Carnosine, leg wellness & cellulite
Carnosine is one of the most important and most widely used anti-ageing actives. It is widely researched for it's action against glycation. Glycation is the main cause of collagen damage (caused by sugar consumption) and thereby skin ageing, blood vessel wall damage and also a major contributor to the formation of cellulite. For all those reasons, carnosine is of great importance as active ingredient in anti-ageing, anti-cellulite, leg wellness, skin firming and under-eye creams.
CARNOSINE CELLULITE CREAMS, BY Celluence®
The carnosine used for the Celluence® cellulite creams is of the highest quality, of >95% purity and in a highly bioavailable form for enhanced absorption by the skin. We are proud to feature high quality, highly purified carnosine in our formulations, together with multiple other natural active ingredients, for maximum synergy and effectiveness. No other cellulite creams offer ALL the important anti-cellulite / leg wellness ingredients, in one package (learn how our creams differ from any other cellulite formulation).
Carnosine: Papers & articles
(Disclaimer: please note that the information and the research presented on this page is for informational purposes only and does not constitute efficacy claims for the Celluence® creams, neither does it constitute or aim to replace medical advice)
Glycation: the silent assassin of youth
Glycation refers to the damage of proteins, lipids and DNA/RNA by sugars and by high temperature cooking.
Increased consumption of sugars, especially fructose, sucrose/sugar, and high fructose corn syrup, as well as high temperature cooking, leads to the creation of advanced glycation end products (AGEs).
AGEs cause widespread damage to all tissues of the body, from blood vessels to skin to organs, by increasing inflammation, oxidative damage and collagen cross linking.
Skin is particularly prone to glycation damage, with loss of elasticity and firmness and an unhealthy grey complexion usually indicating damage by AGEs. Glycation is also an important cause of cellulite.
According to the authors of this review, "elevated circulating AGEs are associated with increased risk of developing many chronic diseases that disproportionally affect older individuals".
Fighting glycation on all fronts
Following a diet high in vegetables, herbs and spices (with the exception of chilli), avoiding high temperature grilling and frying and avoiding sugary foods, are the best things you can do to avoid glycation damage on your skin, blood vessels and other tissues.
Chlorogenic acid (found in green coffee), carnosine (found in meat) and quercetin (found in citrus fruits) are the most well-known natural compounds that can fight glycation.
All three natural chemicals can also be used topically in the form of anti-ageing / anti-cellulite creams.
Drugs that aim to inhibit or break AGEs are also being developed. Existing drugs known to fight glycation include aminoguanidine (pimagedine) and alagebrium chloride (ALT-711), with neither of them being commercially available.
- Paper: Does accumulation of advanced glycation end products contribute to the aging phenotype?
- Abstract: BACKGROUND: Aging is a complex multifactorial process characterized by accumulation of deleterious changes in cells and tissues, progressive deterioration of structural integrity and physiological function across multiple organ systems, and increased risk of death. METHODS: We conducted a review of the scientific literature on the relationship of advanced glycation end products (AGEs) with aging. AGEs are a heterogeneous group of bioactive molecules that are formed by the nonenzymatic glycation of proteins, lipids, and nucleic acids. RESULTS: Humans are exposed to AGEs produced in the body, especially in individuals with abnormal glucose metabolism, and AGEs ingested in foods. AGEs cause widespread damage to tissues through upregulation of inflammation and cross-linking of collagen and other proteins. AGEs have been shown to adversely affect virtually all cells, tissues, and organ systems. Recent epidemiological studies demonstrate that elevated circulating AGEs are associated with increased risk of developing many chronic diseases that disproportionally affect older individuals. CONCLUSIONS: Based on these data, we propose that accumulation of AGEs accelerate the multisystem functional decline that occurs with aging, and therefore contribute to the aging phenotype. Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers. Modification of intake and circulating levels of AGEs may be a possible strategy to promote health in old age, especially because most Western foods are processed at high temperature and are rich in AGEs.
