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The Integrative Coronary Heart Disease (CHD) Prevention Program
Published in Mark C Houston, The Truth About Heart Disease, 2023
Clinical studies in CHD and coronary artery calcification are very positive regarding vitamin K2. The Nurses Health Study (NHS) of 72,874 female nurses showed a 16% reduction in CHD from lowest to highest quintile of vitamin K1 intake. In the Health Professional Study (HPFS) of 40,087 men, there was a 13–16% reduction in CHD. In a population-based study of 4807 subjects, the incident risk for CHD was reduced by vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). Vitamin K2 MK 7 reduced CHD by 57% in upper vs lower tertile and reduced all-cause mortality by 26% in upper vs lower tertile. K2 reduced aortic calcification by 52% in upper vs lower tertile and reduced total mortality by 26%. Evidence linking vitamin K2 intakes to cardiovascular benefits started to come to light in 2004 with the landmark Rotterdam Study, which showed that high dietary intake of vitamin K2—but not vitamin K1—has a strong protective effect on cardiovascular health. Findings from this ten-year population-based study indicated that eating foods rich in natural vitamin K2 (at least 32 mcg/day) resulted in 50% reduction of arterial calcification, 50% reduction of cardiovascular risk, and 25% reduction of all-cause mortality. In 2009, these findings were confirmed by another population-based study with 16,000 subjects (ranging in age from 49 to 70) from the Prospect-EPIC cohort population. After following female participants for up to eight years, the researchers found that for every 10 mcg vitamin K2 (MK-7, MK-8, and MK-9) consumed—again, not vitamin K1—the risk of coronary heart disease was reduced by 9%.
An Overview of Molecular Nutrition
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Vincent W. Li, Catherine Ward, Delaney K. Schurr
Vitamin K1, or phytomenadione, is the most common form of vitamin K in the diet and is found mainly in green leafy vegetables. It’s most commonly known for its role in blood clotting. There is another less recognized form of vitamin K known as vitamin K2 (menaquinone) that is particularly notable for its antiangiogenic properties. In 2009, a research group in Japan found that vitamin K2 was capable of suppressing blood vessel growth and through this mechanism also suppressing colon cancer cells (Kayashima et al., 2009). Another study demonstrated this antiangiogenic effect in prostate cancer cells (Samykutty et al., 2013). Vitamin K2 is found in specific age-ripened hard cheeses like Gouda, Edam, and Müenster cheese but not in other cheeses such as feta, mozzarella, Pecorino, or Parmesan (Vermeer et al., 2018).
Personalization of Nutrition Advice
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Vitamin K2 acts in bone as a cofactor for gamma-carboxylase, which converts the glutamic acid in osteocalcin molecules to gamma-carboxyglutamic acid (Kidd 2010). It is also a transcriptional regulator of bone-specific genes that act through steroid and xenobiotic receptors to favor the expression of osteoblastic markers. Vitamin K deficiency has been shown to be a risk factor for hip fractures in the elderly, and vitamin K2 supplementation increases serum levels of osteocalcin and has a modest effect on bone mineral density.
Should vitamin K be supplemented instead of antagonised in patients with idiopathic pulmonary fibrosis?
Published in Expert Review of Respiratory Medicine, 2018
Bart De Brouwer, Ianthe Piscaer, Jan H. Von Der Thusen, Jan C Grutters, Roger EG. Schutgens, Emiel FM. Wouters, Rob Janssen
A specific shortfall in vitamin K2 could be suspected in patients with IPF based on the high prevalence of certain comorbidities. Various studies have shown that coronary artery disease is associated with IPF [44–46]. The presence of coronary artery calcification (CAC) is pathognomonic for coronary artery disease, and CAC scores are elevated in patients with IPF [45]. An observational study demonstrated that a higher consumption of vitamin K2 was associated with a lower incidence of CAC [47]. This is most likely explained by the fact that vitamin K-activated MGP can inhibit calcium salt precipitation in the coronary artery wall, thereby preventing CAC [23]. On the other hand, VKAs will induce a pronounced vitamin K deficiency; this is most likely the mechanism underlying the association between the use of VKAs and CAC [32].
