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CirculationPro

Capillary Protection & Antioxidant Support

$46.74


90 Tablets 

  • Capillary and blood vessel protection
  • Protein and fat metabolism
  • Antioxidant support
  • Cartilage and connective tissue support

 

• Capillary and blood vessel protection
• Antioxidant support
 
Blood plays a very important role in regulating the body’s system and maintain balance. It does so by supplying oxygen and nutrients, removing waste and transporting hormones and other signaling molecules throughout our body. But how does the blood travel inside the body? How does it know where to go? The answer lies with the circulatory system which include arteries, veins and capillaries that help blood to travel to the extremities of the body. Without these blood vessels the extremities of our body (finger tips, toes, and brain) would not be able to receive oxygen and other nutrients. These blood vessels are prone to damage due to increased age, high or low blood pressure and injuries. CirculationPro provides the body with quercetin, an ingredient that is found in red wine, green tea, berries, Ginkgo biloba, among other sources. Its main benefit is that it helps the protect blood vessels and capillaries, thereby making them more durable, longer lasting and less prone to damage.

 

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

Quercetin (500 mg), Vitamin C (750 mg).

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

*2X stronger than HerbalGenn Quercetin & Vitamin C 250/375 mg

 

 





Circulex

 

NPN:

80054285

Quantity:

90 Tablets 

Product Type:

Quercetin+

Cautions & Warnings:

Consult a physician prior to use if you are pregnant or breastfeeding. Keep out of reach of children.





Biogenique Structurally Active-Orthogenic (SAO) technology


Vitamin B12 has the largest and most complex chemical structure of all the vitamins. The stomach acid is required for the release of vitamin B12 from the proteins in the food and to convert it into Methylcobalamin and 5-deoxyadenosyl cobalamin forms used in the human body. Cobalamin is a compound rich with metal ion and cobalt. Biogenique SAO technology makes vitamin B12 containing the most active form of cobalamin, cyanocobalamin, having maximum vitamin B12 activity. This cyanocobalamin is readily converted to 5-deoxyadenosyl and methylcobalamin forms in the body making vitamin B12 available immediately after its consumption.

Our research says, people at risk for vitamin B12 deficiency include strict vegetarians, elderly people, breastfed infants, and people with increased vitamin B12 requirements associated with pregnancy, thyrotoxicosis, hemolytic anemia, hemorrhage, malignancy, or liver or kidney disease. Administering Biogenique vitamin B12 is effective for preventing and treating dietary vitamin B12 deficiency.

SAO Analysis - Cyanocobalamin functions


Vitamin B12 deficiency is estimated to affect 10%-15% of individuals over the age of 60. Absorption of vitamin B12 from food requires normal function of the stomach, pancreas, and small intestine. Vitamin B12 can also be absorbed by passive diffusion, but this process is very inefficient.

Biogenique vitamin B12 containing cyanocobalamin bypasses this procedure of absorption by stomach and then converting it into the forms to be utilized by the body. Thus, giving you the maximum benefit under any circumstances.

Active form – Methylcobalamin:
Methylcobalamin is co-factor for methionine synthase, an enzyme required for synthesis of methionine from homocysteine. Methionine is a methyl group donor, used in biological methylation of number of sites within DNA and RNA. Methylation of DNA is essential for cancer prevention. Inadequate function of methionine synthase can lead to an accumulation of homocysteine, which has been associated with increased risk of cardiovascular diseases. 

Active form - 5-Deoxyadenosylcobalamin:
5-Deoxyadenosylcobalamin is a co-factor for enzyme that produces Succinyl CoA. This biochemical reaction plays an important role in the production of energy from fats and proteins. Succinyl CoA is also required for the synthesis of hemoglobin, the oxygen carrying pigment in red blood cells..

