detoxification, it is recommended to take with Hepatonic.


Why Jensens Vitamins?

The application of Structurally Active-Orthogenic (SAO) technology by Jensens Vitamins' research and production team ensures that all available products are of a heightened quality. 

SAO technology produces active ingredients with strong molecular composition and the highest bioavailability (ratio of inactive/active ingredients) in order to ensure synergistic applications occur within the body. In other words, the Jensens Vitamins label ensures that all our products are able to be optimally absorbed by the bloodstream at the molecular level, and don’t just pass through the body undigested. 

Jensens Vitamins is pharmaceutically tested and clinically verified by careful examination at every stage of production. The protocols are measured and confirmed for international standard compliance before the product is introduced to market. 

Jensens Vitamins only uses 100% natural ingredients. 

Active Ingredients

Silybum Marianum (200 mg), Matricaria Chamomilla (150 mg), Choline (100 mg), Arctium Lappa (50 mg), Curcuma Longa (50 mg), D-L-Alpha Lipoic Acid (30 mg), Vitamin C (30 mg), Chromium (35 mcg), Vitamin D2 (10 mcg).


Dicalcium phosphate, magnesium stearate, stearic acid, microcrystalline cellulose, silicon dioxide, croscarmellose sodium.

Does not contain gelatin, gluten, artificial colours, preservatives or GMOs.






60 Tablets

Recommended Dose:

Adults: Take 1 tablet once daily with a meal. Diuretic: for occasional use only.


Consult a physician prior to use if you have diabetes or if symptoms persist or worsen. Do not use this product if you are pregnant or if you are allergic to plants of Asteraceae/Compositae/Daisy family.  Discontinue use if hypersensitivity. Keep out of reach of children.

Biogenique Structurally Active-Orthogenic (SAO) technology

Vitamin A is a fat-soluble vitamin important for normal vision, the immune system, and reproduction. Vitamin A also helps the heart, lungs, kidneys, and other organs work properly. Biogenique SAO technology designed vitamin A with a unique formula of compounds in their active form. These compounds are preformed vitamins – retinol, retinal, retinoic acid – together termed as retinoids i.e. vitamin A acetate. 
Preformed vitamins in Biogenique vitamin A are readily available for utilization. They do not depend on bile or fat in the intestines for their absorption. This means, it is specifically beneficial for people with poor digestion or impaired absorption. 
After consuming Biogenique vitamin A, SAO helps this pre-formed vitamin A to be metabolized intracellularly to retinal and retinoic acid (the active forms of vitamin A). SAO supports the vitamin’s important biological functions and maintains healthy reservoirs of vitamin A by storing it in the liver, when not in use. 

Our research says,

Groups at Risk of Vitamin A Inadequacy include:
Premature Infants
In developed countries, clinical vitamin A deficiency is rare in infants and occurs only in those with malabsorption disorders. Preterm infants do not have adequate liver stores of vitamin A at birth and their plasma concentrations of retinol often remain low throughout the first year of life. Preterm infants with vitamin A deficiency have an increased risk of eye, chronic lung, and gastrointestinal diseases. 

Infants and Young Children
Women with vitamin A deficiency, breast milk volume and vitamin A content are suboptimal and not sufficient to maintain adequate vitamin A stores in infants who are exclusively breastfed. The most common and readily recognized symptom of vitamin A deficiency in infants and children is xerophthalmia. 

Pregnant and Lactating Women in developing countries.
Pregnant women need extra vitamin A for fetal growth and tissue maintenance and for supporting their own metabolism. The World Health Organization estimates that 9.8 million pregnant women around the world have xerophthalmia as a result of vitamin A deficiency. Other effects of vitamin A deficiency in pregnant and lactating women include increased maternal and infant morbidity and mortality, increased anemia risk, and slower infant growth and development. 

People with Cystic Fibrosis
Most people with cystic fibrosis have pancreatic insufficiency, increasing their risk of vitamin A deficiency due to difficulty absorbing fat. However, improved pancreatic replacement treatments, better nutrition, and caloric supplements have helped most patients with cystic fibrosis become vitamin A sufficient. 

SAO Analysis

Vitamin A and Vision
The retina is located at the back of the eye. When light passes through the lens, it is sensed by the retina and converted to a nerve impulse for interpretation by the brain. Retinol is transported to the retina via the circulation and accumulates in retinal pigment epithelial cells. It is further shuttled across to the rod cell where it binds to a protein called opsin to form the visual pigment, rhodopsin (also known as visual purple). Rod cells with rhodopsin can detect very small amounts of light, making them important for night vision. Inadequate retinol available to the retina results in impaired dark adaptation, known as "night blindness." 

