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Healthy Hair, Skin & Nails


60 VegeCaps 

  • Healthy hair, skin and nails
  • Tissue formation
  • Nutrient metabolism
  • Antioxidant support


• Healthy hair, skin and nails
• Tissue formation
• Antioxidant support

BeautyRenu is a product that is specially designed to help maintain healthy hair, skin and nails. This product includes ingredients such as Biotin, Coconut Oil and Zinc which are known to help maintain the health of your hair, skin and nails. Furthermore, silicon is also part of the formulation and helps optimize collagen production in the body which in return helps improve skin strength and elasticity. As we go on with our everyday schedule, our skin encounters free radicals from the outside environment but also from within due to chemical processes occurring inside our body. These free radicals have been proved to be harmful for the body and the skin as it may lead to early aging, Vitamin E is a powerful antioxidant to prevent damage from free radicals and it is also included in this product.


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

Biotin (250 mcg), Coconut Oil (100 mg), Iron (4 mg), Silicon (40 mg), Vitamin E (100 mg AT, 140 IU), Zinc (15 mg).

Hypromellose, magnesium stearate, microcrystalline cellulose, silicon dioxide.






60 VegeCaps

Product Type:

Biotin, Coconut, +

Cautions & Warnings:

Do not use if you are pregnant or breastfeeding. If you have cancer, consult a physician prior to use. Ensure your health care provider is aware if you are taking high dose biotin prior to any blood test. Hypersensitivity can occur; in which case discontinue use. Keep out of reach of children.

Biogenique Structurally Active-Orthogenic (SAO) technology

Vitamin E exists in eight different forms: four tocopherols (alpha-, beta-, gamma-, and delta-) and four tocotrienols (alpha-, beta-, gamma-, and delta-) Alpha-tocopherol is the most active form in human body and of greatest nutritional interest. Some of the other vitamin E molecules commonly found in food such as Beta and Gamma tocopherols and tocotrienols exert little biological activity.
Biogenique SAO technology makes vitamin E containing alpha-tocopherol from pure and natural sources. Since naturally occurring vitamin E provided by foods is easily denatured by heat, light, storage and cooking processes, SAO provides vitamin E benefits in a protected form called the "acetate ester" An ester is very stable to food storage and processing conditions. It is easily cleaved to the natural form by pancreatic esterase’s in the small intestine and absorbed into the bloodstream readily.
Our research says, Vitamin E deficiency has been observed in individuals with severe malnutrition, genetic defects affecting the alpha-tocopherol transfer protein, and fat malabsorption syndromes. People who have an impaired capacity to absorb dietary fat and therefore fat-soluble vitamins, may develop symptomatic vitamin E deficiency. 

SAO Analysis

Alpha-tocopherol function:
The main function of alpha-tocopherol in humans appears to be that of an antioxidant. Free radicals are formed primarily in the body during normal metabolism and also upon exposure to environmental factors, such as cigarette smoke or pollutants. Fats, which are an integral part of all cell membranes, are vulnerable to destruction through oxidation by free radicals. The fat-soluble vitamin, alpha-tocopherol, is uniquely suited to intercept free radicals and thus prevent a chain reaction of lipid destruction. 
Aside from maintaining the integrity of cell membranes throughout the body, alpha-tocopherol also protects the fats in low density lipoproteins (LDLs) from oxidation. Lipoproteins are particles composed of lipids and proteins that transport fats through the bloodstream. LDLs specifically transport cholesterol from the liver to the tissues of the body. Oxidized LDLs have been implicated in the development of cardiovascular diseases. 

Scientific Evidence

Cardiovascular disease

Observational studies have suggested that supplemental alpha-tocopherol might have value in the treatment of cardiovascular disease. For example, a small observational study of men who had previously undergone a coronary artery bypass surgery found those who took at least 100 IU of supplemental alpha-tocopherol daily had a reduction in the progression of coronary artery atherosclerosis measured by angiography compared to those who took less than 100 IU/day of alpha-tocopherol. A randomized, placebo-controlled intervention found that supplementing heart disease patients with either 400 IU or 800 IU of alpha-tocopherol for an average of 18 months dramatically reduced the occurrence of nonfatal heart attacks by 77%. It has been suggested that hemodialysis patients may be under increased oxidative stress and therefore may benefit from the chronic use of antioxidants (particularly for the reduction of risk of heart disease). 