Scientific Evidence


Megaloblastic anemia - due to vitamin B12 deficiency

Vitamin B12 deficiency is a cause of megaloblastic anemia, in which red blood cells are larger than normal and the ratio of nucleus size to cell cytoplasm is increased. There are other potential causes of megaloblastic anemia, including folate deficiency or various inborn metabolic disorders. Pernicious anemia is a type of megaloblastic anemia caused by vitamin B12 deficiency, and it should be treated with vitamin B12. Patients with anemia should be evaluated by a physician in order to diagnose and address the underlying cause.

Cardiovascular disease/hyperhomocysteinemia

The amount of homocysteine in the blood is regulated by at least three vitamins: folate, vitamin B12, and vitamin B6. High homocysteine levels in the blood (hyperhomocysteinemia) has been suggested as being a risk factor for cardiovascular disease, blood clotting abnormalities, atherosclerosis, myocardial infarction (heart attack), and ischemic stroke. Some evidence indicates that vitamin B12 deficiency is a major cause of elevated homocysteine levels in people over the age of 60. However, several randomized placebo-controlled trials are presently being conducted to determine whether homocysteine lowering through folic acid and other B vitamin supplementation reduces the incidence of cardiovascular diseases.

Angioplasty

Recent evidence suggests that lowering homocysteine levels with prescription-strength folic acid and vitamins B12 and B6 for six months following coronary angioplasty reduced the risk of revascularization of target lesions and overall adverse cardiac events.

Neural tube defects

Neural tube defects (NTD) may result in anencephaly or spina bifida, devastating and sometimes fatal birth defects. The defects occur between the 21st and 27th days after conception, a time when many women do not realize they are pregnant. Randomized controlled trials have demonstrated 60% to 100% reductions in NTD cases when women consumed folic acid supplements in addition to a varied diet during the month before and the month after conception. Increasing evidence indicates that the homocysteine-lowering effect of folic acid plays a critical role in lowering the risk of NTD. Homocysteine may accumulate in the blood when there is inadequate folate and/or vitamin B12 for effective functioning of the methionine synthase enzyme. Decreased vitamin B12 levels in the blood and amniotic fluid of pregnant women have been associated with an increased risk of NTD, suggesting that adequate vitamin B12 intake in addition to folic acid may be beneficial in the prevention of NTD. 

Alzheimer's disease and dementia

Some patients diagnosed with Alzheimer's disease have been found to have abnormally low vitamin B12 levels in their blood. A case-control study of 164 patients with dementia of Alzheimer's type included 76 cases in which the diagnosis of Alzheimer's disease was confirmed by examination of brain cells after death. Compared to 108 control subjects without evidence of dementia, subjects with dementia of Alzheimer's type and confirmed Alzheimer's disease had higher blood homocysteine levels and lower blood levels of folate and vitamin B12.

Breast cancer

Researchers have reported that women with breast cancer tend to have lower vitamin B12 levels in their blood serum than do women without breast cancer. Stratification of the data revealed that the inverse association between dietary vitamin B12 intake and breast cancer risk was stronger in postmenopausal women compared to premenopausal women. However, high dietary folate intakes have been associated with reduced risk for breast cancer in several studies, and some studies have reported that vitamin B12 intake may modify this association.

Circadian rhythm sleep disorders

Taking vitamin B12 by mouth, in methylcobalamin form, does not seem to be effective for treating delayed sleep phase syndrome. Supplemental methylcobalamin with bright light therapy may be helpful for adolescents with circadian rhythm sleep disorders. More research is needed in this area.

Selected references


1. Albert CM, Cook NR, Gaziano JM, et al. Effect of folic acid and B vitamins on risk of cardiovascular events and total mortality among women at high risk for cardiovascular disease: a randomized trial. JAMA. 2008 May 7; 299(17):2027-36. 

2. Andres E, Serraj K, Mecili M, Ciobanu E, Vogel T, Weitten T. Update of oral vitamin B12. Ann Endocrinol (Paris). 2009 Dec; 70(6):455-61. Epub 2009 Aug 15. 

3. Bjørke-Monsen AL, Torsvik I, Saetran H, et al. Common metabolic profile in infants indicating impaired cobalamin status responds to cobalamin supplementation. Pediatrics 2008 Jul; 122(1):83-91. 