Regulation of gene expression
Retinoic acid (RA) act as hormones to affect gene expression and thereby influence numerous physiological processes. Through the stimulation and inhibition of transcription of specific genes, retinoic acid plays a major role in cellular differentiation (the specialization of cells for highly specific physiological roles). Many of the physiological effects attributed to vitamin A appear to result from its role in cellular differentiation. 

Vitamin A is commonly known as the anti-infective vitamin, because it is required for normal functioning of the immune system. The skin and mucosal cells (cells that line the airways, digestive tract, and urinary tract) function as a barrier and form the body's first line of defense against infection. Retinol is required to maintain the integrity and function of these cells. 

Growth and development
Both vitamin A excess and deficiency are known to cause birth defects. Retinol and retinoic acid (RA) are essential for embryonic development. During fetal development, RA functions in limb development and formation of the heart, eyes, and ears. Additionally, RA has been found to regulate expression of the gene for growth hormone. 

Red blood cell production
Red blood cells, like all blood cells, are derived from precursor cells called stem cells. Stem cells are dependent on retinoids for normal differentiation into red blood cells. Additionally, vitamin A appears to facilitate the mobilization of iron from storage sites to the developing red blood cell for incorporation into hemoglobin, the oxygen carrier in red blood cells. 

Nutrient interactions
Zinc: Zinc deficiency is thought to interfere with vitamin A metabolism in several ways: (1) zinc deficiency results in decreased synthesis of retinol binding protein (RBP) (2) zinc deficiency results in decreased activity of the enzyme that releases retinol from its storage form, in the liver; and (3) zinc is required for the enzyme that converts retinol into retinal Iron: Vitamin A deficiency may exacerbate iron-deficiency anemia. Vitamin A supplementation has beneficial effects on iron deficiency anemia and improves iron nutritional status among children and pregnant women. The combination of supplemental vitamin A and iron seems to reduce anemia more effectively than either supplemental iron or vitamin A alone. 

Scientific Evidence


According to our studies, people with diabetes tend to be deficient in vitamin A. An observational study suggests that vitamin A supplements may improve blood sugar control in people with diabetes. However, due to safety concerns, you should not supplement with vitamin A except under medical supervision. 

Menorrhagia (Heavy Menstruation)

Recent study suggests that women with heavy menstrual bleeding can benefit from taking vitamin A daily. But vitamin A cannot be recommended as an ongoing treatment for menorrhagia, since women who menstruate can become pregnant, and even fairly low doses of supplemental vitamin A may cause birth defects. 

Lower Respiratory Tract Infections

Lower respiratory tract infections include conditions like pneumonia and bronchiolitis. Young children are especially susceptible to these infections. A review of 10 trials involving over 3000 children under age 7 years found that, in the majority of cases, vitamin A did not reduce the incidence of infection or severity of symptoms. However, in two of the studies, vitamin A was beneficial for undernourished children. 

Diseases of the skin

Both natural and synthetic retinoids have been used as pharmacologic agents to treat disorders of the skin like psoriasis, acne etc. Retinoids most likely affect the transcription of skin growth factors and their receptors. Use of pharmacological doses of retinoids by pregnant women causes birth defects. 

Do high intakes of vitamin A increase the risk of osteoporosis?

Results of some prospective studies suggest that long-term intakes of preformed vitamin A in excess are associated with increased risk of osteoporotic fracture and decreased BMD (Bone mineral density) in older men and women. Only excess intakes of preformed vitamin A (retinol), not beta-carotene, were associated with adverse effects on bone health. Although these observational studies cannot provide the reason for the association between excess retinol intake and osteoporosis, limited experimental data suggest that excess retinol may stimulate bone resorption or interfere with the ability of vitamin D to maintain calcium balance. 

Pharmacologic doses of retinoids

Retinoids are used at pharmacologic doses to treat several conditions, including retinitis pigmentosa, acute promyelocytic leukemia, and various skin diseases. It is important to note that treatment with high doses of natural or synthetic retinoids overrides the body's own control mechanisms; therefore, retinoid therapies are associated with potential side effects and toxicities. Additionally, all of the retinoid compounds have been found to cause birth defects. Thus, women who have a chance of becoming pregnant should avoid treatment with these medications. Retinoids tend to be very long acting: side effects and birth defects have been reported to occur months after discontinuing retinoid therapy. 


