MCT Oil

MCT Oil

June 01, 2025

 MCT Oil: Boosting Energy and HealthIn an era where health is paramount in daily life, many are keenly interested in choosing highly nutritious products that benefit the body. One popular health product today is MCT Oil, or "Medium-Chain Triglyceride Oil," a natural oil with diverse benefits, widely recognized among health-conscious and active individuals. What is MCT Oil?MCT Oil is a type of fat commonly found in foods. It's extracted from coconut oil and palm oil, with coconut oil being a particularly rich source. This oil is rapidly absorbed by the body and can be used immediately as energy, without undergoing the complex digestive processes required by other fats. Benefits of MCT OilMCT Oil is popular among those looking to boost their energy and aid in weight loss. This type of oil offers numerous benefits for the body, including enhancing energy, improving exercise performance, and helping to control fat metabolism. It provides quick energy because the fatty acids in MCT are rapidly absorbed and converted into usable energy.Studies also show that MCT Oil helps increase the body's fat burning and supports healthy weight management. Consuming MCT Oil allows the body to efficiently draw energy from fat.Another significant benefit of MCT Oil is its role in brain health. MCT Oil can help boost brain energy, especially for those on weight loss journeys or ketogenic (Keto) diets, where the body often requires more energy from fats. MCT Oil ensures the brain receives necessary energy without relying on carbohydrates.Additionally, MCT Oil aids in digestion. The fatty acids in MCT Oil stimulate the digestive system and enhance nutrient absorption, enabling the body to fully utilize the benefits of food. Using MCT Oil in Daily LifeMCT Oil can be incorporated into daily life in various ways, whether in cooking, smoothies, or taken directly. You can mix MCT Oil with coffee for an energy boost and enhanced performance in the morning. Adding MCT Oil to your favorite beverage helps ensure you get the necessary energy to start your day.For those aiming for weight loss or management, using MCT Oil in your diet can increase the body's fat-burning capacity. It helps boost fat metabolism and reduces appetite, allowing for better portion control. Choosing Quality MCT OilIf you're seeking high-quality MCT Oil, we recommend Coconut Oil Plus MCT Oil. This product combines the properties of coconut oil and MCT Oil. It's extracted from pure coconut oil and boasts high purity. This oil contains MCT fatty acids that effectively boost energy, aid in weight loss, and support brain health.High-quality MCT Oil is an excellent choice for maintaining health and helping you achieve your weight loss and energy goals effectively. Key Features of Coconut Oil Plus MCT OilExtracted from pure coconut oilContains MCT fatty acids that boost energy and fat metabolismSupports brain health and enhances body function 

Astaxanthin for eyes and skin

Astaxanthin for eyes and skin

March 24, 2025

Astaxanthin Astaxanthin is a lipid-soluble, reddish-orange pigment that belongs to a group of carotenoids called xanthophylls, which includes β-cryptoxanthin, canthaxanthin, lutein and zeaxanthin [1]. It is obtained from primary sources such as higher plants; microscopic phytoplankton algae Haematococcus pluvialis, Chlorella zofingiensis, Chlorococcum sp.; and some microorganisms, i.e., Xanthophyllomyces dendrorhous (anamorph Phaffia rhodozyma) yeasts and bacteria such as Mycobacterium lacticola, Brevibacterium, Agrobacterium aurantiacum, Alcaligens sp. strain PC-1. and Paracoccus carotinifaciens [2]. Although plants, bacteria, and microalgae can also produce astaxanthin, the chlorophyte alga Haematococcus pluvialis is considered to have the highest capacity to accumulate astaxanthin [3].The structure of astaxanthin is similar to β-carotene but it has 40 times stronger antioxidant activity since its polar ionone rings on both ends can quench free radicals and other reactive oxygen species (ROS), and the thirteen conjugated double, polyunsaturated bonds can remove high energy electrons. Its amphipathic structure with polar-nonpolar-polar characteristics allows astaxanthin to be inserted into the bilayers of cell membranes, confines lipoperoxidation promoters to penetrate across the lipid bilayer and thus reduces peroxidation-caused damages [4]. Due to astaxanthin's structural characteristics, it can pass through the blood-brain barrier to the brain and be absorbed from the small intestine into the plasma and erythrocytes, including the epidermis and dermis, and the skin [5].Numerous studies have shown that astaxanthin's exceptional antioxidant potential may be used in the prevention and treatment of diseases related to reactive oxygen species, such as Type 2 diabetes, artherosclerosis, neurodegenerative diseases, and eye diseases [2]. In addition, astaxanthin has several essential biological functions, including pigmentation, protection against ultraviolet (UV), immune response, reproductive capacity, stress tolerance, and protection against oxidation of macromolecules [3].Health Effects of AstaxanthinSkin-Protective Mechanisms Antioxidant ActivityThe aging process and cutaneous damage in humans are greatly influenced by oxidative stress. Both intrinsic (chronological) and extrinsic (photo-) aging have mechanisms that involve the generation of ROS as a result of oxidative metabolism and exposure to sun ultraviolet (UV) light, respectively. Consequently, the generation of ROS is a key factor causing skin aging. Oxidant events of skin aging involve damage to DNA, the inflammatory response, reduced production of antioxidants, and the generation of matrix metalloproteinases (MMPs) that degrade collagen and elastin in the dermal skin layer leading to the formation of wrinkles and loss of skin elasticity [3, 4]. Astaxanthin has attracted the attention of researchers, because of its potent antioxidant activity and its unique molecular and biochemical messenger properties with potential for treating and preventing skin diseases. In comparison studies exploring the photoprotective properties of carotenoids, astaxanthin was found to have a higher antioxidant capacity in human dermal fibroblasts than canthaxanthin and β-carotene. In particular, astaxanthin regulates the expression of oxidative stress-responsive enzymes such heme oxygenase-1 (HO-1), a sign of oxidative stress and a regulatory mechanism involved in the cell's defense against oxidative damage, and prevents the production of ROS. HO-1 is regulated via various stress-sensitive transcription factors, including nuclear factor erythroid 2-related factor (Nrf2), which binds to antioxidant response elements in the promoter regions of enzymes of the detoxifying metabolism. Several authors demonstrated that astaxanthin activates the Nrf2/HO-1 antioxidant pathway by generating small amounts of ROS. Consistent with these studies, observed that astaxanthin upregulated Nrf2 expression in irradiated cells. Furthermore, in the presence of astaxanthin, irradiation cells markedly increased the Nrf2-targeted proteins HO-1, superoxide dismutase 2 (SOD2), catalase (CAT), and glutathione peroxidase 1 (GPX1), as well as several other antioxidative enzymes. As a result, astaxanthin exerts strong antioxidant effects not only by directly scavenging free radicals but also by triggering the cellular antioxidant defense system via altering the Nrf2 pathway [3]. Astaxanthin may also inhibit the synthesis of lipid peroxides, so assisting in preserving the sebum content that naturally declines with age, avoiding the oxidation of sebum lipids, and reducing rough skin and the odor associated with aging [4].Anti-Inflammatory PropertiesThe mechanism by which continued oxidative stress causes chronic inflammation, which in turn mediates the majority of chronic diseases like neurodegeneration, cancer, and skin damage, has been extensively studied over the past 20 years. It is widely known that various proinflammatory markers in skin are increased as a result of UV exposure. Keratinocytes are essential in the photodamage response after UV exposure by releasing proinflammatory mediators. It has been demonstrated that astaxanthin treatment prevents the deleterious effects of UV by decreasing UV-induced reactive nitrogen species production, inflammatory cytokine expression, and apoptosis in keratinocytes. Inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2 levels were significantly reduced by astaxanthin, and it also decreased the release of prostaglandin E2 from keratinocytes after UV irradiation [3].Effects on Skin DamageCollagen, elastin, and glycosaminoglycans (GAGs) are the most significant and prevalent components of the dermal extracellular matrix (ECM). Changes in these structures are seen in both intrinsic and extrinsic aging. These alterations result in wrinkle formation, dryness, loss of tensile strength and rebound capability, and slowed wound healing. Additionally, UV-induced ROS stimulate the synthesis of MMPs that are responsible for the degradation of ECM, particularly those that may completely destroy collagen. In vitro, astaxanthin effectively suppresses cell damage caused by free radicals and induction of MMP-1 in skin after UV irradiation. Some similar studies also reported that astaxanthin inhibited the expression of MMPs in different cells, including macrophages and chondrocytes. The ECM at the wound site dramatically reorganizes during wound healing. It has been demonstrated that astaxanthin is an effective compound for accelerating wound healing in full-thickness dermal wounds in mice. Wounds treated with astaxanthin had considerably higher levels of biological indicators for wound healing like basic fibroblast growth factor (bFGF) and collagen type I α 1 (Col1A1) [3].Cardiovascular and Metabolic SyndromeAstaxanthin has three stereoisomers: (3R,3'R), (3R,3'S) and (3S,3'S). Disodium disuccinate astaxanthin (DDA), a synthetic derivative of astaxanthin composed of the three stereoisomers, has been created by Cardax Pharmaceuticals. DDA has been used predominantly in experimental myocardial ischaemia-reperfusion models. In order to determine whether prior DDA treatment was effective in lessening myocardial damage, the myocardial ischemia-reperfusion paradigm has been applied to a variety of animals, including the rat, rabbit, and dog. After four days of intravenous DDA therapy at dosages of 25, 50, and 75 mg/Kg/d, myocardial infarct size was significantly reduced in Sprague-Dawley rats. The effects were dose related, with less myocardial damage at higher doses [6].The oxidative stress biomarkers including malondialdehyde, isoprostanes, superoxide dismutase, and total antioxidant capacity were all decreased in 23 obese and overweight healthy people when astaxanthin was taken at doses of 5 and 20 mg/day. In another study, astaxanthin enhanced apolipoprotein B, oxidative stress indicators, and low-density lipoprotein cholesterol in 27 obese and overweight patients. In an uncontrolled, open-label clinical study, 17 volunteers who were at risk of developing the metabolic syndrome received astaxanthin 8 mg twice daily. Participants who received astaxanthin experienced a significant increase in adiponectin levels as well as significant decreases in HbA1c and tumor necrosis factor-alpha (TNF-α). Thus, astaxanthin shows promise at improving a range of metabolic factors that may have benefits in cardiovascular risk reduction [6].Diabetes-protective activitiesDiabetes mellitus (DM) leads to high blood sugar and is associated with oxidative stress and inflammation. Activating the NF-κB pathway, generating VEGF to prevent microvascular damage, and anti-apoptotic activity via modulation of MAPKs and PI3K/Akt pathways all contribute to the effectiveness of astaxanthin in the treatment of diabetic retinopathy and diabetic neuropathy. Furthermore, astaxanthin inhibited NF-κB translocation, transforming growth factor-beta (TGF-β) generation, inflammation, and fibrosis. In addition, due to its ability to reduce inflammation and oxidative stress through the NF-κB pathway and vasoconstriction, astaxanthin has demonstrated effectiveness in treating cardiovascular problems related to diabetes [7].Neuroprotective Activities The central nervous system (CNS) is one of the most important systems in the human body and it contains billions of neuronal and glial cells. The blood-brain barrier (BBB) is a selectively permeable barrier between capillaries and the brain that isolates the CNS from other systems of the body. This barrier is crucial for maintaining brain homeostasis and protecting the neuronal environment from harmful materials. However, the BBB occasionally prevents the transportation of therapeutic agents to the CNS for the treatment of neurological disorders. As mentioned previously, astaxanthin is a lipid-soluble that may penetrate the BBB, which is essential for the treatment of neurological diseases. There is a study found that astaxanthin accumulates in the hippocampi and cerebral cortexes of rat brains after single and repeated dietary ingestion. The accumulation of astaxanthin in the cerebral cortex may help to preserve and enhance cognitive function. Astaxanthin treatment has been shown in some studies to enhance the gene expression of proteins necessary for brain recovery, including glial fibrillary acidic protein (GFAP), microtubule associated protein 2 (MAP-2), brain-derived neurotrophic factor (BDNF) and growth-associated protein 43 (GAP-43) [1].     Enhancement of Immune FunctionThe mechanism by which astaxanthin enhances immunity has not been reported. It is hypothesized that it may be closely related to astaxanthin's antioxidant properties [8]. The immunological system of the animal is cytotoxically affected by singlet oxygen. It facilitates the production of free radicals that lead to the degradation of macrophage cell membranes, resulting in decreased phagocytic efficiency and antigen presentation capability. T lymphocytes and B lymphocytes can both be attacked by free radicals. T lymphocytes mediate cellular immunity, and the immune response depends heavily on the activation and proliferation of these cells. T cells stimulate an immune response and eliminate the antigen after being aroused by an antigen. B cells can produce antibodies like IgG, IgA, IgE, and IgM after being stimulated, which attach to antigens and remove them from the body. When these two immune cells are attacked by free radicals, the entire immune system is affected. Astaxanthin can directly scavenge oxygen-free radicals, quench singlet oxygen, stabilize the membrane structure of immune cells, and improve immunity by protecting the integrity of various immune cells [8].There is a comprehensive study to examine the action of dietary astaxanthin in regulating immune response, oxidative damage and inflammation in humans. In young, healthy females, dietary astaxanthin improved both cell-mediated and humoral immune responses. The immune markers significantly enhanced by feeding astaxanthin included T cell and B cell mitogen-induced lymphocyte proliferation, NK cell cytotoxic activity, IFN-γ and IL-6 production, and LFA-1 expression. An increase in the quantity of circulating total T and B cells was correlated with an improvement of these ex vivo immunological markers [9].Dry Eye DiseaseDry eye disease (DED) is a condition brought on by a variety of elements, including the environment, nutrition, trauma, medicines, localized inflammation, living habits, and changes in body hormone levels [10].Astaxanthin has been shown to boost local antioxidants, neutralize and scavenge oxygen free radicals, and suppress the rise of age-related oxidative stress markers like p53, p21, and p16 in a number of in vitro and in vivo cell and animal tests. Moreover, it downregulates the inflammatory factors, such as interleukin (IL)-1β, IL-6, and TNF-α, and its antioxidant and anti-inflammatory effects are dose-dependent [10].

