When it comes to the common cold, just about everyone claims to have a cure or a treatment — some real, some bogus. But researchers now believe they’ve found something that works to ward off the cold and other upper respiratory infections: vitamin E.
Menstruation is a basic part of life. Many go through it without incident, but for some women, the experience can be agonizing. The pain brought by dysmenorrhea or menstrual cramps can be so severe that it prevents sufferers from functioning as they would on a normal day.
Over-the-counter pain relievers are easy to obtain, but their potential side effects make them a risky gamble. Long-term supplementation of vitamin E, says a study, makes for a natural and more wholesome alternative.
New evidence on a key nutrient offers hope to cancer patients; will the FDA snuff it out?
A new study on annatto-sourced delta-tocotrienol (one of the compounds contained in vitamin E) has shown incredible results for extending the life of ovarian cancer patients. It is a stunning finding that should be hailed as a major breakthrough, but don’t expect to hear much about it from the crony medical establishment, which does everything it can to prevent you from learning about the benefits of natural products.
I have a friend who takes large doses of vitamin E because he says the vitamin is an antioxidant that prevents cancer, heart disease, and aging? Is he right? What are antioxidants?
Triple‑negative breast cancers (TNBCs) lack the estrogen receptor, progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2). Therefore, hormone or targeted therapies are not effective in the treatment of TNBC and thus the development of novel therapeutic strategies is crucial. Methotrexate (MTX), a folate antagonist, has been used in the treatment of various types of cancer; however, the anticancer effects of MTX treatment on breast cancer have thus far been ineffective. Vitamin E variants and derivatives have been applied for cancer therapy. Previous studies have indicated that vitamin E variants and derivatives exert distinct anticancer effects on different types of cancer. However, whether MTX plus vitamin E variants or its derivatives can inhibit TNBC remains unclear. The aim of the present study was to examine the anticancer effects and mechanisms of action of MTX in combination with vitamin E variants (α‑tocopherol) and derivatives (α‑tocopherol succinate) on TNBC. In the present study, MTT assay and western blot analysis were used to determine the cell survival rates and protein levels. The results demonstrated that combination treatment with MTX and α‑tocopherol suppressed TNBC cell proliferation. In addition, various concentrations of MTX exerted distinct cytotoxic effects on α‑tocopherol succinate‑treated cells. Furthermore, high‑dose MTX enhanced α‑tocopherol succinate‑induced anticancer activity; however, low‑dose MTX inhibited α‑tocopherolsuccinate‑induced anticancer activity. The present study also demonstrated that caspase‑3 activation and poly(adenosine diphosphate‑ribose) polymerase cleavage were observed in the α‑tocopherol succinate/MTX‑treated cells. In conclusion, the findings of the present study demonstrated that high‑dose MTX enhanced anticancer activity in α‑TOS‑treated TNBC, while low‑dose MTX reduced anticancer activity in α‑TOS‑treated TNBC.
Delta tocotrienol has anti-neoplastic activity as demonstrated in several in-vitro and in-vivo investigations. The effect relies on inhibition of different pathways. It also has antiangiogenic activity, and an additive effect to bevacizumab may be expected. The present study was a phase II trial of bevacizumab combined with tocotrienol in chemotherapy refractory ovarian cancer. The study also included analysis of circulating tumor specific HOXA9 methylated DNA (HOXA9 meth-ctDNA) during treatment. The study included 23 patients. The rate of disease stabilization was 70% with very low toxicity. The median PFS was 6.9 months and the median OS 10.9 months, which is rather high compared to the current literature. A division of the patients according to level of HOXA9 meth-ctDNA already after the first cycle of chemotherapy resulted in two groups of patients with different prognoses. Patients with an increasing level of HOXA9 meth-ctDNA had a median PFS and OS of 1.4 and 4.3 months, respectively, compared to 7.8 and 12 months in the group with stable or decreasing levels. The combination of bevacizumab and tocotrienol is potent in chemotherapy refractory ovarian cancer. The level of HOXA9 meth-ctDNA after one cycle of chemotherapy holds important prognostic information.
BACKGROUND AND PURPOSE:
Atherosclerosis is characterized by chronic low-grade inflammation with concomitant lipid accumulation in the arterial wall. Anti-inflammatory and anti-atherogenic properties have been described for a novel class of endogenous nitroalkenes (nitrated-unsaturated fatty acids), formed during inflammation and digestion/absorption processes. The lipid-associated antioxidant α-tocopherol is transported systemically by LDL particles including to the atheroma lesions. To capitalize on the overlapping and complementary salutary properties of endogenous nitroalkenes and α-tocopherol, we designed and synthesized a novel nitroalkene-α-tocopherol analogue (NATOH) to address chronic inflammation and atherosclerosis, particularly at the lesion sites.
We synthesized NATOH, determined its electrophilicity and antioxidant capacity and studied its effects over pro-inflammatory and cytoprotective pathways in macrophages in vitro. Moreover, we demonstrated its incorporation into lipoproteins and tissue both in vitro and in vivo, and determined its effect on atherosclerosis and inflammatory responses in vivo using the Apo E knockout mice model.
NATOH exhibited similar antioxidant capacity to α-tocopherol and, due to the presence of the nitroalkenyl group, like endogenous nitroalkenes, it exerted electrophilic reactivity. NATOH was incorporated in vivo into the VLDL/LDL lipoproteins particles to reach the atheroma lesions. Furthermore, oral administration of NATOH down-regulated NF-κB-dependent expression of pro-inflammatory markers (including IL-1β and adhesion molecules) and ameliorated atherosclerosis in Apo E knockout mice.
CONCLUSIONS AND IMPLICATIONS:
In toto, the data demonstrate a novel pharmacological strategy for the prevention of atherosclerosis based on a creative, natural and safe drug delivery system of a non-conventional anti-inflammatory compound (NATOH) with significant potential for clinical application.
Popular alternative health expert Bryce Wylde recently told his nearly 13,000 combined Instagram and Facebook followers about the health benefits of palm-derived tocotrienols. In his lead paragraph he states, “Best supplemental sources of tocotrienols are derived from Malaysian sustainable red palm fruit oil.” Wylde describes how palm-derived tocotrienols support the brain, heart, skin, hair, liver and immune function.
Vitamin E (VE) is an indispensable vitamin in piglet feed formula. Among other things, it affects tissues including small intestine tissues and in particular its major unit intestinal epithelial cells. Previously, limited in vivo experiments have focused on the effect of VE on the intestine, particularly digestion and absorption. VE has been shown to inhibit proliferation of some types of cells. This experiment was conducted to test the hypothesis that VE affects intestinal functions by influencing the intestinal epithelial cell proliferation. Thirty 21-d old weaned [(Yorkshire × Landrace) × Duroc] piglets with BWs of 6.36 ± 0.55 kg were randomly divided into five VE-containing feeding formula groups. The treatments were (i) 0 IU (control), (ii) 16 IU, (iii) 32 IU, (iv) 4. 80 IU, and (v) 5. 160 IU. The treatments lasted 14 d. At the end of the experiment, all subjects were sacrificed to obtain blood and tissue samples. The results suggest that VE did not affect the growth performance. VE did tend to decrease jejunal crypt depth (linear, P = 0.056) and villus width (linear, P < 0.05). Sucrase activity significantly decreased in the adding 80 IU VE compared with the control (P < 0.05). Jejunal crypt, cell proliferation in 80 IU group significantly decreased compared with the control group (P < 0.05). This study suggests that dietary VE may affect intestinal morphology and functions by inhibiting weaned piglet jejunal epithelial cell proliferation.