It is thought that dosages of vitamin A above 50,000 IU per day taken for several years can cause liver injury, bone problems, fatigue, hair loss, headaches, and dry skin. Nonetheless, we do not recommend using vitamin A at doses over the upper levels, except under close physician supervision. Some people may be more likely to develop toxic symptoms than others. 

If you already have liver disease, check with your doctor before taking vitamin A supplements, because even small doses may be harmful. 

It is thought that people with diabetes may have trouble releasing vitamin A stored in the liver. This may mean that they are at greater risk for vitamin A toxicity. 

Excessive intake of vitamin A appears to accelerate liver injury in people with alcoholism. In addition, relatively high intake of vitamin A has been associated with increased risk of osteoporosis. 

Women should avoid supplementing with vitamin A during pregnancy, because at toxic levels it might increase the risk of birth defects. 

Vitamin A may increase the anticoagulant effects of warfarin (Coumadin). In addition, because vitamin A chemically resembles the drug isotretinoin (Accutane), it may amplify its toxic effects. 

Interactions You Should Know About 
If you are taking:
• Isotretinoin (Accutane): Don't take vitamin A, as the two might enhance each other's toxicity.

• Valporic acid (Depakote, Depacon, or Depakene) and you are pregnant: Do not take vitamin A supplements unless advised to do so by a physician.

• Warfarin (Coumadin): Do not take vitamin A supplements unless advised to do so by a physician. 

Selected references

1. Johnson EJ, Russell RM. Beta-Carotene. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:115-20.

2. Ross CA. Vitamin A. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:778-91.

3. Solomons NW. Vitamin A. In: Bowman B, Russell R, eds. Present Knowledge in Nutrition. 9th ed. Washington, DC: International Life Sciences Institute; 2006:157-83.

4. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc . Washington, DC: National Academy Press; 2001.

5. Tanumihardjo SA. Vitamin A: biomarkers of nutrition for development. Am J Clin Nutr 2011;94:658S-65S. [PubMed abstract]

6. Dietary Reference Intakes: The Essential Guide to Nutrient RequirementsUSDA National Nutrient Database for Standard Reference, Release 24Bailey RL, Gahche JJ, Lentino CV, Dwyer JT, Engel JS, Thomas PR, et al. Dietary supplement use in the United States, 2003-2006. J Nutr 2011;141:261-6. [PubMed abstract]

7. What We Eat in America, 2007-2008Global Prevalence of Vitamin A Deficiency in Populations at Risk 1995–2005: WHO Global Database on Vitamin A DeficiencyMayo-Wilson E, Imdad A, Herzer K, Yakoob MY, Bhutta ZA. Vitamin A supplements for preventing mortality, illness, and blindness in children aged under 5: systematic review and meta-analysis. BMJ 2011;343:d5094. [PubMed abstract]

8. Sommer A. Vitamin A deficiency and clinical disease: An historical overview. J Nutr 2008;138:1835-9. [PubMed abstract]

9. Mactier H, Weaver LT. Vitamin A and preterm infants: what we know, what we don't know, and what we need to know. Arch Dis Child Fetal Neonatal Ed 2005;90:F103-8. [PubMed abstract]

10. Darlow BA, Graham PJ. Vitamin A supplementation to prevent mortality and short and long-term morbidity in very low birthweight infants. Cochrane Database Syst Rev 2007:CD000501. [PubMed abstract]

11. Oliveira-Menegozzo JM, Bergamaschi DP, Middleton P, East CE. Vitamin A supplementation for postpartum women. Cochrane Database Syst Rev 2010:CD005944. [PubMed abstract]

12. van den Broek N, Dou L, Othman M, Neilson JP, Gates S, Gulmezoglu AM. Vitamin A supplementation during pregnancy for maternal and newborn outcomes. Cochrane Database Syst Rev 2010:CD008666. [PubMed abstract]

13. Graham-Maar RC, Schall JI, Stettler N, Zemel BS, Stallings VA. Elevated vitamin A intake and serum retinol in preadolescent children with cystic fibrosis. Am J Clin Nutr 2006;84:174-82. [PubMed abstract]

14. O'Neil C, Shevill E, Chang AB. Vitamin A supplementation for cystic fibrosis. Cochrane Database Syst Rev 2010:CD006751.pub2. [PubMed abstract]

15. Michel SH, Maqbool A, Hanna MD, Mascarenhas M. Nutrition management of pediatric patients who have cystic fibrosis. Pediatr Clin North Am 2009;56:1123-41. [PubMed abstract]

16. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and CarotenoidsPubMed abstract 


I)Vitamin A and fish oils for retinitis pigmentosa.