EVIDENCE-BASED HEALTH BENEFITS OF COCONUT OIL

EVIDENCE-BASED HEALTH BENEFITS OF COCONUT OIL

March 23, 2025

EVIDENCE-BASED HEALTH BENEFITS OF COCONUT OILCoconut is one of the world's most significant tree crops, providing food and shelter to millions of people in the tropical region. Virgin coconut oil was introduced to the world at the end of twentieth century. Because of its wide range of applications in medication, food, cosmetics, and hair care products, virgin coconut oil is gaining worldwide popularity. Various methods have been employed to extract the coconut oil, but whichever method have been used it is still the best to avoid oil that has been refined, bleached or deodourized. This is because the health benefits, flavor, and scent of coconut oil are lost when it goes through these processes [1].Cold extraction and hot extraction are the two most used conventional methods of oil extraction. Low yield of oil is a challenge for these two procedures, and the heating process in the hot extraction approach reduces the antioxidant properties of the oil. The cold extraction method separates coconut oil from coconut milk without using any heat to break the emulsion. This technique has several advantages, including lower production costs because it does not require solvents or refinement operations like deodorizing and bleaching. As a result, the required amount of energy is reduced, making this procedure more environmentally friendly. Furthermore, when the coconut oil is refined, phytonutrients and polyphenols within the oil will be lost [1].Coconut oil comprises 90-95% of saturated fatty acids. Unlike long-chain fatty acids found in plant-based oil, medium-chain fatty acids are smaller in size, allowing higher cell permeability for immediate energy conversion instead of being stored as fat. Medium-chain fatty acids can also be digested more easily than long-chain fatty acids present in plant-based oil [1].At temperatures of 30°C and above, coconut oil is a colorless liquid. At a temperature of 25°C, it will solidify. Coconut oil contains of mainly saturated triglycerides, with medium chain acid which is lauric and myristic predominating. The main fatty acids in triglycerides oils are caprylic (C8) and capric (C10), which are both classed as medium-chain fatty acids, although lauric acid (C12), the main fatty acid in coconut oil, can be classified as either medium-chain fatty acids or long-chain fatty acids. Because the majority (70–75%) of lauric acid is absorbed with chylomicrons, it behaves more like a long-chain fatty acid in terms of digestion, whereas 95% of medium-chain fatty acids are absorbed directly into the portal vein. Medium-chain fatty acids are weak electrolytes and are highly ionized at neutral pH which increases their solubility. This marks the difference in solubility that occurs at chain lengths of C:10 and less, which excludes lauric acid [1]. HEALTH BENEFIT OF COCONUT OILInsulin Resistance, Inflammation, and ObesityObesity is characterized by an accumulation of adipose tissue either subcutaneously (underneath the skin) or ectopically (in and around organs). Certain fatty acids are more likely to be stored in adipose tissue rather than burned for energy when consumed. This can be measured by the fatty acid oxidation rate after fatty acid ingestion. When compared to certain long-chain saturated fats, medium-chain saturated fatty acids (C6-C12), such as lauric acid found in coconut oil, have relatively high oxidation rates [2].The overall evidence in the literature suggests that medium-chain saturated fatty acids is less likely to promote insulin resistance, inflammation, and fat storage compared to long-chain saturated fatty acids (such as stearic acid found in large quantities in butter, but particularly palmitic acid found in palm oil). While it is well known that fatty acids enter muscle tissue in order to be oxidized for ATP production used for muscle contraction, it is less commonly known that medium-chain saturated fatty acids may be directed more towards oxidation than long-chain saturated fatty acids. Thus, long-chain saturated fatty acids are more likely to be stored in muscle versus medium-chain saturated fatty acids, especially on top of a diet high in refined carbohydrates. This is why long-chain saturated fatty acids may cause greater muscle insulin resistance via increased intramyocellular lipid accumulation. Moreover, long-chain saturated fatty acids, as compared to unsaturated fats, are more readily incorporated into diacylglycerol (DAG) versus triacylglycerol (TAG), which may enhance inflammation and insulin resistance [2].In eight weeks of daily supplementation with coconut oil, Oliveira-de-Lira et al.  observed a higher adjuvant effect on weight loss and %body fat, with an emphasis on the reduction of anthropometric parameters associated with abdominal adiposity. Their findings are consistent with those reported by Assunção et al. and Cardoso et al., who reported a reduction in waist circumference that was associated with a significant increase in high-density lipoprotein cholesterol (HDL-C) after coconut oil supplementation as compared to placebo oil (a source of long-chain fatty acids) supplementation in obese women. Their findings regarding the reduction in waist circumference and conicity index reinforce the potential effects of coconut oil in causing a decrease in abdominal adiposity [3]. Coconut Oil on Blood Lipids Extra virgin coconut oil has recently been promoted as a healthy oil. Despite being high in saturated fat, the principal saturated fatty acid, lauric acid (C12), has been suggested to have different metabolic and hence health effects compared with other saturated fatty acids such as palmitic acid (C16), predominant in butter, palm oil and animal fat. In particular, it has been suggested that coconut oil does not raise total cholesterol (TC) or low density lipoprotein cholesterol (LDL-C) as much as butter [4].For a variety of reasons, the results were unexpected. Coconut oil is predominantly saturated fat which is generally held to have an adverse effect on blood lipids by increasing blood LDL-C concentrations. However, the saturated fatty acids profiles of various dietary fats differ significantly; coconut oil is predominantly (around 48%) lauric acid (C12) compared with butter (66% saturated fat) which is about 40% palmitic acid (C16) and stearic acid (C18), suggesting that coconut oil may not have the same health effects as other saturated fat-rich foods. Nevertheless, though reviews on coconut oil and cardiovascular disease risk factors have concluded that the evidence of an association between coconut oil consumption and blood lipids or cardiovascular risk was mostly poor quality, trials have generally reported that coconut oil consumption raises LDL-C in comparison to polyunsaturated oil such as safflower oil, though not as much in comparison to butter [4].Despite inconsistent findings in the literature, women who took coconut oil supplements had no negative alterations in their lipid profile. On the contrary, they experienced beneficial effects, such as an increased HDL-C levels and decreased triglycerides /HDL-C ratio as compared to the long-chain fatty acids group [3]. In addition, Nevin and Rajamohan  found that virgin coconut oil reduced total cholesterol, triglycerides, phospholoipids, low density lipoprotein (LDL), very-low-density lipoprotein (VLDL), and increased high density lipoprotein (HDL)-cholesterol levels. In vitro, LDL oxidation was reported to be prevented by the polyphenol component of virgin coconut oil [5].Other BenefitsVisna virus, Cytomegalovirus (CMV), Epstein-Barr virus, Influenza virus, Leukemia virus, Pneumonovirus, and Hepatitis C virus are all lipid-coated viruses that coconut oil is very effective against. Coconut oil's medium chain saturated fatty acids destroy these organisms by disrupting their membranes and interfering virus assembly and maturation. Monoglycerides are active against these viruses, but diglycerides and triglycerides are inactive. Lauric acid has more antiviral action than caprylic, capric, or myristic acids among the saturated fatty acids [5].Several authors have found that cold pressed oil has antimicrobial activity against Gram-positive and Gram-negative bacteria in vitro, in situ, and in vivo. Coconut oil exhibits antibacterial activity against Gram-positive and Gram-negative bacteria, according to Nevin and Rajamohan. Additionally, coconut oil has been used as a feed additive owing to its beneficial applications and health benefits such as antioxidant and anti-inflammatory activities [6].El-Abasy et al. found that coconut supplementation played a role in enhancing immune parameters and health. Furthermore, enhanced lysozyme activity with supplementation of coconut oil may indicate improved immunity in rabbits. More than 90% of the fatty acids in coconut oil are saturated and just less than 10% are unsaturated. Saturated fatty acids in coconut oil have been found to significantly enhance the innate immune responses [6].