4. Erol I, Alehan F, G;uuml;m;uuml;s A. West syndrome in an infant with vitamin B12 deficiency in the absence of macrocytic anaemia. Dev Med Child Neurol 2007 Oct; 49(10):774-6. 

5. Eussen SJ, de Groot LC, Clarke R, et al. Oral cyanocobalamine supplementation in older people with vitamin B12 deficiency: a dose-finding trial. Arch Intern Med 2005 May 23; 165(10):1167-72. 

6. Force RW, Meeker AD, Cady PS, et al. Increased vitamin B12 requirement associated with chronic acid suppression therapy. Ann Pharmacother 2003; 37:490-3. 

7. Haggarty P, McCallum H, McBain H, Effect of B vitamins and genetics on success of in-vitro fertilisation: prospective cohort study. Lancet 2006 May 6; 367(9521):1513-9. 

8. Lehman JS, Bruce AJ, Rogers RS. Atrophic glossitis from vitamin B12 deficiency: a case misdiagnosed as burning mouth disorder. J Periodontol 2006 Dec; 77(12):2090-2. 

9. Malouf R, Grimley Evans J. Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people. Cochrane Database Syst Rev 2008 Oct 8 ;( 4):CD004514. 

10. Molloy AM, Kirke PN, Brody LC, et al. Effects of folate and vitamin B12 deficiencies during pregnancy on fetal, infant, and child development. Food Nutr Bull 2008 Jun; 29(2 Suppl):S101-11; discussion S112-5. 

11. Ryan-Harshman M, Aldoori W. Vitamin B12 and health. Can Fam Physician 2008 Apr; 54(4):536-41. 

12. Seal EC, Metz J, Flicker L, et al. A randomized, double-blind, placebo-controlled study of oral vitamin B12 supplementation in older patients with subnormal or borderline serum vitamin B12 concentrations. J Am Geriatr Soc 2002; 50:146-51. 

13. Suzuki DM, Alagiakrishnan K, Masaki KH, et al. Patient acceptance of intranasal cobalamin gel for vitamin B12 replacement therapy. Hawaii Med J 2006 Nov; 65(11):311-4. 

14. Toole JF, Malinow MR, Chambless LE, et al. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial. JAMA 2004; 291:565-75. 

15. Yajnik CS, Lubree HG, Thuse NV, et al. Oral vitamin B12 supplementation reduces plasma total homocysteine concentration in women in India. Asia Pac J Clin Nutr 2007; 16(1):103-9. 

16. http://www.mayoclinic.com/health/vitamin-B12/NS_patient-vitaminb12

 




I) Vitamin B12 deficiency: The great masquerader.


Source

Department of Pediatrics, Section of Hematology/Oncology, Medical College of Wisconsin/Children's Research Institute of the Children's Hospital of Wisconsin, Milwaukee, Wisconsin. 

ABSTRACT

Vitamin B12 deficiency is rare in children, with nonspecific symptoms including failure to thrive, vomiting, anorexia, and neurologic changes with or without hematologic disturbances. The neuropathy can be severe and irreversible. We report four cases of children with B12 deficiency secondary to adult type pernicious anemia, a presumed transport protein abnormality, and a metabolic defect. All demonstrated neurologic compromise that improved after initiation of B12 therapy. Hematologic manifestations may be preceded by constitutional, gastrointestinal, or neurologic changes, and must raise concern for B12 deficiency.

II) II) High folate and low vitamin B-12 intakes during pregnancy are associated with small-for-gestational age infants in South Indian women: a prospective observational cohort study.


Source

Division of Nutrition (PD and AVK) and the Epidemiology and Biostatistics Unit (TT), St John's Research Institute, St John's National Academy of Health Sciences, Bangalore, India; Harvard College, Cambridge, MA (JRB); the Department of Obstetrics and Gynecology, St John's Medical College, St John's National Academy of Health Sciences, Bangalore, India (AT); and the Department of Pediatrics, St John's Medical College, St John's National Academy of Health Sciences, Bangalore, India (SB).