Rayapudi S, Schwartz SG, Wang X, Chavis P. 

BACKGROUND:v Retinitis pigmentosa (RP) comprises a group of hereditary eye diseases characterized by progressive degeneration of retinal photoreceptors. It results in severe visual loss that may lead to legal blindness. Symptoms may become manifest during childhood or adulthood, and include poor night vision (nyctalopia) and constriction of peripheral vision (visual field loss). This field loss is progressive and usually does not reduce central vision until late in the disease course.The worldwide prevalence of RP is one in 4000, with 100,000 patients affected in the USA. At this time, there is no proven therapy for RP. 


The objective of this review was to synthesize the best available evidence regarding the effectiveness and safety of vitamin A and fish oils (docosahexaenoic acid (DHA)) in preventing the progression of RP. 


We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (2013, Issue 7), Ovid MEDLINE, Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, Ovid OLDMEDLINE (January 1946 to August 2013), EMBASE (January 1980 to August 2013), Latin American and Caribbean Health Sciences Literature Database (LILACS) (January 1982 to August 2013), the metaRegister of Controlled Trials (mRCT) (www.controlled-trials.com), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. We last searched the electronic databases on 20 August 2013. 


We included randomized controlled trials (RCTs) evaluating the effectiveness of vitamin A, fish oils (DHA) or both, as a treatment for RP. We excluded cluster-randomized trials and cross-over trials. 


We reviewed 394 titles and abstracts and nine ClinicalTrials.gov records and included three RCTs that met our eligibility criteria. The three trials included a total of 866 participants aged four to 55 years with RP of all forms of genetic predisposition. One trial evaluated the effect of vitamin A alone, one trial evaluated DHA alone, and a third trial evaluated DHA and vitamin A versus vitamin A alone. None of the RCTs had protocols available, so selective reporting bias was unclear for all. In addition, one trial did not specify the method for random sequence generation, so there was an unclear risk of bias. All three trials were graded as low risk of bias for all other domains. We did not perform meta-analysis due to clinical heterogeneity of participants and interventions across the included trials.The primary outcome, mean change of visual field from baseline at one year, was not reported in any of the studies. No toxicity or adverse events were reported in these three trials. No trial reported a statistically significant benefit of vitamin supplementation on the progression of visual field loss or visual acuity loss. Two of the three trials reported statistically significant differences in ERG amplitudes among some subgroups of participants, but these results have not been replicated or substantiated by findings in any of the other trials. 


Based on the results of three RCTs, there is no clear evidence for benefit of treatment with vitamin A and/or DHA for people with RP, in terms of the mean change in visual field and ERG amplitudes at one year and the mean change in visual acuity at five years follow-up. In future RCTs, since some of the studies in this review included unplanned subgroup analysis that suggested differential effects based on previous vitamin A exposure, investigators should consider examining this issue. Future trials should take into account the changes observed in ERG amplitudes and other outcome measures from trials included in this review, in addition to previous cohort studies, when calculating sample sizes to assure adequate power to detect clinically and statistically meaningful difference between treatment arms. 

II)Effects of vitamin a on in vitro maturation of pre-pubertal mouse spermatogonial stem cells.


Travers A1, Arkoun B1, Safsaf A1, Milazzo JP1, Absyte A1, Bironneau A1, Perdrix A1, Sibert L2, Macé B1, Cauliez B3, Rives N1. 