Age-related macular degeneration

Like other antioxidants, vitamin E has been suggested to prevent, slow progression, or improve macular degeneration. The scientific evidence in this area is not conclusive, although there is some suggestion that vitamin E alone, or in combination with beta-carotene, may not be beneficial. 

Cancer prevention

Cancer cells proliferates rapidly and are resistant to death by apoptosis (programmed cell death). Cell culture studies indicate that the vitamin E ester, alpha-tocopherol, can inhibit proliferation and induce apoptosis in a number of cancer cell lines. The ester form alpha-tocopherol, is required to effectively inhibit proliferation or induce cancer cell death. There have been laboratory, population, and other human trials examining vitamin E and its benefits in preventing various types of cancer, including prostate, colon, or stomach cancer. Patients interested in using high-dose antioxidants such as vitamin E during chemotherapy or radiation should discuss this decision with their medical oncologist or radiation oncologist. 

Cataract prevention

Cataracts appear to be formed by protein oxidation in the lens of the eye; such oxidation may be prevented by antioxidants like alpha-tocopherol. Several observational studies have examined the association between vitamin E consumption and the incidence and severity of cataracts. Results of these studies are mixed: some report increased vitamin E intake protects against cataract development, while others report no association. 

Immune Function

Alpha-tocopherol has been shown to enhance specific aspects of the immune response that appear to decline as people age. For example, elderly adults given 200 mg/day of alpha-tocopherol for several months displayed increased formation of antibodies. A randomized, placebo-controlled trial in elderly nursing home residents reported that daily supplementation with 200 IU of alpha-tocopherol for one year significantly lowered the risk of contracting upper respiratory tract infections, especially the common cold. 

Dementia (impaired cognitive function)

The brain is particularly vulnerable to oxidative stress, which is thought to play a role in the pathology of neurodegenerative diseases like Alzheimer’s disease. Additionally, some studies have documented low levels of vitamin E in cerebrospinal fluid of patients with Alzheimer's disease. There is some evidence that alpha-tocopherol) is similar in efficacy to selegiline and superior to placebo for slowing cognitive function decline in patients with moderately severe Alzheimer's disease. Retrospective data suggest that long-term combination therapy with donepezil may help slow cognitive decline in patients with Alzheimer's disease. 

Supplementation in preterm and very low birth weight infants

Premature infants are at risk of vitamin E deficiency, particularly when they are born with very low birth weight. There are numerous studies of vitamin E given to premature infants to try to prevent potentially serious complications, such as intraventricular hemorrhage (bleeding into the brain), retinopathy (eye damage), or death. Premature infants should be under strict medical supervision. Decisions regarding vitamin supplementation should be made with the infant's physician. 

Selected references

1. Bjelakovic G, Nikolova D, Simonetti RG, et al. Antioxidant supplements for preventing gastrointestinal cancers. Cochrane Database Syst Rev 2008 Jul 16;(3):CD004183. 

2. Boshtam M, Rafiei M, Golshadi ID, et al. Long term effects of oral vitamin E supplement in type II diabetic patients. Int J Vitam Nutr Res 2005 Sep;75(5):341-6. 

3. Fillenbaum GG, Kuchibhatla MN, Hanlon JT, et al. Dementia and Alzheimer's disease in community-dwelling elders taking vitamin C and/or vitamin E. Ann Pharmacother 2005 Dec;39(12):2009-14.

4. Gao J, Gao X, Li W, et al. Observational studies on the effect of dietary antioxidants on asthma: a meta-analysis. Respirology 2008 Jun;13(4):528-36. 

5. Gaziano JM, Glynn RJ, Christen WG, et al. Vitamins E and C in the prevention of prostate and total cancer in men: the Physicians' Health Study II randomized controlled trial. JAMA 2009 Jan 7;301(1):52-62.

6. Isaac MG, Quinn R, Tabet N. Vitamin E for Alzheimer's disease and mild cognitive impairment. Cochrane Database Syst Rev 2008 Jul 16;(3):CD002854. 

7. Karlson EW, Shadick NA, Cook NR, et al. Vitamin E in the primary prevention of rheumatoid arthritis: the Women's Health Study. Arthritis Rheum 2008 Nov 15;59(11):1589-95. 

8. Lin J, Cook NR, Albert C, et al. Vitamins C and E and beta carotene supplementation and cancer risk: a randomized controlled trial. J Natl Cancer Inst 2009 Jan 7;101(1):14-23. 

