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Preventing, Treating, and Reversing Chronic Disease With Nutritional Interventions
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Alexandra Lessem, Caroline Trapp
In a separate study, a portfolio diet with high intake of specific foods thought to be effective for lowering cholesterol was shown to be comparable to statin medication and superior to a low-fat diet. Cholesterol levels were compared after following a diet high in the portfolio foods (plant sterols, soy protein, almonds, and soluble fiber) or a very low-fat diet either with or without lovastatin 20 mg daily for four weeks each (Jenkins et al., 2005). At the end of the study period, LDL reductions were −8.5 ± 1.9%, −33.3 ± 1.9%, and −29.6 ± 1.3% for low-fat diet alone, low-fat diet plus lovastatin, and portfolio diet respectively (Jenkins et al., 2005). A systematic review and meta-analysis of studies combining the Portfolio Diet and the National Cholesterol Education Program (NCEP) Step II diet found the addition of the portfolio diet reduced LDL by an additional 17% as compared to the Step II diet alone (Chiavaroli et al., 2018).
Macronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
Sterols are lipid compounds containing a phenanthrene skeleton, and have 27–30 carbon atoms with a hydroxy group (alcohol) at C-3 of the first ring of phenanthrene structure and a side chain of at least seven carbons at C-17. Sterols are quite different from triglycerides and phospholipids made up of fatty acids. Sterols are abundant in nature: animals, plants and fungi (mushrooms) and comprise over 300 compounds (69, 118–119). According to their source, sterols are divided into three groups: zoosterols derived from animals, phytosterols or plant sterols, and mycosterols present in fungi. The most important animal sterol is cholesterol, while phytosterols are abundant in plants. Ergosterol is a common mycosterol found in cell membranes of fungi, yeast and protozoa. Cholesterol in humans and animals is precursor of steroid hormones, vitamin D3 and bile salts. Sterols (cholesterol, phytosterol, mycosterol) play an important role as structural components of cell membranes, and have a broad range of biological activities and physical properties (69, 118–119).
Apiaceae Plants Growing in the East
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Ethnopharmacology of Wild Plants, 2021
Sherweit El-Ahmady, Nehal Ibrahim, Nermeen Farag, Sara Gabr
Coriander seeds are particularly rich in sterols with a total sterol content ranging from 36.93 to 51.86 mg/g seed oil followed by fruits. β-sitosterol is the main sterol in coriander fruits and is especially concentrated in the pericarp where it accounts for 49.4% of total sterols. Stigmasterol is found mainly in seed oil (Sriti et al. 2009). Sterols have received considerable attention due to their inhibitory effect on dietary cholesterol absorption which can be beneficial in hyperlipidemic patients.
Simvastatin suppresses renal cell carcinoma cells by regulating DDX5/DUSP5
Published in Scandinavian Journal of Urology, 2021
Yu Qiu, Yakun Zhao, Haipng Wang, Wei Liu, Chengluo Jin, Wanhai Xu
Our results found that simvastatin exerts a strong inhibitory effect on RCC cell viability, migration, and invasion. Moreover, a low concertation of simvastatin could regulate the cell cycle and induce apoptosis; however, the underlying mechanism is unclear. Statins are specific inhibitors of the mevalonate pathway, which is responsible for the de novo synthesis of cholesterol and other, non-sterol isoprenoids. In this pathway, statins inhibit the conversion of HMG68 CoA to MVA by inhibiting the rate-limiting enzyme, HMG-CoA reductase (HMGCR) [25]. Many researches have proved that the mevalonate pathway supports tumorigenesis and is deregulated in human cancers [26]. Meanwhile, the mevalonate pathway is a source of various important biochemical compounds and plays important roles in normal physiology. Therefore, the changes in DXX5/DUSP5 might be one cellular change caused by simvastatin treatment. Considering the abnormal expression of DDX5 and DUSP5 in RCC, we explored whether simvastatin was closely related to DDX5 and DUSP5; our results revealed that simvastatin could inhibit RCC by regulating DDX5/DUSP5. Limitations of our study should also be noted. Firstly, addition of extracellular cholesterol in cell culture is able to rescue the cells from statin-induced growth inhibition. The cholesterol level in cell culture medium should be tested in this study. Secondly, the mechanism of how simvastatin regulates DDX5/DUSP5 should be explored. Further evidence, including animal experiments, is needed to determine the underlying mechanism, which will be the focus of future studies.
Evaluating the Lipid-Lowering Effects of α-lipoic Acid Supplementation: A Systematic Review
Published in Journal of Dietary Supplements, 2020
Nicole Erickson, Michelle Zafron, Scott V. Harding, Christopher P.F. Marinangeli, Todd C. Rideout
Within-study variability may be due to subject-specific factors that contribute to a heterogeneity of responses with study populations. Although genetics and other more readily identifiable subject characteristics, including body weight/composition and baseline lipids levels, have been shown to influence individual responses to a range of nutraceuticals, including dietary fiber (Ganji and Kuo 2008), omega 3 fatty acids (Lovegrove and Gitau 2008), and plant sterols (Rideout et al. 2009), we are not aware of any studies that have specifically examined metabolic and genetic determinants of blood lipids in response to α-lipoic acid supplementation. Previous work suggests that LDL-C responsiveness to cholesterol-lowering therapies such as plant sterols is greater in individuals with elevated baseline cholesterol (Abumweis, Barake, and Jones 2008). In the included studies, El-Farok et al. (El-Farok et al. 2013), the only study to specifically examine the lipid-lowering responses in hypercholesterolemic individuals, reported reductions in total and LDL-C after daily α-lipoic acid (600 mg) for two months. Although other disease states represented in our review, including obesity and type 2 diabetes, are associated with characteristic hypercholesterolemia, no clear pattern of responsiveness based on metabolic disease state was evident. Further well-controlled studies designed and powered to detect improvements in lipid profile in hypercholesterolemic individuals are warranted.
Homozygous familial hypercholesterolemia and its treatment by inclisiran
Published in Expert Opinion on Orphan Drugs, 2020
A David Marais, Dirk J Blom, Frederick J Raal
Since the measurements of PCSK9 have not been fully standardized, reports of concentrations may differ as discussed by Malo et al. in a recent review [25]. Some assays include the inactive furin-cleaved product, which may be about 15% of the mature form in hoFH. Plasma PCSK9 has a short half-life of 5 minutes. This will result in rapid adaptation of LDL receptor activity. The plasma PCSK9 concentration follows a diurnal rhythm, and responds to changes in estrogen such that postmenopausally the concentration of PCSK9 may rise and could at least partially explain the rise in plasma cholesterol concentration postmenopausally. The fasting state, resistin, thyroxin, diet, and exercise also influence the concentration of PCSK9. Apart from statins, fibrates and ezetimibe also increase PCSK9 expression. Regulation of PCSK9 synthesis occurs through a sterol response element in the promoter region of this gene. The response to cholesterol depletion in the intracellular membranes, through a finely tuned process, involves proteolysis and the production of sterol regulatory element binding protein 2 (SREBP2) which then acts on the promoter of the genes in the nucleus of the cell. In addition, there is a cooperating hepatic nuclear factor 1 site that promotes synthesis of PCSK9. PCSK9 may also be activated through the mTORC1 mechanism as indicated in Figure 1. High fructose diets may also increase plasma PCSK9 levels.