Testicular tissue cryopreservation is the only potential option for fertility preservation in pre-pubertal boys exposed to gonadotoxic treatment. Completion of spermatogenesis after in vitro maturation is one of the future uses of harvested testicular tissue. The purpose of the current study was to evaluate the effects of vitamin A on in vitro maturation of fresh and frozen-thawed mouse pre-pubertal spermatogonial stem cells in an organ culture system. Pre-pubertal CD1 mouse fresh testes were cultured for 7 (D7), 9 (D9) and 11 (D11) days using an organ culture system. Basal medium was supplemented with different concentrations of retinol (Re) or retinoic acid (RA) alone or in combination. Seminiferous tubule morphology (tubule diameter, intra-tubular cell type), intra-tubular cell death and proliferation (PCNA antibody) and testosterone level were assessed at D7, D9 and D11. Pre-pubertal mouse testicular tissue were frozen after a soaking temperature performed at -7°C, -8°C or -9°C and after thawing, were cultured for 9 days, using the culture medium preserving the best fresh tissue functionality. Retinoic acid at 10(-6)M and retinol at 3.3.10(-7)M, as well as retinol 10(-6)M are favourable for seminiferous tubule growth, maintenance of intra-tubular cell proliferation and germ cell differentiation of fresh pre-pubertal mouse spermatogonia. Structural and functional integrity of frozen-thawed testicular tissue appeared to be well-preserved after soaking temperature at -8°C, after 9 days of organotypic culture using 10(-6)M retinol. RA and Re can control in vitro germ cell proliferation and differentiation. Re at a concentration of 10(-6)M maintains intra-tubular cell proliferation and the ability of spermatogonia to initiate spermatogenesis in fresh and frozen pre-pubertal mouse testicular tissue using a soaking temperature at -8°C. Our data suggested a possible human application for in vitro maturation of cryopreserved pre-pubertal testicular tissue. 

III)Retinoic acid inhibits pancreatic cancer cell migration and EMT through the downregulation of IL-6 in cancer associated fibroblast cells.


Guan J1, Zhang H1, Wen Z2, Gu Y1, Cheng Y1, Sun Y1, Zhang T1, Jia C1, Lu Z1, Chen J3. 


Retinoic acid (RA) is a small molecular derivative of vitamin A that is stored in quiescent stellate cells in pancreas stroma. Cancer associated fibroblasts (CAFs) are activated fibroblast cells in pancreatic ductal adenocarcinoma tumor microenvironment. We treated CAFs with RA and found that these cells became static due to the low expression of α-SMA, FAP, and IL-6 and decreased production of extracellular matrix (ECM). Furthermore, we verified that the low secretion of IL-6 from CAFs was related to RA-induced inhibition of migration and epithelial-mesenchymal transition (EMT) of tumor cells. However, RA could not inhibit the migration and EMT of tumor cells directly. Therefore, our study showed that one of the therapeutic effects of RA on tumor cells is through its modulation of CAFs in tumor microenvironment. The tumor microenvironment plays an important role in promoting tumor migration and might be a promising target of biological treatment. Copyright © 2013. Published by Elsevier Ireland Ltd. 

IV)α-Retinol and 3,4-didehydroretinol support growth in rats when fed at equimolar amounts and α-retinol is not toxic after repeated administration of large doses.


Riabroy N, Dever JT, Tanumihardjo SA. 


Dietary α-carotene is present in oranges and purple-orange carrots. Upon the central cleavage of α-carotene in the intestine, α-retinal and retinal are formed and reduced to α-retinol (αR) and retinol. Previous reports have suggested that αR has 2 % biopotency of all-trans-retinyl acetate due in part to its inability to bind to the retinol-binding protein. In the present work, we carried out three studies. Study 1 re-determined αR's biopotency compared with retinol and 3,4-didehydroretinol in a growth assay. Weanling rats (n 40) were fed a vitamin A-deficient diet for 8 weeks, divided into four treatment groups (n 10/group) and orally dosed with 50 nmol/d retinyl acetate (14•3 μg retinol), α-retinyl acetate (143 μg αR), 3,4-didehydroretinyl acetate (14•2 μg DR) or cottonseed oil (negative control). Supplementation was continued until the control rats exhibited deficiency signs 5 weeks after the start of supplementation. Body weights and AUC values for growth response revealed that αR and DR had 40-50 and 120-130 % bioactivity, respectively, compared with retinol. In study 2, the influence of αR on liver ROH storage was investigated. The rats (n 40) received 70 nmol retinyl acetate and 0, 17•5, 35 or 70 nmol α-retinyl acetate daily for 3 weeks. Although liver retinol concentrations differed among the groups, αR did not appreciably interfere with retinol storage. In study 3, the accumulation and disappearance of αR over time and potential liver pathology were determined. The rats (n 15) were fed 3•5 μmol/d α-retinyl acetate for 21 d and the groups were killed at 1-, 2- and 3-week intervals. No liver toxicity was observed. In conclusion, αR and didehydroretinol are more biopotent than previously reported at sustained equimolar dosing of 50 nmol/d, which is an amount of retinol known to keep rats in vitamin A balance.


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