The contribution of gut bacterial metabolites in the human immune signaling pathway of non-communicable diseases
Published in Gut Microbes, 2021
F. Hosseinkhani, A. Heinken, I. Thiele, P. W. Lindenburg, A. C. Harms, T. Hankemeier
Another category of bacterial metabolites that are essential for host metabolism are vitamins. Microbial fermentation and modulation are essential for acquiring vitamin B and vitamin K, as the host is not capable to perform the necessary biosynthetic reactions.40 The members of the vitamin K group are mainly vitamin K1 (phylloquinone), and vitamin K2 (menaquinone) which are absorbed in the small intestine in a bile salt-, and pancreatic dependent solubilization.117 Vitamin K1 is obtained from ingested food and is mainly found in green leafy vegetables, while vitamin K2 is synthesized by certain intestinal bacteria, especially Enterobacter spp., Eggerthella lenta, Veillonella sp. and Bacteroides sp.118,119 Deficiency of vitamin K2 has been reported in several diseases such as cardiovascular, and neurodegenerative diseases, and the bacterial flora composition is significantly altered in patients suffering from these diseases.120,121 Besides the well-known role in blood coagulation, preventing osteoporosis and cardiovascular disease, recent studies indicate the significant effect of vitamin K on the immune system. Multiple studies showed that vitamin K2 is able to suppress the lipopolysaccharide-induced expression of inflammatory cytokines such as IL-6 by inhibiting the NF-κB pathway in vitro. Pan et al.122 showed that vitamin K2 was able to dose-dependently (10–100 μM) inhibit TNF-α, IL-1 α, and IL-1 β gene expression in human monocyte-derived macrophages in vitro. Moreover, vitamin K was shown to exert a protective effect against colitis through downregulation of the pro-inflammatory cytokine IL-6 in mice fed with a vitamin K-supplemented diet.123
Vitamin K2 protects PC12 cells against Aβ (1-42) and H2O2-induced apoptosis via p38 MAP kinase pathway*
Published in Nutritional Neuroscience, 2020
Elham Hadipour, Zahra Tayarani-Najaran, Masoud Fereidoni
In addition cellular oxidation and damage in the cell function occur in many neurodegenerative diseases including AD.8 Reactive oxygen species (ROS) includes all highly active oxygen species and free radicals such as OH•, O−2, H2O2, O•2, NO, and different lipid Peroxides.9 ROS can react with membrane lipids, nucleic acids, proteins, enzymes and other small molecules leading to the cellular damages.10 The imbalance ROS production disturbs the physiologic function of the mitochondria.9 Also, the precipitation of Aβ plaques and tau protein neurofibrillary tangles in neurons increase the oxidative stress and contribute to the pathophysiology of the AD.11 In fact, oxidative stress happens by the occurrence of imbalance between the production of free radicals and antioxidant defense and fortunately, the production of free radical can be controlled by antioxidants.12 Vitamin K is a family of fat-soluble compounds with some similar structure. Naturally, vitamin K has two forms including phylloquinone (K1) and menaquinone (K2) and one industrial analog named methylnaphthoquinone (K3) which is used in cancer chemotherapy. Vitamin K2 has a bacterial origin13,14 and is made as a result of the activity of intestinal bacteria.15 Furthermore, vitamin K2 has a high concentration in the nervous system.16 Vitamin K has a ring structure, naphthoquinone with a methyl group and an aliphatic side chain at position two and three, respectively. The number of isoprenoid residues varies from four to thirteen, and all residues are unsaturated.17,18 Evidence suggests that vitamin K2 contributes to inflammatory response regulation and has the potential to interfere with oxidative damage. Recent studies indicate the protective role of vitamin K2 in mitochondria.13,14 However, the mechanism by which vitamin K2 can contribute to the regulation of inflammation and oxidative stress is unclear. Based on the given information for inducing factors of Alzheimer’s and the mentioned effects of vitamin K2, it is possible that vitamin K2 have a protective or inhibitory role in Alzheimer’s disease. So, the aim of this study was to distinguish the protective effect of vitamin K2 on toxicity and oxidative damage induced by Aβ (1-42) and H2O2 in PC12 cells as an appropriate model of cell damages in Alzheimer’s disease.