THE ROLE OF CALCIUM AND VITAMIN D

THE ROLE OF CALCIUM AND VITAMIN D

March 22, 2025

THE ROLE OF CALCIUM AND VITAMIN DCalciumCalcium is the most abundant mineral in the body. Approximately 1.2 kg (equivalent to about 300 mmol) is contained within the human body, with 99% of this calcium being located within the bones and teeth. Calcium is also located in body fluids and soft tissues. It has two key roles: (1) supporting structural integrity; (2) regulating metabolic function. Cellular structure, intercellular and intracellular metabolism, signaling, heart muscle contractions, nerve function, enzyme activity, and normal blood clotting are all dependent on calcium. There is no functional marker of calcium status, since its role in normal blood clotting takes priority and hence plasma calcium is maintained within very narrow limits [1].The jejunum, ileum, and colon are the primary sites for calcium absorption. Uptake occurs by active transport and simple passive diffusion. Active transport is more prevalent when calcium intake is low, but when intake rises, more calcium is absorbed through non-specific routes. The metabolite of vitamin D (1,25-dihydroxycholecalciferol) stimulates calcium transport across the intestinal cells by inducing the production of a calcium-binding protein. This process occurs within the villus cells through the normal process of receptor binding, DNA interaction and messenger RNA production. Hence, vitamin D is critical for effective calcium absorption [1].Vitamin D Vitamin D refers to vitamin D2 (ergocalciferol) or vitamin D3 (cholecalciferol). Ergocalciferol is produced from irradiated fungi or yeast. Cholecalciferol is produced in skin or found naturally in fatty fish such as salmon or mackerel. Although food can be fortified with both types of vitamin D, only cholecalciferol can be produced endogenously in skin. 7-dehydrocholesterol, a substance found in the skin, is converted into previtamin D3, which isomerizes to form vitamin D3, when exposed to ultraviolet B (UVB) radiation between the wavelengths of 290 and 315 nm. The amount of vitamin D3 made in the skin can be affected by an individual's skin color, age, and use of sunscreen products, as well as the time of day, season, and latitude [2]. Once vitamin D is made in the skin (D3) or obtained in the diet (D2 or D3), it enters the circulation bound to vitamin D–binding protein. The main form of vitamin D that circulates in the body is 25-hydroxyvitamin D (25(OH)D), which is created in the liver by the hydroxylation of vitamins D2 and D3 complex. The best marker for determining vitamin D level is 25(OH)D, which reflects both endogenous and exogenous sources. To generate the physiologically active form of vitamin D, 25(OH)D undergoes hydroxylation by the 1α-hydroxylase enzyme in the kidneys to produce 1,25-dihydroxyvitamin D (1,25(OH)2D; calcitriol). 1,25(OH)2D circulates bound to vitamin D–binding protein, enters the target cell, and binds to the vitamin D receptor (VDR) in the cytoplasm, which then enters the nucleus and heterodimerizes with the retinoic acid X receptor to increase transcription of vitamin D–dependent genes important for bone metabolism, calcium absorption, and other nonclassical functions (e.g., inhibition of genes important in cancer growth) [2, 3]. The Advantage of Calcium and Vitamin DOsteoporosisOsteoporosis is defined as a metabolic bone disease characterized by low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk. According to estimates, three million people worldwide, roughly one in three women and one in twelve men aged > 50 years, will have osteoporosis at some point in their lives [1].Bone is a living tissue. Active bone formation (through the activity of osteocytes and osteoblasts) and bone resorption (involving osteoclasts) occur continuously. Osteoclasts are attracted to a quiescent bone surface and then excavate an erosion cavity. Mononuclear cells smooth off the erosion cavity, which is a subsequent site for the attraction of osteoblasts that synthesize an osteoid matrix. Continuous new bone matrix synthesis is followed by calcification of the newly-formed bone. When complete, lining cells once more overlie the trabecular surface [1]. It is well known that vitamin D promotes calcium absorption in the gut and kidney and helps to maintain adequate serum calcium concentrations to enable normal mineralization of the bone. Osteoblasts and osteoclasts need vitamin D to develop bones and repair them [4]. Bone matrix formation and bone maturation are stimulated by vitamin D. Additionally, it enhances osteoclastic activity and some evidence points to the possibility that it may influence differentiation of bone cell precursors [1]. Although vitamin D is utilized to enhance bone health, there is currently limited and conflicting evidence that vitamin D supplements alone have an impact on fracture outcomes. Thus, calcium and vitamin D work together synergistically on the bone [4]. Skeletal Benefits  Several randomized, placebo-controlled trials in both institutionalized and ambulatory elderly subjects have been shown that vitamin D with or without calcium reduced the incidence of hip and/or nonvertebral fractures by 20% to 30%. According to meta-analysis, taking vitamin D supplements along with calcium considerably lowers the risk of hip fractures (by 18%) and other nonvertebral fractures (by 12%). The majority of studies used at least 800 IU of vitamin D and the minimum 25(OH)D level of 29.7 ng/mL (74 nmol/L) was found to be effective in preventing fractures, suggesting a threshold for optimal vitamin D status [2].The Role in Cancer  There is a strong biological rationale for the association between a vitamin D deficiency and an elevated risk of cancer, as well as for the use of vitamin D or its bioactive analogues in the prevention and treatment of cancer. VDR is expressed in most cancerous tissues; in vitro cell culture studies and in vivo animal studies demonstrate that 1,25(OH)2D inhibits cell proliferation, angiogenesis, invasion and promotes differentiation and apoptosis. In cancer cells, 1,25(OH)2D/VDR stimulates TGF-β activity, activates cyclin-dependent kinase inhibitors (e.g., p21, p27), and inhibits mitogenic growth factors including IGF-1 and EGF, thus inhibiting cell proliferation and cancer growth. 1,25(OH)2D/VDR signaling has the capacity to downregulate cyclooxygenase-2, prostaglandin, and NF-kB pathways, which prevents inflammation associated with tumors. It can also suppress antiapoptotic proteins (e.g., Bcl2) and to activate proapoptotic proteins (e.g., Bax, RAK). Acting together, all these can suppress cancer growth [5].Oral HealthIt indicates that 1,25(OH)2D/VDR plays a role in maintaining the homeostasis of oral epithelium and of oral immunity. Oral keratinocytes contain VDR, which has a ligand-independent role in limiting keratinocyte proliferation. 1,25(OH)2D/VDR signaling has an even stronger inhibitory effect on keratinocytes proliferation. Studies conducted in vitro and in vivo demonstrate that vitamin D deficiency causes oral keratinocyte proliferation to increase but without any morphological or histological alterations [5].The anti-inflammatory, antimicrobial, and immunomodulating effects of the 1,25(OH)2D/VDR pathway most probably play roles in maintaining the homeostasis of oral tissues in general, thus providing some protection against the development of bacterial plaque-induced periodontal diseases. There is evidence that vitamin D deficiency or VDR polymorphism are associated with increased risk of chronic periodontitis. Therefore, administering biologically active vitamin D may be a useful addition to the standard treatment for chronic periodontitis [5].MenopauseIn post-menopausal women, estrogen loss affects calcium homeostasis in a variety of ways, including increasing bone resorption, reducing calcium absorption and increasing in urinary calcium loss. Ovariectomy does not reduce serum 1,25(OH)2D levels in rats, despite the fact that low estrogen levels seen in post-menopausal women are associated with reduced serum levels of 1,25(OH)2D. On the other hand, oophorectomy decreased 1,25(OH)2D-induced intestinal calcium absorption in young women and this was restored by estrogen repletion. Although the loss of tissue VDR levels following estrogen loss is not observed in all studies, other findings imply that the effect of estrogen loss on the intestine responsiveness to 1,25(OH)2D is caused by reduced VDR levels [6].High intakes of calcium and vitamin D have been found to be modestly associated with lower risk of early menopause. Contrarily, supplemental calcium intake was positively related with early menopause but supplemental vitamin D intake was not [7]. Side EffectsCalciumCalcium supplement users are aware of their propensity to cause gastrointestinal upset, particularly constipation. The latter can be a serious concern for frail elderly, who are already prone to this issue. There is evidence that calcium supplements increase the risk of myocardial infarction and, possibly, stroke. Studies on nephrology patients who were given calcium to bind phosphate also show an increase in mortality. As previously mentioned, calcium supplementation acutely elevates serum calcium concentration and higher serum calcium levels have been associated in cohort studies with increased risk of myocardial infarction, stroke, and mortality [8].Vitamin DMost studies of vitamin D supplements have used doses of 400–1000 IU/day. These doses have not been associated with evidence of adverse effects, and it is generally held that doses up to 2000 IU/day are safe. However, trials have shown that vitamin D 4000 IU/day, 60,000 IU/month, or 300,000–500,000 IU/year increase the risk of falls and/or fractures, and a recent 3-year study found that 4000 IU/day and 10,000 IU/day both accelerate bone loss. Use of these large doses is not justified because the threshold for vitamin D's advantages on bones is fulfilled with doses of 400–1000 IU/day. Supplemental doses above 2000 IU/day should only be used under strict control and in unusual cases [8]. ReferencesLanham-New S. Importance of calcium, vitamin D and vitamin K for osteoporosis prevention and treatment. Proceedings of the Nutrition Society. 2008 [cited 2022 November 30]; 67: 163-76. Available form: https://www.cambridge.org/core/journals/proceedings-of-the-nutrition-society/article/importance-of-calcium-vitamin-d-and-vitamin-k-for-osteoporosis-prevention-and-treatment/C30A29EDA3064CC8313079BAF4C486C6Khazai N, Judd S, Tangpricha V. Calcium and vitamin D: skeletal and extraskeletal health. Current Rheumatology Reports. 2008 [cited 2022 November 30]; 10: 1-13. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669834/Heravi A, Michos E. Vitamin D and Calcium Supplements: Helpful, Harmful, or Neutral for Cardiovascular Risk? Methodist Debakey Cardiovascular Journal. 2019 [cited 2022 November 30]; 15: 207-13. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6822648/Weaver C, Alexander D, Boushey C, Dawson-Hughes B, Lappe J, LeBoff M, et al. Calcium plus vitamin D supplementation and risk of fractures: an updated meta-analysis from the National Osteoporosis Foundation. Osteoporosis International. 2016 [cited 2022 November 29]; 27: 367-76. Available form: https://link.springer.com/article/10.1007/s00198-015-3386-5Khammissa R, Fourie J, Motswaledi M, Ballyram R, Lemmer J, Feller L. The Biological Activities of Vitamin D and Its Receptor in Relation to Calcium and Bone Homeostasis, Cancer, Immune and Cardiovascular Systems, Skin Biology, and Oral Health. BioMed Research International. 2018 [cited 2022 November 30]; 2018: 1-10. Available form: https://www.hindawi.com/journals/bmri/2018/9276380/Fleet J. The role of vitamin D in the endocrinology controlling calcium homeostasis. Molecular and Cellular Endocrinology. 2017 [cited 2022 November 30]; 453: 1-24. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5529228/Purdue-Smithe A, Whitcomb B, Szegda K, Boutot M, Manson J, Hankinson S, et al. Vitamin D and calcium intake and risk of early menopause. The American Journal of Clinical Nutrition. 2017 [cited 2022 November 30]; 105: 1493-1501. Available form: https://academic.oup.com/ajcn/article/105/6/1493/4633994?login=falseReid I, Bolland M. Calcium and/or Vitamin D Supplementation for the Prevention of Fragility Fractures: Who Needs It? Nutrients. 2020 [cited 2022 November 30]; 12: 1-9. Available form: https://www.mdpi.com/2072-6643/12/4/1011