- Comment: In a paper about how obesity affects tendons published today, a group of Italian and Spanish scientists state that advanced glycation end products (AGEs), caused by the consumption of sugar-laden foods, can potentially affect tendons
- This is because AGEs are known to damage the structure and functionality of collagen fibres in tendons, ligaments and skin, along with chronic, sub-clinical low grade inflammation, which also typically accompanies chronic sugar consumption, overweight/obesity and pre-diabetic metabolic syndrome states.
- In these cases, the scientists advise low impact exercise, but we would also add sugar avoidance (most important) and also supplementation with carnosine, which is known to prevent the formation of AGEs in the body.
- Source: How Obesity Affects Tendons?
- Abstract: Several epidemiological and clinical observations have definitely demonstrated that obesity has harmful effects on tendons. The pathogenesis of tendon damage is multi-factorial. In addition to overload, attributable to the increased body weight, which significantly affects load-bearing tendons, systemic factors play a relevant role. Several bioactive peptides (chemerin, leptin, adiponectin and others) are released by adipocytes, and influence tendon structure by means of negative activities on mesenchymal cells. The ensuing systemic state of chronic, sub-clinic, low-grade inflammation can damage tendon structure. Metabolic disorders (diabetes, impaired glucose tolerance, and dislipidemia), frequently associated with visceral adiposity, are concurrent pathogenetic factors. Indeed, high glucose levels increase the formation of Advanced Glycation End-products, which in turn form stable covalent cross-links within collagen fibers, modifying their structure and functionality. Sport activities, so useful for preventing important cardiovascular complications, may be detrimental for tendons if they are submitted to intense acute or chronic overload. Therefore, two caution rules are mandatory: first, to engage in personalized soft training program, and secondly to follow regular check-up for tendon pathology.
- Abstract: L-carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities.
- Abstract: Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.
- Abstract: Skin beautification with oral non-hydrolized versions of carnosine and carcinine: Effective therapeutic management and cosmetic skincare solutions against oxidative glycation and free-radical production as a causal mechanism of diabetic complications and skin aging.
- Abstract: Advanced glycation Maillard reaction end products (AGEs) are causing the complications of diabetes and skin aging, primarily via adventitious and cross-linking of proteins. Long-lived proteins such as structural collagen are particularly implicated as pathogenic targets of AGE processes. The formation of α-dicarbonyl compounds represents an important step for cross-linking proteins in the glycation or Maillard reaction. The purpose of this study was to investigate the contribution of glycation coupled to the glycation free-radical oxidation reactions as markers of protein damage in the aging of skin tissue proteins and diabetes. To elucidate the mechanism for the cross-linking reaction, we studied the reaction between a three-carbon α-dicarbonyl compound, methylglyoxal, and amino acids using EPR spectroscopy, a spectrophotometric kinetic assay of superoxide anion production at the site of glycation and a chemiluminescence technique. The transglycating activity, inhibition of transition metal ions peroxidative catalysts, resistance to hydrolysis of carnosine mimetic peptide-based compounds with carnosinase and the protective effects of carnosine, carcinine and related compounds against the oxidative damage of proteins and lipid membranes were assessed in a number of biochemical and model systems. A 4-month randomized, double-blind, controlled study was undertaken including 42 subjects where the oral supplement of non-hydrolized carnosine (Can-C Plus® formulation) was tested against placebo for 3 months followed by a 1-month supplement-free period for both groups to assess lasting effects. Assessment of the age-related skin parameters and oral treatment efficacy measurements included objective skin surface evaluation with Visioscan® VC 98 and visual assessment of skin appearance parameters. The results together confirm that a direct one-electron transfer between a Schiff base methylglyoxal dialkylimine (or its protonated form) and methylglyoxal is responsible for the generation of the cross-linked radical cation and the radical counteranion of methylglyoxal. Under aerobic conditions, molecular oxygen can then accept an electron from the methylglyoxal anion to generate the superoxide radical anion causing the propagation of oxidative stress chain reactions in the presence of transition metal ions. Carnosine stabilized from enzymatic hydrolysis, carcinine and leucyl-histidylhydrazide in patented formulations thereof, demonstrate the Schiff bases' transglycating activities concomitant with glycation site specific antioxidant activities and protection of proprietary antioxidant enzymes in the skin during aging and with diabetes lesions. During oral supplementation with stabilized from enzymatic hydrolysis carnosine (Can-C Plus® formulation), the skin parameters investigated showed a continuous and significant improvement in the active group during the 3 months of supplementation as compared to placebo. Visual investigation showed improvement of the overall skin appearance and a reduction of fine lines. No treatment-related side effects were reported. The finding that already-formed AGE cross-links can be pharmacologically severed and attendant pathology thereby reversed by non-hydrolized carnosine or carcinine in patented oral formulations thereof has broad implications for the skin beautification and therapeutics of the complications of diabetes and skin diseases associated with aging
- Source: The Possible Mechanism of Advanced Glycation End Products (AGEs) for Alzheimer's Disease.