ABSTRACT

BACKGROUND: 

Folic acid supplementation in those with a low vitamin B-12 intake or status may have adverse effects. These effects are unknown with regard to birth outcome in pregnant Indian women who are routinely supplemented with high doses of folic acid.

OBJECTIVE: 

The objective was to examine the association of unbalanced vitamin B-12 and total folate (folic acid supplement + dietary folate) intakes during pregnancy with outcomes in small-for-gestational-age (SGA) infants.

DESIGN: 

This was a prospective observational cohort study of 1838 pregnant women in South India. Low intake of dietary vitamin B-12 in the presence of high total folate intake was examined as the ratio of vitamin B-12 intake to total folate intake.

RESULTS: The inadequacy of vitamin B-12 intake (

CONCLUSIONS: 

These findings suggest that vitamin B-12 and folate deficiencies may have adverse birth outcomes associated with unbalanced vitamin B-12 and folate intakes or status during pregnancy. Supplementation with vitamin B12 and folic acid in women prior to becoming pregnant or during pregnancy can be effective. 

III) Effect of Cyanocobalamine (vitamin B12) in the Induction and Expression of Morphine Tolerance and Dependence in Mice.


Source

Department of Pharmacodynamy and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, IR. Iran.

ABSTRACT

The antinociceptive effect of cyanocobalamine (Vit B12) has been reported in animal models and human studies. Our previous study showed the effect of Vit B12 on morphine tolerance. The dependence and tolerance were induced in male mice using subcutaneous morphine injections, 3 times a day (50, 50 and 75 mg/kg/day) for 3 days. Mice also received Vit B12 (100, 250 and 500 µg/kg), clonidine, memantine and saline intraperitoneally before morphine administration. On fourth day mice received only 7 mg /kg morphine just before tail-flick test. To determine the expression of morphine dependence and tolerance, all compounds were injected once intraperitoneally on the day of experiment. The tolerance was evaluated by the tail-flick test. The effect of Vit B12 and other agents on dependence were evaluated by counting the number of jumps (induced by naloxone 5 mg/kg). Co-administration of Vit B12 (100-500 µg/kg) and morphine in 3 days reduced the development of tolerance to morphine analgesic effect (8.2±0.5 and 7.83±0.5 s. vs. normal saline, 3.57±0.3 s). Repeated administration of Vit B12, also, diminished the reduced naloxane withdrawal signs of naloxone withdrawal test (100-500 µg/kg: 5±1.9 and 1.2±0.8 jumps vs. normal saline 72.6±12.2). However, Vit B12 had no effect on the expression of morphine tolerance and physical dependence. It is concluded that co-administration of Vit B12 and morphine could reduce tolerance to analgesic effect of morphine chronic administration and also reduce its withdrawal symptoms. 

IV) [Vitamins and oxidative stress].


Kodentsova VM, Vrzhesinskaia OA, Mazo VK.

Abstract

The central and local stress limiting systems, including the antioxidant defense system involved in defending the organism at the cellular and systemic levels from excess activation response to stress influence, leading to damaging effects. The development of stress, regardless of its nature [cold, increased physical activity, aging, the development of many pathologies (cardiovascular, neurodegenerative diseases, diseases of the gastrointestinal tract, ischemia, the effects of burns), immobilization, hypobaric hypoxia, hyperoxia, radiation effects etc.] leads to a deterioration of the vitamin status (vitamins E, A, C). Damaging effect on the antioxidant defense system is more pronounced compared to the stress response in animals with an isolated deficiency of vitamins C, A, E, B1 or B6 and the combined vitamins deficiency in the diet. Addition missing vitamin or vitamins restores the performance of antioxidant system. Thus, the role of vitamins in adaptation to stressors is evident. However, vitamins C, E and beta-carotene in high doses, significantly higher than the physiological needs of the organism, may be not only antioxidants, but may have also prooxidant properties. Perhaps this explains the lack of positive effects of antioxidant vitamins used in extreme doses for a long time described in some publications. There is no doubt that to justify the current optimal doses of antioxidant vitamins and other dietary antioxidants specially-designed studies, including biochemical testing of initial vitamin and antioxidant status of the organism, as well as monitoring their change over time are required.

V) Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens.


Source

Parkinson's Disease and Movement Disorders Centre, Neurology Unit, San Pio X Clinic, Fondazione Opera San Camillo, Milan, Italy. Electronic address: francesca.mancini@tin.it. 

ABSTRACT

BACKGROUND: 

Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PD patients undergoing different therapeutic regimens. 

METHODS: Three groups of consecutive PD patients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PN patients was performed. 

RESULTS: 

Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDII patients and all O-LD and ODT PN patients displayed a sub-acute sensory PN. In contrast, 29% of CLDII patients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN. 

CONCLUSION: Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases. 

VI) Biologically active vitamin B12 compounds in foods for preventing deficiency among vegetarians and elderly subjects.


Source

Watanabe F, Yabuta Y, Tanioka Y, Bito T Division of Applied Bio resources Chemistry, The United Graduate School of Agricultural Sciences, Tottori University, Tottori 680-8553, Japan. watanabe@muses.tottori-u.ac.jp 
ABSTRACT

The usual dietary sources of vitamin B12 are animal-source based foods, including meat, milk, eggs, fish, and shellfish, although a few plant-based foods such as certain types of dried lavers (nori) and mushrooms contain substantial and considerable amounts of vitamin B12, respectively. Unexpectedly, detailed characterization of vitamin B12 compounds in foods reveals the presence of various corrinoids that are inactive in humans. The majority of edible blue-green algae (cyanobacteria) and certain edible shellfish predominately contain an inactive corrinoid known as pseudovitaminB12. Various factors affect the bioactivity of vitamin B12 in foods. For example, vitamin B12 is partially degraded and loses its biological activity during cooking and storage of foods. The intrinsic factor-mediated gastrointestinal absorption system in humans has evolved to selectively absorb active vitamin B12 from naturally occurring vitamin B12 compounds, including its degradation products and inactive corrinoids that are present in daily meal foods. The objective of this review is to present up-to-date information on various factors that can affect the bioactivity of vitamin B12 in foods. To prevent vitamin B12 deficiency in high-risk populations such as vegetarians and elderly subjects, it is necessary to identify plant-source foods that contain high levels of bioactive vitamin B12 and, in conjunction, to prepare the use of crystalline vitamin B12-fortified foods. 

VII) Clinical and neurological findings of severe vitamin B12 deficiency in infancy and importance of early diagnosis and treatment.


Source

Demir N, Koc A, Ustyol L, Peker E, Abuhandan M. Department of Pediatrics, YYU School of Medicine, Istanbul, Turkey 

ABSTRACT

AIM 

Nutritional vitamin B12 deficiency among children in developing countries may lead to a severe clinical status. In this article, the clinical manifestations of vitamin B12 deficiency and the consequences of delay in its diagnosis have been evaluated. 

METHODS: A total of 41 patients who were hospitalised and treated with the diagnosis of severe vitamin B12 deficiency in the paediatric haematology department of the hospital were enrolled in the trial. The diagnosis of severe vitamin B12 deficiency was based on haematological values, a serum vitamin B12 level of

RESULTS: 

The mean age of 25 male and 16 female patients was determined as 12 (6-18 months) months. Almost all of the children had been fed with breast milk and a poor nutritional state was found in all of the mothers. Non-specific findings such as growth retardation (78%), hyperpigmentation of the skin (78%), diarrhoea (63.4%), convulsion (14.6%), weakness, reluctance to eat, vomiting, irritability and tremor were found in all the patients, in addition to hypotonia, motor retardation and pallor. Treatment with vitamin B12 provided recovery in all the patients. The mean age of the patients with full recovery was 11.7 months, while the mean age of patients with partial recovery was 12.9 months. 

CONCLUSION: As a delay in the diagnosis causes irreversible neurological damage, early diagnosis and treatment is highly important. 






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