Can Lutein Benefit Your Eye Health?

Can Lutein Benefit Your Eye Health?

March 21, 2025

Can Lutein Benefit Your Eye Health? Lutein and its isomer zeaxanthin commonly found in nature, is a lipophilic pigment belonging to the xanthophyll family of dietary carotenoids [1]. Carotenoids can be divided into carotenes, e.g., α-carotene, β-carotene, lycopene, torulene, isorenieratene, and their oxygen derivatives, xanthophylls, containing oxygen in the molecule in the form of hydroxyl, epoxy, or carbonyl groups, e.g., lutein, zeaxanthin, canthaxanthin, astaxanthin, and echinaxanthin. Xanthophylls are more polar molecules than carotenoids because they have hydroxyl groups in the carbon ring of the molecule, which allows them to absorb light with shorter wavelengths. Xanthophylls are abundant in nature, with a group of compounds showing both chemical and physicochemical similarity [2]. The most prevalent isomer in the tissues that are involved in vision (the eye and brain) is lutein. Except for the vitreous, cornea, and sclera, almost all of the human ocular structures contain lutein, zeaxanthin, and metabolites. The highest concentration of lutein and zeaxanthin in the eye is in the macula of the retina [3]. One of the most prevalent carotenoids in the human diet, lutein is frequently consumed along with zeaxanthin. Approximately 20% of all carotenoids are composed of lutein and zeaxanthin together. The richest food sources of lutein are all dark green leafy vegetables, especially kale, spinach, lettuce, and broccoli. Vegetables are a better source of these xanthophylls than fruits. The highest amount among fruits is found in nectarines, blackberries, avocados, raspberries, gooseberries, kiwi fruits, and black currants [1, 2].Relation to DiseasesAge-related Macular Degeneration (AMD)Strong evidence suggests that lutein and zeaxanthin protect against the development of Age-related Macular Degeneration (AMD), the cause of blindness in persons over 40 years of age in the United States. AMD is a condition that causes progressive vision loss and develops as a result of a complex interplay of environmental, multiple dietary and genetic factors that affect oxidative stress, inflammation, and light damage [3].There is an abundance of oxygen in the retina of the human eye. Long-chain polyunsaturated fatty acids in the retina are reduced by prolonged or repetitive exposure to light, which also causes an increase in lipid-conjugated dienes, selective photoreceptor degradation, and retinal damage. Reactive oxygen species (ROS), produced by oxidative stress and including free radicals, hydrogen peroxide, and singlet oxygen, cause cellular damage, promote the aging process in the retina, and eventually lead to the progression of AMD. For quenching these ROS and protecting retina from AMD, a particular transmembrane orientation of macular xanthophylls has been proposed. Macular xanthophylls located transversely in the lipid bi-layer of the retinal membrane are able to prevent AMD and protect the retina against peroxidation and photo-damage by acting as antioxidants that quench free radicals and ROS. Additionally, they significantly prevent blue light exposure to the photoreceptors in the fovea [4]. In addition to retinal effects, supplementation with lutein has been demonstrated to lower circulating levels of a rate-limiting enzyme of the alternative complement activation pathway that may play an important role in inflammatory response and the development of AMD [3]. Diabetic Retinopathy (DR)A third of people with diabetes are affected by Diabetic Retinopathy (DR), one of the most prevalent microvascular consequences of diabetes [5]. Diabetes causes alterations in the retina's metabolism, structure, and function because of the high glucose levels that weaken the electron transport chain system, produce superoxide, damage mitochondrial DNA, and reduce the amount of proteins that are encoded by the mitochondrial DNA [4].Carotenoids, tocopherol, and ascorbate are antioxidants that protect against ocular oxidative damage. Carotenoids have the ability to neutralize free radicals, scavenge reactive oxygen species, regulate gene expression, reduce inflammation, and prevent diabetes-related microvascular complications, including diabetic retinopathy, nephropathy, and neuropathy. Due to its potent anti-inflammatory and antioxidant properties, macular pigment (MP), which includes lutein, zeaxanthin, and mesozeaxanthin, also contributes to the protection of the retinal tissue in diabetics. It has been established that patients with type 2 diabetes have a lower level of MP as compared to healthy controls. Supplemental lutein has been shown to protect the retina against oxidative damage [4]. The protective effects of carotenoids on visual function in the diabetic state were demonstrated in a retrospective study of type 2 diabetic patients, which found that supplementing with lutein and zeaxanthin can improve retinal thickness and function as measured by optical coherence tomography (OCT) and multifocal electroretinography (mfERG) [5]. CataractCataract is one of the most common age-related eye diseases. It is thought to affect 95 million people worldwide and is a major factor in about 90% of blindness in developed countries. It is characterized by the clouding or opacification of the lens, which reduces the amount of light passing through to reach the retina and causes vision to become blurry. Although there are several contributing factors to cataracts, aging is thought to be the most common risk factor [5].The lens, which is located in the front of the eye, is constantly exposed to oxidative stress from sources including UV light. A number of antioxidant defense systems including antioxidant enzymes such as superoxide dismutase and antioxidants are utilized in the lens to protect against oxidative stress-mediated damages [5]. For many years, antioxidant properties of carotenoids have been understood. In a pioneering study, Kellogg III and Fridovich discovered that β-carotene significantly inhibits lipid peroxidation caused by xanthine oxidase. Chemical antioxidants like α-tocopherol, β-carotene, ascorbate, and glutathione (GSH) are implicated in preventing oxidative damage of the ocular tissues. According to some theories, the antioxidants lutein and zeaxanthin are continually transported from the body pool to the epithelial/cortical layer of the lens, where they scavenge ROS by enhancing the activities of GSH, catalase, and superoxide dismutase (SOD). Gao et al. (2011) reported that lutein and zeaxanthin could reduce the risk for senile cataract by protecting lens protein, lipid, and DNA from oxidative damage [4]. Dry Eye Syndrome (DES)Dry Eye Syndrome (DES) is a multifactorial disease of the tear film and ocular surface of the eye that causes decreased tear production, discomfort-related symptoms, and visual disturbances, as well as the possibility of ocular surface injury. The prevalence of various DES symptoms has increased further as a result of increased usage of light-emitting diode displays, including those found in computers, flashlights, and cell phones.The pathophysiology of DES includes loss of tear film, tear hyperosmolarity, oxidative stress, and inflammation of ocular surface that result in a vicious cycle of ocular surface damage and inflammation. Patients with dry eyes have higher levels of inflammation in their tears, which is mediated by pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and IL-8. The secretion of lacrimal glands is weakened as a result of these cytokines' inhibition of neurotransmitter release and the activity of sensory nerves on the ocular surface. The macula of the eye contains high concentrations of the xanthophyll carotenoids lutein and zeaxanthin, which absorb high-energy blue light and shield the retina from phototoxicity. These substances also function as antioxidants and scavenge free radicals. Moreover, it is known that lutein and zeaxanthin inhibit inflammatory pathways including lipopolysaccharide-induced secretion of IL-8 and hyper-osmotically induced secretion of IL-6 in corneal epithelial cells [6].   Extra-Eye Action: Cognitive Function Macular Pigment Optical Density (MPOD), considered a stable measure of lutein and zeaxanthin in neural tissues, has been associated with better global cognition, verbal learning and fluency, and processing and perceptual speed in healthy young and old people. Plasma or retinal levels of lutein and zeaxanthin have been linked to improved brain activity, white matter integrity, and neural efficiency. Interventional studies also provide support that taking supplements of lutein and/or zeaxanthin may improve cognitive function and help maintain cognitive health. The effect of lutein and zeaxanthin consumption (supplementation or dietary intervention) on cognitive functioning in healthy young and more mature adults has been studied in 13 randomized, double-blind, controlled interventional trials to date [1]. It has been found through the use of functional magnetic resonance imaging that lutein may improve cerebral perfusion or neural efficiency in older adults, and two studies have shown a relationship between MPOD and some aspects of cognitive function, such as prospective memory or verbal fluency and processing speed [7]. SafetyLutein is a very safe molecule that has been consumed in the diet at various doses for a very long time. In several toxicity studies, including developmental toxicity and dermal irritation, no adverse effects were documented in animals, including monkeys or humans [1]. While there is a lack of conclusive information on the optimal lutein supplementation dosage, numerous studies have found that lutein has a reasonably high safety profile, and the US Food and Drug Administration (FDA) has classified it as Generally Regarded as Safe (GRAS) [5].Excessive lutein consumption appears to have mild and rarely reported side effects. There is one case study reporting bilateral "foveal sparkle" in an elderly Asian woman who consumed a daily 20 mg lutein dose, which resulted in an extraordinarily high lutein level, and a high intake of dietary lutein (broccoli, kale, spinach, and avocado smoothie every morning) for a duration of 8 years. Seven months after stopping the lutein, crystals in the inner layers of the foveal region of her right eye gradually dissolved, but the crystal in her left eye persisted [5]. ReferencesGazzolo D, Picone S, Gaiero A, Bellettato M, Montrone G, Riccobene F, et al. Early Pediatric Benefit of Lutein for Maturing Eyes and Brain-An Overview. Nutrients. 2021 [cited 2023July 17]; 13: 1-26. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8468336/Mrowicka M, Mrowicki J, Kucharska E, Majsterek I. Lutein and Zeaxanthin and Their Roles in Age-Related Macular Degeneration-Neurodegenerative Disease. Nutrients. 2022 [cited 2023 July 17]; 14: 1-14. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8874683/Mares J. Lutein and Zeaxanthin Isomers in Eye Health and Disease. Annu Rev Nutr. 2016 [cited 2023 July 17]; 36: 571-602. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5611842/Johra F, Bepari A, Bristy A, Reza H. A Mechanistic Review of β-Carotene, Lutein, and Zeaxanthin in Eye Health and Disease. Antioxidants (Basel). 2020 [cited 2023 July 19]; 9: 1-21. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7692753/Li LH, Lee JC, Leung HH, Lam WC, Fu Z, Lo ACY. Lutein Supplementation for Eye Diseases. Nutrients. 2020 [cited 2023 July 19]; 12: 1-27. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352796/Muz O, Orhan C, Erten F, Tuzcu M, Ozercan I, Singh P, et al. A Novel Integrated Active Herbal Formulation Ameliorates Dry Eye Syndrome by Inhibiting Inflammation and Oxidative Stress and Enhancing Glycosylated Phosphoproteins in Rats. Pharmaceuticals (Basel). 2020 [cited 2023 July 19]; 13: 1-18. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599565/Buscemi S, Corleo D, Di Pace F, Petroni ML, Satriano A, Marchesini G. The Effect of Lutein on Eye and Extra-Eye Health. Nutrients. 2018 [cited 2023 July 19]; 10: 1-24. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6164534/

Sesame Oil: Is It Good for You?

Sesame Oil: Is It Good for You?