- Abstract: Amyloid precursor protein (APP) has been modified by β and γ-secretase that cause amyloid deposits (plaques) in neuronal cells. Glyceraldhyde-derived AGEs has been identified as a major source of neurotoxicity in Alzheimer's disease (AD). In a previous study, we demonstrated that glyceraldehyde-derived AGEs increase APP and Aβ via ROS. Furthermore, the combination of AGEs and Aβ has been shown to enhance neurotoxicity. In mice, APP expression is increased by tail vein injection of AGEs. This evidence suggests a correlation between AGEs and the development of AD. However, the role played by AGEs in the pathogenesis of AD remains unclear. In this report, we demonstrate that AGEs up-regulate APP processing protein (BACE and PS1) and Sirt1 expression via ROS, but do not affect the expression of downstream antioxidant genes HO-1 and NQO-1. Moreover, we found that AGEs increase GRP78 expression and enhance the cell death-related pathway p53, bcl-2/bax ratio, caspase 3. These results indicate that AGEs impair the neuroprotective effects of Sirt1 and lead to neuronal cell death via endoplasmic reticulum ER stress. Our findings suggest that AGEs increase ROS production, which stimulates downstream pathways related to APP processing, Aβ production, Sirt1, and GRP78, resulting in the up-regulation of cell death related pathway. This in-turn enhances neuronal cell death, which leads to the development of AD.
- Source: Carnosine and the processes of ageing.
- Abstract: The causes of ageing are usually regarded as multifactorial; thus effective regulation might be achieved by intervention at multiple sites. It has been suggested that the endogenous dipeptide carnosine, also available as a food supplement, possesses anti-ageing activity and may achieve its reported age-alleviating effects via a number of mechanisms. Carnosine's possible anti-ageing mechanisms are therefore discussed; the evidence suggests that inhibition of the mechanistic target of rapamycin and carbonyl scavenging may be involved.
- At a recent research paper presentation, we looked into how glycation and hypoxia (low tissue oxygenation, caused by poor circulation) cause fat tissue inflammation throughout the body and cellulite, in particular. at skin level. On this article we provide a simple holistic strategy against hypoxia, inflammation and glycation to help improve the health of your fat tissue and reduce cellulite.
- Hypoxia can be reduced by regular exercise and a healthy diet rich in oily fish, vegetables and fruits and poor in sugar and saturated fat. A highly concentrated anti-cellulite cream that enhances circulation and reduces fat can also be of help, as can a strong anti-cellulite treatment, such as high power radiofrequency or strong anti-cellulite massage.
- Glycation can be reduced by seriously restricting sugar, refined carbohydrates or excessive intake of carbs (even the complex ones). Supplementing with the anti-glycation aminoacid carnosine is essential. Again, a highly concentrated anti-cellulite cream that contains in meaningful quantities the aminoacids carnosine and other anti-glycation plant extracts (such as centella, pine bark extract, green tea extract, dihydromyricetin and other) can also be of help.
- Low grade inflammation can be reduced by a diet poor in sugar, trans fats and omega-6 fatty acids and rich in oily fish, vegetables, fruits and herbs such as turmeric. A highly concentrated anti-cellulite cream, rich in anti-inflammatory ingredients such as curcumin and 18-beta glycyrrhetinic acid may also be of help.