9. Lee IM, Cook NR, Gaziano JM, et al. Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women's Health Study: a randomized controlled trial. JAMA 2005 Jul 6;294(1):56-65. 

10. Mayer-Davis EJ, Nichols M, Liese AD, et al. Dietary intake among youth with diabetes: the SEARCH for Diabetes in Youth Study. J Am Diet Assoc 2006 May;106(5):689-97. 

11. Orrell RW, Lane RJ, Ross M. A systematic review of antioxidant treatment for amyotrophic lateral sclerosis/motor neuron disease. Amyotroph Lateral Scler 2008 Aug;9(4):195-211. 

12. Sesso HD, Buring JE, Christen WG, et al. Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial. JAMA 2008 Nov 12;300(18):2123-33. 

13. Walsh PC. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. J Urol 2005 Nov;174(5):1823-4. 

14. Wluka AE, Stuckey S, Brand C, et al. Supplementary vitamin E does not affect the loss of cartilage volume in knee osteoarthritis: a 2 year double blind randomized placebo controlled study. J Rheumatol 2002;29(12):2585-2591.

15. You WC, Brown LM, Zhang L, et al. Randomized double-blind factorial trial of three treatments to reduce the prevalence of precancerous gastric lesions. J Natl Cancer Inst 2006 Jul 19;98(14):974-83. 

I) A history of vitamin E.


Health Research Institute, AIST, Ikeda, Japan. 


Vitamin E (α-tocopherol) was discovered nearly 100 years ago because it was required to prevent fetal resorption in pregnant, vitamin E-deficient rats fed lard-containing diets that were easily oxidizable. The human diet contains eight different vitamin E-related molecules synthesized by plants; despite the fact that all of these molecules are peroxyl radical scavengers, the human body prefers α-tocopherol. The biological activity of vitamin E is highly dependent upon regulatory mechanisms that serve to retain α-tocopherol and excrete the non-α-tocopherol forms. This preference is dependent upon the combination of the function of α-tocopherol transfer protein (α-TTP) to enrich the plasma with α-tocopherol and the metabolism of non-α-tocopherols. α-TTP is critical for human health because mutations in this protein lead to severe vitamin E deficiency characterized by neurologic abnormalities, especially ataxia and eventually death if vitamin E is not provided in large quantities to overcome the lack of α-TTP. α-Tocopherol serves as a peroxyl radical scavenger that protects polyunsaturated fatty acids in membranes and lipoproteins. Although specific pathways and specific molecular targets have been sought in a variety of studies, the most likely explanation as to why humans require vitamin E is that it is a fat-soluble antioxidant. 

II)Serum levels of vitamin E forms and risk of cognitive impairment in a Finnish cohort of older adults.


Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet , Stockholm, Sweden; Stockholm University, Sweden; Institute of Gerontology and Geriatrics, Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy. Electronic address: francesca.mangialasche@ki.se. 



Vitamin E includes eight natural antioxidant compounds (four tocopherols and four tocotrienols), but α-tocopherol has been the main focus of investigation in studies of cognitive impairment and Alzheimer's disease. 


To investigate the association between serum levels of tocopherols and tocotrienols, markers of vitamin E oxidative/nitrosative damage (α-tocopherylquinone, 5-nitro-γ-tocopherol) and incidence of cognitive impairment in a population-based study. 


A sample of 140 non-cognitively impaired elderly subjects derived from the Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study was followed-up for 8years to detect cognitive impairment, defined as development of mild cognitive impairment (MCI) or Alzheimer's dementia. The association between baseline serum vitamin E and cognitive impairment was analyzed with multiple logistic regression after adjusting for several confounders. 


The risk of cognitive impairment was lower in subjects in the middle tertile of the γ-tocopherol/cholesterol ratio than in those in the lowest tertile: the multiadjusted odds ratio (OR) with 95% confidence interval (CI) was 0.27 (0.10-0.78). Higher incidence of cognitive impairment was found in the middle [OR (95% CI): 3.41 (1.29-9.06)] and highest [OR (95% CI): 2.89 (1.05-7.97)] tertiles of the 5-NO2-γ-tocopherol/γ-tocopherol ratio. Analyses of absolute serum levels of vitamin E showed lower risk of cognitive impairment in subjects with higher levels of γ-tocopherol, β-tocotrienol, and total tocotrienols. 