March 19, 2025

Sesame Oil: Is It Good for You?Sesame (Sesamum indicum L.) is one of the earliest human production and consumption oil crops in the family of Pedaliaceae, rape, soybean, and peanuts, known as China’s four major oil crops. Due to its highly aromatic odor and mellow flavor, sesame is extensively produced and well-liked. Sesame can be divided into three categories based on the color of the germplasm: white sesame, black sesame, and yellow sesame. Black and white sesame are the most prevalent and widely grown dominant species. Black sesame has strong growth ability, lodging resistance, and drought resistance, whereas white sesame has high oil content and good quality and has the largest planting area and distribution [1].Fat, protein, vitamins, minerals, and dietary fiber are all abundant in sesame seeds. Unsaturated fatty acids, fat-soluble vitamins, amino acids, and other nutrients are abundant in sesame oil, which is obtained through traditional oil production methods. Studies have found that sesame seeds contain 21.9% protein and 61.7% fat, and are rich in minerals. In addition to being rich in nutrients, sesame also contains many important functional components such as sesamin, sesamolin, sesamol, sesaminol, sesamolin phenol, and other lignan-like active ingredients. Each component of sesame has a different content depending on the extraction method and external growing conditions, e.g., hot-pressed sesame oil has a higher content of sesamol, sesamin, and total lignans than cold-pressed and refined sesame oil [1].Sesame oil is an aromatic oil extracted from sesame seeds and is a traditional product from the primary processing of sesame seeds, which can be used as edible oil. Linoleic and linolenic acids, as well as large quantities of biologically active compounds such as lignans, natural vitamin E, and phytosterols, are abundant in sesame oil. Sesame seed oil obtained by cold pressing has a high quality and nutritional content. The main unsaturated fatty acid in sesame oil is linoleic acid (46.9%), followed by oleic acid (37.4%). These fatty acids are essential fatty acids because they cannot be synthesized in the organism and must be obtained through the diet [1].Health Benefits of Sesame OilOsteoarthritis (OA) Sesame oil showed an attenuation of quadriceps muscle dysfunction in osteoarthritis (OA) rats. Lower muscle strength and muscle weakness are related to both increased interleukin (IL)-6 production and decreased citrate synthase (CS) activity in a number of animal illness models. Myosin heavy chain (MHC) typing change is one of the major causes of muscle weakness in various pathogenic situations. Lower muscular strength/muscle weakness in the quadriceps is related to decreased MHC IIa fiber in OA patients. In the present study, sesame oil effectively improved muscle dysfunction and elevated MHC IIa gene expression. It is likely that enhancing MHC IIa gene expression may be involved in sesame oil exerted attenuation of muscular dysfunction, at least partially [2].Sesame oil may improve quadriceps muscle dysfunction by inhibiting muscular oxidative stress during the initiation of OA. Increased oxidative stress in skeletal muscle is sufficient to cause muscular atrophy, according to genetic evidence. Elevated reactive oxygen species (ROS) generation can contribute to muscle dysfunction by oxidative damage, degradating contractile proteins, or activating calpain and ubiquitin proteolytic systems. Overproduction of ROS alters the fiber type and muscle function by regulating MHC gene expression. In addition, inhibiting endogenous antioxidant expression in mice results in significant loss of skeletal muscle mass and muscle weakness. In the present study, sesame oil may decrease joint pain by improving oxidative stress associated muscle dysfunction [2].Sesamin has been shown in studies to have anti-inflammatory properties. It is well recognized that TNF-α is crucial in the development of rheumatoid arthritis. Khansai et al., found that sesamin significantly reduced the mRNA expression of IL-6 and IL-1 in human primary synovial fibroblast cell lines, indicating that sesamin inhibited TNF-α-induced pro-inflammatory cytokine mRNA expression. The major sesamin metabolites found in human plasma after oral administration of sesamin are sesamin catechol conjugates. Catechol glucuronides exert anti-inflammatory effects through demyelination in macrophage-like J774.1 cells, thereby inhibiting the expression of interferon beta and inducible nitric oxide synthase. In murine macrophage-like J774.1 cells, it was found that SC1, one of CYP450's sesamin metabolites, has more potent anti-inflammatory properties than sesamin itself [1].Cardiovascular Disease and Lipid and Lipoprotein LevelsIt is generally known that lipids and lipoproteins play a causative role in cardiovascular disease (CVD). LDL-C and HDL-C are raised by dietary saturated fatty acids (SFA), which are present in milk, butter, cheese, cattle, lamb, hog, poultry, palm oil, and coconut oil. The increase in LDL-C is due to a decrease in hepatic LDL clearance and an increase in LDL production secondary to a decrease in hepatic LDL receptors. Sesame oil contains monounsaturated fatty acids (MUFA) which can decrease LDL-C by increasing hepatic LDL receptor activity [3].Not all meta-analyses, but the majority, have been unable to show that MUFA intake reduces cardiovascular events. However, one meta-analysis and the Nurses’ Health Study and Health Professionals Follow-Up Study, two very large observational studies, found that MUFA from plant sources was beneficial while MUFA from other sources was not protective from developing cardiovascular events [3].Metabolic syndromeInsulin resistance, dyslipidemia, hypertension, and abdominal obesity are all part of the metabolic syndrome, which raises the risk of type 2 diabetes and CVD. Inflammation and oxidative stress play a substantial role in the development of metabolic syndrome. Moreover, the metabolic syndrome is diagnosed by metabolic biomarkers such as increased triglycerides (TG) and decreased HDL, hypertension, obesity, insulin resistance, and elevated oxidative stress. These factors are the main causes of increase in mortality of patients with cardiovascular disease, type 2 diabetes, and strokes all over the world. Insulin sensitivity is increased by polyunsaturated fatty acids (PUFA), which have been shown to have various positive impacts on human health. Monounsaturated fatty acids (MUFA) reduce insulin resistance and TG through promoting fatty acid oxidation [4].Sesame oil is rich in MUFA, omega 6 Polyunsaturated fatty acids (PUFA) (83%-90%), such as oleic acid and linoleic acid, respectively. Sesame oil contains tocopherol, sesamin, sesamolin, polyphenols, phytosterols, flavonoids, and sesamol lignans that have anti-inflammatory and anti-mutagenic effects. Moreover, consuming this oil improves blood pressure, insulin levels, and fasting blood glucose (FBG). Vitamin B6, magnesium, calcium, copper, iron, and zinc are all found in sesame oil, which reduces blood pressure, hyperlipidemia, and lipid peroxidation by increasing enzymatic and nonenzymatic antioxidants. Sesamin, which is present in sesame oil, has anti-atherosclerotic effects that help to control blood pressure [4].The current systematic review and meta-analysis includes 12 clinical trials. They provided the evidence to show how consuming sesame oil improved metabolic biomarkers. Overall results showed sesame oil consumption significantly reduced FBG (-3.268 mg/ dl), and malondialdehyde (MDA; -4.847 mg/dl) compared to the control group. Also, HbA1C (-2.057%), systolic blood pressure (SBP; -2.679 mmHg), diastolic blood pressure (DBP; -1.981 mmHg), body weight (-0.346 kg), and body mass index (BMI; -0.385 kg/m2) were all significantly lower than baseline. However, no reduction effect was identified for insulin serum [4].ReferencesWei P, Zhao F, Wang Z, Wang Q, Chai X, Hou G, Meng Q. Sesame (Sesamum indicum L.): A Comprehensive Review of Nutritional Value, Phytochemical Composition, Health Benefits, Development of Food, and Industrial Applications. Nutrients. 2022 [cited 2023 March 10]; 14: 1-26. Available form: https://www.mdpi.com/2072-6643/14/19/4079Hsu D, Chu P, Jou I. Enteral sesame oil therapeutically relieves disease severity in rat experimental osteoarthritis. Food Nutrition Research. 2016 [cited 2023 March 14]; 60: 29807. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816814/Feingold K. The Effect of Diet on Cardiovascular Disease and Lipid and Lipoprotein Levels. Endotext [Internet]. 2021 [cited 2023 March 14]. Available form: https://www.ncbi.nlm.nih.gov/books/NBK570127/Atefi M, Entezari M, Vahedi H, Hassanzadeh A. The effects of sesame oil on metabolic biomarkers: a systematic review and meta-analysis of clinical trials. Journal of Diabetes & Metabolic Disorders. 2022 [cited 2023 March 14]; 21: 1065-80. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9167273/ 

THE POTENTIAL BENEFITS OF ZINC SUPPLEMENTS

THE POTENTIAL BENEFITS OF ZINC SUPPLEMENTS

March 18, 2025

THE POTENTIAL BENEFITS OF ZINC SUPPLEMENTSZinc is a trace element that is required for living organisms and their biological processes. Because the body cannot accumulate zinc, it is essential to take this element consistently in the diet [1].  In the human body, zinc is found in muscles (60%), bones (30%) and skin (5%). Zinc is involved in the activation of various enzymes and proteins, and it aids in the absorption of vitamins A, E, and folate. Low levels of zinc can be associated with an increased chance of developing infections and degenerative pathologies. Zinc also plays an important role in the psychosocial functioning of human behavior [2].Zinc deficiency defined by a plasmic zinc level below 60 µg/dl, exceeds the regulatory capacity of homeostatic mechanisms, clinical symptoms may arise. Zinc deficiency can occur due to inadequate intake, reduced absorption, increased losses, or increased demand. It can also occur due to genetic disorders such as Acrodermatitis enteropathica and sickle cell disease. Inadequate intakes as a result of a zinc-deficient diet or a phytate rich diet is the most common worldwide cause of zinc deficiency. Individuals most susceptible to zinc deficiency caused by inadequate intake are those with the greatest physiological demand. Due to age-related declines in absorption and poor diet, the elderly is particularly at risk [3]. Bullous-pustular dermatitis, alopecia, diarrhea, weight loss, intercurrent infections, and hypogonadism are all symptoms of severe zinc insufficiency in males. Unrecognized severe zinc deficiency is fatal. Growth retardation, delayed puberty, hypogonadism in males, rough skin, poor appetite, delayed wound healing, and abnormalities in gustation, olfaction, and night vision are all symptoms of moderate zinc deficiency. Oligospermia, weight loss, and hyperammonemia are all symptoms of mild zinc deficiency [3].THE BENEFITS OF ZINC SUPPLEMENTAcne VulgarisSince Michaelsson discovered zinc's beneficial effect on acne in a patient with acrodermatitis enteropathica, and subsequent studies demonstrated low serum zinc in acne patients, zinc has been widely used both topically and systemically for the treatment of acne vulgaris. Oral zinc sulfate is reportedly more effective in the treatment of severe acne than for the treatment of mild to moderate acne but nausea, vomiting, and diarrhea occur frequently. Oral zinc gluconate has also been reported to be effective in the treatment of inflammatory acne, but the initial loading dose is ineffective. However, acne treatment with zinc salts appears to be equal or less effective compared with systemic tetracyclines (minocycline, oxytetracycline). The exact mechanism of zinc in acne treatment remains poorly elucidated and is considered to act directly on microbial inflammatory equilibrium and facilitate antibiotic absorption when used in combination. Another mechanism for zinc's acne benefit is its antiandrogenic action, which suppresses sebum production [4].AlopeciaAndrogenetic alopecia is a prevalent condition in males over the age of 20, with an estimated 90% of males over the age of 20 experiencing some degree of frontal recession. The mainstay of treatment is minoxidil and finasteride, as well as surgical methods like hair transplantation. Zinc has been discovered to have antiandrogen properties and to alter the activities of 5𝛼-reductase types 1 and 2 [4]. ImmunityZinc is a trace element that is required for the activity of several enzymes and transcription factors in humans. It plays a key role in regulating the function of both the adaptive and the innate immune system. Dietary sources of zinc are animal products such as meat, fish, eggs, and dairy, but it is also contained in whole grains, nuts, and legumes. When compared to zinc obtained from plant products, zinc from animal sources has a higher bioavailability. Phytate, some dietary fibers, and lignin are plant ligands that chelate zinc and prevent it from being absorbed [5].Zinc’s effect on the immune system is complex; it can promote and inhibit various immunological activities to achieve a proper balance of pro and anti-inflammatory effects via a variety of methods. A correct intake of zinc is essential to limit the overproduction of inflammatory cytokines: in vitro and human studies show that zinc deficiency is associated with an increased inflammatory response and excessive release of pro inflammatory cytokines such as IL-2, IL-6, and TNF-alfa, regulated through the NF-κB signaling pathway. Zinc also enhances the number of inducible regulatory T cells. Another important role played by zinc is the maintenance of membrane barrier integrity, which is essential in the pulmonary and intestinal epithelia that constitute the first barrier to protect the organism from pathogens. Zinc supplementation has also been proven to have a direct antiviral effect on RSV, Dengue virus, and coronaviruses, as well as reducing oxidative stress and minimizing the duration of cold symptoms in adults. Lastly, some authors suggested that combining chloroquine with zinc would increase the toxicity of chloroquine against viruses [5].Zinc supplementation has also been investigated against acute lower respiratory infection. Two studies found that zinc therapy decreased infection episodes and increased recovery rates from illness and fever, however the latter study's effect was only significant in boys. Lower respiratory infection may be caused by a variety of bacteria or viruses, the nature of which was not explored in these studies. Hence it can be concluded that zinc treatment reduces the symptoms, but there is no evidence that zinc has an effect on the immune response to the underlying infections based on these findings. A pooled analysis of four trials in which continuous supplementation was investigated confirmed that zinc is efficient for the prevention of pneumonia. In this study, zinc supplementation reduced the incidence of pneumonia in children in developing countries by 41%. Pneumonia is a major cause of childhood mortality; it accounts for approximately 20% of childhood deaths in developing countries, making zinc supplementation a promising approach for a significant reduction in childhood mortality. Furthermore, a recent study suggests that zinc may be beneficial to the elderly. Zinc supplementation was found to be associated with a lower risk of pneumonia in nursing home residents, suggesting that zinc supplementation could be used to prevent pneumonia in the elderly [6].Wound HealingZinc, a trace mineral, is found to be in low concentration in tissues and across cell membranes in post-neurosurgical wound-healing patients. As such, zinc is firmly regulated through gene transcription rule, ion carriers, cellular homeostasis, and extracellular supplies. Extracellular vesicles contain a modest amount of zinc during physiological processes. Zinc is normally taken up by the zinc transporter protein (ZIP) in intracellular vesicles. The cytosol contains free zinc ions, which have been identified as secondary messengers capable of targeting proteins to regulate a variety of chemical and physiological pathways. Therefore, the availability of zinc and its regulation are essential components of cellular physiology [7].Zinc shortage has been blamed for delays in wound healing. Zinc deficiency plays a role in inflammation by increasing the inflammatory response and causing damage to the host tissue. Post-neurosurgical and severely ill patients, patients with severe burn injury, hypodermic sore, insignificant surgery, and pressure ulcers have all received zinc supplements [7].  INTERACTIONZinc–IronStudies showed that high concentrations of iron can have a negative effect on zinc absorption in human adults when zinc and iron are given in solution and on an empty stomach. It has been suggested that suppression of zinc absorption by iron occurs when given in an aqueous medium because of a competition for common nonspecific pathways. This suppression cannot occur when iron and zinc are given during a meal because zinc can be absorbed via an alternate pathway with the aid of ligands formed during protein digestion [8].Zinc–VitaminsFinally, the interaction of zinc with some vitamins (A, D, and E) is intriguing because zinc influences the vitamins' trans-porters, such as retinol-binding protein for vitamin A and tocopherol for vitamin E. The interaction between zinc and vitamin D is suggestive because zinc participates in the constitution of vitamin D (especially D3 isoform) receptor DNA binding domain through two zinc finger-like motifs, favoring the re-absorption of calcium at kidney level and phosphorus at intestinal level. As a result, the interaction of zinc and vitamin D is critical for the proper functioning of a variety of organs and tissues, including the brain and bone [8].Zinc–CalciumAlthough different mechanisms of zinc and calcium absorption in small intestine have been proposed through the binding with prostaglandin E and vitamin D, respectively, experiments in rats have however shown that calcium may interfere in intestinal zinc absorption because a competition between zinc and calcium for the same transcellular transporting carriers on the mem-brane surface occurs [8]. REFERENCESSanna A, Firinu D, Zavattari P, Valera P. Zinc Status and Autoimmunity: A Systematic Review and Meta-Analysis. Nutrients. [Internet]. 2018 [cited 2022 Feb 1]; 10: 1-17. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793296/Uwitonze AM, Ojeh N, Murererehe J, Atfi A, Razzaque MS. Zinc Adequacy Is Essential for the Maintenance of Optimal Oral Health. Nutrients. [Internet]. 2020 [cited 2022 Feb 1]; 12: 1-14. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7230687/Kogan S, Sood A, Garnick MS. Zinc and Wound Healing: A Review of Zinc Physiology and Clinical Applications. Wounds. [Internet]. 2017 [cited 2022 Feb 1]; 29: 102-6. Available form: https://www.hmpgloballearningnetwork.com/site/wounds/article/zinc-and-wound-healing-review-zinc-physiology-and-clinical-applicationsGupta M, Mahajan VK, Mehta KS, Chauhan PS. Zinc therapy in dermatology: a review. Dermatology Research and Practice. [Internet]. 2014 [cited 2022 Feb 1]; 2014: Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120804/Pecora F, Persico F, Argentiero A, Neglia C, Esposito S. The Role of Micronutrients in Support of the Immune Response against Viral Infections. Nutrients. [Internet]. 2020 [cited 2022 April 21]; 12: 1-45. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7589163/Overbeck S, Rink L, Haase H. Modulating the immune response by oral zinc supplementation: a single approach for multiple diseases. Archivum Immunologiae et Therapiae Experimentalis. [Internet]. 2008 [cited 2022 April 21]; 56: 15-30. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7079749/Adjepong D, Jahangir S, Malik B. The Effect of Zinc on Post-Neurosurgical Wound Healing: A Review. Cureus. [Internet]. 2020 [cited 2022 April 21]; 12: 1-7. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039353/Mocchegiani E, Romeo J, Malavolta M, Costarelli L, Giacconi R, Diaz LE, Marcos A. Zinc: dietary intake and impact of supplementation on immune function in elderly. Age (Dordr). [Internet]. 2013 [cited 2022 Feb 1]; 35: 839-60. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636409/