Elevated levels of tocopherol and tocotrienol forms are associated with reduced risk of cognitive impairment in older adults. The association is modulated by concurrent cholesterol concentration. Various vitamin E forms might play a role in cognitive impairment, and their evaluation can provide a more accurate measure of vitamin E status in humans. 

III)Structural consequences of mutations to the α-tocopherol transfer protein associated with the neurodegenerative disease ataxia with vitamin E deficiency.


Division of Biomedical and Health Informatics, Department of Biomedical Informatics and Medical Education, University of Washington, Seattle, Washington 98195, USA. 


The α-tocopherol transfer protein (α-TTP) is a liver protein that transfers α-tocopherol (vitamin E) to very-low-density lipoproteins (VLDLs). These VLDLs are then circulated throughout the body to maintain blood α-tocopherol levels. Mutations to the α-TTP gene are associated with ataxia with vitamin E deficiency, a disease characterized by peripheral nerve degeneration. In this study, molecular dynamics simulations of the E141K and R59W disease-associated mutants were performed. The mutants displayed disruptions in and around the ligand-binding pocket. Structural analysis and ligand docking to the mutant structures predicted a decreased affinity for α-tocopherol. To determine the detailed mechanism of the mutation-related changes, we developed a new tool called ContactWalker that analyzes contact differences between mutant and wild-type proteins and highlights pathways of altered contacts within the mutant proteins. Taken together, our findings are in agreement with experiment and suggest structural explanations for the weakened ability of the mutants to bind and carry α-tocopherol. 

IV) Chronic vitamin E deficiency promotes vitamin C deficiency in zebrafish leading to degenerative myopathy and impaired swimming behavior.


Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA. 


We hypothesized that zebrafish (Danio rerio) undergoing long-term vitamin E deficiency with marginal vitamin C status would develop myopathy resulting in impaired swimming. Zebrafish were fed for 1 y a defined diet without (E-) and with (E+) vitamin E (500 mg α-tocopherol/kg diet). For the last 150 days, dietary ascorbic acid concentrations were decreased from 3500 to 50 mg/kg diet and the fish sampled periodically to assess ascorbic acid concentrations. The ascorbic acid depletion curves were faster in the E- compared with E+ fish (P < 0.0001); the estimated half-life of depletion in the E- fish was 34 days, while in it was 55 days in the E+ fish. To assess swimming behavior, zebrafish were monitored individually following a "startle-response" stimulus, using computer and video technology. Muscle histopathology was assessed using hematoxylin and eosin staining on paramedian sections of fixed zebrafish. At study end, E- fish contained 300-fold less α-tocopherol (p < 0.0001), half the ascorbic acid (p = 0.0001) and 3-fold more malondialdehyde (p = 0.0005) than did E+ fish. During the first minute following a tap stimulus (p < 0.05), E+ fish swam twice as far as did E- fish. In the E- fish, the sluggish behavior was associated with a multifocal, polyphasic, degenerative myopathy of the skeletal muscle. The myopathy severity ranged from scattered acute necrosis to widespread fibrosis and was accompanied by increased anti-hydroxynonenal staining. Thus, vitamin E deficiency in zebrafish causes increased oxidative stress and a secondary depletion of ascorbic acid, resulting in severe damage to muscle tissue and impaired muscle function. 

V) Vitamin E: a dark horse at the crossroad of cancer management Cardenas E, Ghosh R.


Department of Urology, School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. 


It appears that the story on vitamin E and its role in human health remains incomplete. It is apparent that vitamin E supplementation involves many variables, some of which include its uptake from the intestine, the preference for α-tocopherol, transport by tocopherol specific proteins and lipid transporters and the differential metabolism of different vitamin E isoforms. The fundamental differences within population genetics can have significant implications for the effect that dietary supplementation might have on human health. When evaluating the efficacy of vitamin E prophylactic or therapeutic use in previous and future studies, it is critical to consider dosage to be administered, form of vitamin E and source (such as whether from synthetic or purified from natural sources). Further studies are needed to determine the effects of all vitamin E isoforms on cell growth, tumorigenicity, to clarify its possible use as an adjuvant to existing chemotherapeutics. The Alpha-Tocopherol, Beta Carotene (ATBC) Cancer Prevention Study Group and Selenium and Vitamin E Cancer Prevention Trial (SELECT) studies along with the numerous studies of vitamin E should help guide the next chapter of vitamin E research. 

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