The benefits of “Ginkgo Biloba Extract”

The benefits of “Ginkgo Biloba Extract”

March 16, 2025

The benefits of “Ginkgo Biloba Extract”Ginkgo biloba is one of the oldest living species on the planet. The leaves and seeds of this plant have been used for medicinal purposes in China for centuries, initially being used for asthma and problems in the digestive system. In Europe and the USA, they have been sold since the sixties, and now they represent one of the most popular phytotherapeutic products in the world [1].In the early 1970s, Dr. Willmar Schwabe Pharmaceuticals (Karlsruhe, Germany) effectively developed a method for the extraction and standardization of ginkgo biloba extract preparation and produced highly concentrated and stable extract from ginkgo biloba leaves. The standardized extract of ginkgo biloba leaves contains 6% terpenoids (in which 3.1% are ginkgolides A, B, C, and J and 2.9% is bilobalide), 24% flavonoid glycosides (containing quercetin, kaempferol, isorhamnetin etc.), and 5–10% organic acids [2].The active compounds for ginkgo biloba extract is flavonoids and terpenoids. The content of flavonoids promotes blood circulation, especially cerebral blood circulation. Therefore, it is used in disorders such as Alzheimer’s disease and memory loss that are caused by decreased blood flow. In addition, the extract also has antioxidant [3] and neuroprotective properties [2]. Ginkgo Biloba Extracts PropertiesDementia and Alzheimer’s diseaseThe rapid aging of the global population is resulting in an increasing prevalence of mild cognitive impairment, dementia, and Alzheimer's disease. Age is a key risk factor for these diseases; after the age of 65 years, the prevalence of dementia doubles every five years. It is higher among women than men, largely because women tend to live longer [4].There are studies performed that the positive effect of ginkgo biloba extract has been reported on Alzheimer’s disease, memory enhancement, dementia of vascular origin, and cognitive disorders. The extract modifies the cerebral blood flow and may help to reduce fatigue and inattention [2]. But some studies of ginkgo biloba extract have not been demonstrated to prevent the progression of dementia. However, several studies showed that ginkgo biloba extract encourage efficacy in terms of improvement in cognition, behavior, and ability to maintain activities of daily living in patients with dementia or Alzheimer's disease, as well as reducing caregiver burden [4]. Age-related macular degeneration (AMD)Age-related macular degeneration (AMD) is a condition affecting the central area of the retina (the back of the eye). The retina can deteriorate with age and some people get lesions that lead to loss of central vision. Vascular factors and oxidative damage are two potential mechanisms in the pathology of the disease. Ginkgo biloba extract contains two constituents (flavonoids and terpenoids) which have antioxidant properties. It is believed these may help to slow down the progression of AMD through several mechanisms of action including increased blood flow, inhibiting platelet-activating factor, and prevention of membrane damage caused by free radicals[5]. GlaucomaGlaucoma is the leading cause of irreversible visual impairment and blindness. Although the mechanism of glaucoma is still largely unknown, oxidative stress, optic nerve ischemia, and neuroinflammation were found to be a certain role in the development of glaucomatous optic nerve degeneration. It has been suggested that ginkgo biloba extract may protect tissue against free radical damage like other antioxidants such as vitamin C and E. However, unlike the others, the extract acts at the level of organelles by stabilizing the mitochondria due to abnormal mitochondrial changes can lead to glaucoma [6].   Ginkgo biloba extract was also found to have vasodilatory properties that could improve coronary and peripheral circulation that could improve blood viscosity [6]. Moreover, it was associated with positive effects on the improvement of deteriorated visual field in patients with open-angle glaucoma [7]. Due to its antioxidant, vasoregulatory, and anti-inflammatory benefits, ginkgo biloba extract is considered a neuroprotective agent and improve the vision of people with glaucoma [6].Oxidative stressOxidative stress is caused by destructive and progressive modifications in one or more body tissues, leading to dysfunction of organs, premature aging, and sometimes disease and death. Stress exposure, radiation, infections, and smoke exposure cause significant damage, inducing alterations in DNA, can lead to several oxidative disorders such as cardiovascular diseases and cancer. It is possible that the usage of ginkgo biloba extract may delay this process [1].Ginkgo biloba extract has antioxidant properties since it regulates the expression of antioxidant enzymes positively and reduces reactive oxygen and nitrogen species. It also exhibits anti-inflammatory properties, inhibits the expression of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α so it minimizes the risk factors for diseases that are caused by the oxidative stress process [1].Warnings, Interactions, and Adverse Effects of Ginkgo Biloba ExtractThe most important clinical problem with ginkgo biloba is caused by its inhibition of the platelet-activating factor, so the use of ginkgo in conjunction with warfarin, aspirin, or other antiplatelet agents should be consulted with a specialist. Ginkgo biloba is generally well tolerated, with side effects being rare, usually mild, and including nausea, vomiting, diarrhea, headaches, dizziness, palpitations, restlessness, weakness, or skin rashes. Although no studies have been performed to support any restrictions on the use of ginkgo during pregnancy or lactation, it seems careful not to administer ginkgo in the absence of any data[8]. ReferencesAchete de Souza G, de Marqui SV, Matias JN, Guiguer EL, Barbalho SM. Effects of Ginkgo biloba on Diseases Related to Oxidative Stress. Planta Medica. [Internet]. 2020 [cited 2022 Jan 6]; 86: 376-86. Available from: https://www.thieme-connect.com/products/ejournals/abstract/10.1055/a-1109-3405Singh SK, Srivastav S, Castellani RJ, Plascencia-Villa G, Perry G. Neuroprotective and Antioxidant Effect of Ginkgo Biloba Extract Against AD and Other Neurological Disorders. Neurotherapeutics. [Internet]. 2019 [cited 2022 Jan 6]; 16: 666-74. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6694352/Sellami M, Slimeni O, Pokrywka A, Kuvačić G, D Hayes L, Milic M, Padulo J. Herbal medicine for sports: a review. Journal of the International Society of Sports Nutrition. [Internet]. 2018 [cited 2022 Jan 6]; 15: 1-14. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5856322/Kandiah N, Ong PA, Yuda T, Ng LL, Mamun K, Merchant RA, et al. Treatment of dementia and mild cognitive impairment with or without cerebrovascular disease: Expert consensus on the use of Ginkgo biloba extract, EGb 761®. CNS Neuroscience & Therapeutics. [Internet]. 2018 [cited 2022 Jan 6]; 25: 288-98. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488894/Evans J. Ginkgo biloba extract for age-related macular degeneration (Review). Cochrane Database of Systematic Reviews. [Internet]. 2013 [cited 2022 Jan 7]; 1-15. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061350/Ige M, Liu J. Herbal Medicines in Glaucoma Treatment. Yale Journal of Biology and Medicine. [Internet]. 2020 [cited 2022 Jan 7]; 93: 347-53. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7309662/Bungau S, Abdel-Daim MM, Tit DM, Ghanem E, Sato S, Maruyama-Inoue M, et al. Health Benefits of Polyphenols and Carotenoids in Age-Related Eye Diseases (Review). Oxidative Medicine and Cellular Longevity. [Internet]. 2019 [cited 2022 Jan 7]; 1-22. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390265/Sierpina VS, Wollschlaeger B, Blumenthal M. Ginkgo Biloba. Complementary and Alternative Medicine. [Internet]. 2003 [cited 2022 Jan 7]; 68: 923-6. Available from: https://www.aafp.org/afp/2003/0901/p923.html

Pomegranate extract

Pomegranate extract

March 14, 2025

POMEGRANATE EXTRACTThe pomegranate (Punica granatum L.), belonging to Punica L. genus, Punicaceae family, is an ancient fruit native to Central Asia in regions spanning from Iran and Turkmenistan to northern India as well as in the Mediterranean area and the Middle East. Pomegranate and its components have been shown in studies conducted over the last several decades to have potent anti-oxidative and anti-inflammatory capabilities. In addition to in vivo and in vitro studies showed that pomegranate exhibits anti-hypertensive and anti-proliferative properties [1].Pomegranate fruit is abundant in flavonoids, proanthocyanidins, and natural polyphenols. It is frequently used as nutritional food, for medicinal purposes, health promotion, and strong anti-oxidant action. As pomegranate seeds include vitamin C, vitamin K, folic acid, and bioactive chemicals rich in polyphenols, they have been shown to scavenge reactive oxygen species (ROS). Furthermore, the pomegranate fruit peel was estimated to primarily contain 25 - 28% of the polyphenols with gallic acid and tannins for scavenging ROS, while the pomegranate fruit pericarp mainly contains potent bioactive compounds, such as gallagic, ellagic acid, ellagitannins, punicalagin, anthocyanins delphinidin, pelargonidin, and luteolin [2]. The Benefits of Pomegranate ExtractVasculoprotective Effects  The presence of hydrolyzable tannins (ellagitannins and gallotannins), pomegranate derivative ellagic acid, or their common metabolites urolithins was hypothesized to be the reason for the protective benefits [1].In hypertensive patients, daily consumption of pomegranate juice for 2 weeks reduced the activity of angiotensin-converting enzyme (ACE) by 36% as well as diminished systolic blood pressure by 5%. The group also reported that patients with carotid artery stenosis significantly decreased their blood pressure, low-density lipoprotein (LDL) oxidation, and common carotid intima-media thickness by consuming pomegranate juice over 3 years. In a cohort of 51 healthy women, pomegranate juice drinking for four weeks significantly lowered blood pressure (without significantly changing serum ACE activity). A subsequent study involving 21 hypertensive patients revealed that pomegranate juice consumption effectively lowered both systolic and diastolic blood pressure [1]. Inflammatory DiseaseConsuming pomegranates has a generally positive effect on patients with chronic inflammatory disorders. In patients with hypertension or metabolic syndrome, as well as those undergoing dialysis, pomegranate juice appears to offer promising hypotensive properties. It also resulted in a slight amelioration of lipid profiles in patients with cardiovascular disease (CVD), as pomegranate intake elevated endogenous levels of high-density lipoprotein (HDL) cholesterol and reduced triglyceride (TG) levels. However, several studies have been unable to confirm pomegranate’s TG and cholesterol lowering effect. With regards to risk factors for CVD, one dose of 150 mL of pomegranate juice per day did not influence the level of circulating soluble adhesion molecules or indicators of atherosclerosis and subclinical coronary heart disease (CHD) in hypertensive people. Long-term consumption (100 mL per day for a year) or a higher intake of juice (500 mL per day) were both used to demonstrate the beneficial effects of pomegranate on CVD [3].Several groups have studied the effects of pomegranate on the prevention and amelioration of atherosclerosis and other CVD symptoms. In a rat model of the metabolic syndrome, de Nigris et al. (2007) found that supplementation with pomegranate juice or pomegranate fruit extract decreased the expression of vascular inflammatory markers and transforming growth factor β-1 (TGFβ-1), and, likewise, elevated endothelial nitric oxide synthase (eNOS) levels. Additionally, Labsi et al. (2016) demonstrated that Swiss albino mice treated intraperitoneally with pomegranate peel extract for two months after the induction of echinococcosis significantly reduced the nitric oxide (NO) and TNF-α levels [3].Anti-oxidantReactive oxygen species (ROS) are a by-product of the natural metabolism of oxygen in mammalian bodies, and are neutralized by the anti-oxidant system. Increased ROS production due to exposure to toxic chemicals and xenobiotics leads to an imbalance between the production of ROS and their elimination by anti-oxidant systems. The increased ROS attack cell membranes and damage biomolecules such as proteins and DNA [4].Natural anti-oxidants found in pomegranates, such as anthocyanins, catechins, quercetin, gallotannins, ellagitannins, ellagic, ferulic, and gallic acid, are abundant and show promise as anti-oxidants. The most prevalent polyphenols in the peel are ellagitannins (punicalagin and its derivatives), which are known for their strong anti-oxidant properties [4].Pomegranate is a rich source of polyphenols and several studies have shown the beneficial role of both pomegranate and its bioactives on reducing oxidative stress and lipid peroxidation through the direct neutralization of ROS, upregulating anti-oxidant enzymes, and modulating transcription factors such as nuclear factor κB (NF-κB) or peroxisome proliferator-activated receptor g (PPARg), among others. The primary bioactive components of pomegranate fruit extract that support skin health are ellagic acid and punicalagin, which have anti-oxidant and anti-inflammatory properties as well as the ability to inhibit the tyrosinase enzyme. Additionally, pomegranate extract stimulates type I procollagen synthesis and inhibits MMP-1 (collagenase) production by dermal fibroblasts [5].As confirmed by the reduced histopathological damage, the pomegranate-peel extract meaningfully restored the liver markers. This is consistent with the results in, where the authors revealed that pomegranate’s anti-oxidant properties could reduce oxidative-stress-induced liver injury. It has been discovered that pomegranate phenolic compounds contain anti-oxidant and free-radical-scavenging characteristics, and they also considerably enhanced the kidney weight to body weight ratio [4].  ReferencesWang D, Özen C, Abu-Reidah I, Chigurupati S, Patra J, Horbanczuk J, et al. Vasculoprotective Effects of Pomegranate (Punica granatum L.). Frontiers in Pharmacology. 2018 [cited 2022 November 24]; 9: 1-15. Available form: https://www.frontiersin.org/articles/10.3389/fphar.2018.00544/full#B108Singh M, Lee K, Vinayagam R, Kang S. Antioxidant and Antibacterial Profiling of Pomegranate-pericarp Extract Functionalized-zinc Oxide Nanocomposite. Biotechnology and Bioprocess Engineering. 2021 [cited 2022 November 29]; 26: 728-37. Available form: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8548265/Danesi F, Ferguson L. Could Pomegranate Juice Help in the Control of Inflammatory Diseases? Nutrients. 2017 [cited 2022 December 6]; 9: 1-23. Available form: https://www.mdpi.com/2072-6643/9/9/958Sayed S, Alotaibi S, El-Shehawi A, Hassan M, Shukry M, Alkafafy M, et al. The Anti-Inflammatory, Anti-Apoptotic, and Antioxidant Effects of a Pomegranate-Peel Extract against Acrylamide-Induced Hepatotoxicity in Rats. Life (Basel). 2022 [cited 2022 December 6]; 12: 1-16. Available form: https://www.mdpi.com/2075-1729/12/2/224Quiles J, Cabrera M, Jones J, Tsapekos M, Caturla N. In Vitro Determination of the Skin Anti-Aging Potential of Four-Component Plant-Based Ingredient. Molecules. 2022 [cited 2022 December 6]; 27: 1-23. Available form: https://www.mdpi.com/1420-3049/27/22/8101