Calorie Restriction Mimetics and Aging

Resveratrol-procyanidin blend: nutraceutical and antiaging efficacy evaluated in a placebo-controlled, double-blind study

“…Dietary intake is 6–8 mg daily, and recent clinical data show that resveratrol may possess bioactivity at μg doses, when provided as part of a synergistic combination of phytochemicals in foods and supplements. Accordingly, the use of supplements that bring the dose into a medium to low range may have specific effects on the aging process 42. In addition, our study is the first to demonstrate that, as well as improving systemic oxidative stress, antioxidant nutraceutical treatment also enhances antioxidant capacity in the stratum corneum of the skin.…”

Resveratrol – pills to replace a healthy diet?

“… Structure of resveratrol. Genes and products affected by exposure to the compound [7, 17, 25, 56] . CDK – 1/2/4/7, cyclin‐dependant kinase 1/2 /4/7; HDAC‐2, histone deacetylase 2; P53, tumour protein 53; Rb, retinoblastoma tumour suppressor gene; c‐Myc, gene myelocytomatosis; PTEN, phosphatase and tensin homolog; p21 Waf1/Cip1 , cyclin‐dependent kinase inhibitor 1A; P27, cyclin dependant kinase inhibitor 27; Rbf‐E2F/DP pathway, Retinoblastoma‐family protein/ E2F transcription factor/ DP transcription factor; P300/CBP, CREB binding protein; PARP, poly(ADP)‐ribose polymerase; EGF, endothelial growth factor; HGF, human growth factor; GAD45, DNA damage inducible gene 45; FOXO‐1/3a/4, forkhead transcription factor 1/3a/4; NFκB, nuclear factor kappa B; AP‐1, activating protein‐1;NRF‐2, nuclear respiratory factor‐2; STAT3, signal transducer and activator of transcription 3; PPARγ, peroxisome proliferator activated receptor gamma; HIF‐1α, hypoxia inducible factor 1‐alpha; Erg‐1, ets‐related gene; E2F, transcription factor E2F; SP‐1, Sp1 transcription factor; CREB, cyclic‐AMP response element binding proteins; NF1B, neurofibromin 1b; PI3K, phosphoinositide 3 kinases; ERK1/2, extracellular signal regulated kinase 1 /2; PKC, protein kinase C; PKD, protein kinase D; PKA, protein kinase A; MAPK, mitogen activated protein kinase; JNK‐1, c‐Jun N‐terminal kinases; Akt, serine/threonine protein kinase; IKKβ, IkB kinase beta; JAK, Janus kinase; Src, sarcoma pro‐oncogenic tyrosine kinase; syk, spleen tyrosine kinase gene; CKII, casein kinase 2; Cu‐Zn‐Mn SOD, copper‐zinc‐manganese superoxide dismustase; Trx1, cytosolic thioredoxin; p47 phox , enzyme for production of superoxide; ROS, reactive oxygen species; AMPK, adenosine monophosphate activated protein kinase; GLUT4, glucose transporter 4; UCP‐1, uncoupling protein 1; PGC‐1α, PPARgamma coactivator 1 proliferator‐activated receptor‐gamma; PTB1B, protein tyrosine phosphatase 1 B; ER, eostrogen receptor; AR, andogen receptor; CYP isoforms, cytochrome P450 isoforms; NQO2, NADPH dehydrogease quinone 2; hTERT, human telomerase reverse transcriptase; IGF‐1, insulin like growth factor‐1; IRS‐1, insulin receptor substrate 1; IGFBP‐3, Insulin‐like growth factor‐binding protein 3; TNFα, tumour necrosis factor alpha; COX‐2, cyclo‐oxygenase 2; iNOS, inducible nitric oxide synthase, eNOS, endothelial nitric oxide synthase; NO, nitric oxide; CRP, C‐ reactive protein; 5‐LOX, 5‐lipoxygenase‐ activating protein; NAG‐1, nonsteroidal anti‐inflammatory drug‐activated gene; IFNγ, interferon gamma; ILs, interleukins; MPO, myeloperoxidase; GM‐CSF, granulocyte‐macrophage colony stimulating factor; TBARS, thiobarbituric acid reactive substances; SOCS3, Suppressor of cytokine signaling 3; MCP‐1, monocyte chemotactic protein‐1; TGFβ, transforming growth factor beta; Bcl‐2, B‐cell lymphoma 2; Bcl‐XL, BCL2‐like 1; TRAF2, TNF receptor‐associated factor 2; AP‐2α, activating protein 2; XIAP, X‐linked Inhibitor of apoptosis protein; mTOR, mammalian target of rapamycin; PUMA, BCL2 binding component 3; noxA, nitrate reductase, NADH oxidase subunit; Bim, BCL2‐like 11 apoptosis facilitator; Cyt.…”

“…It is too soon to comment on the most suitable dose and source, or the effects and safety of chronic intake, until further clinical data are available. In the mean time, nutraceutical RSV is easily available commercially, and uncontrolled self‐prescribing is encouraged by claims of calorie‐restriction mimetic and anti‐ageing activity, following initial in vivo reports [7].…”

“… The potential clinical applications of resveratrol and main proposed mechanisms of action [6, 7, 24, 56, 70]. NFκB, nuclear factor kappa B; STAT3, signal transducer and activator of transcription 3; COX‐1/2, cyclo‐oxygenase 1 /2; IL's, interleukins; CRP, C‐reactive protein; AMPK, adenosine monophosphate activated protein kinase; TNFα, tumour necrosis factor alpha; TG, triglycerides; HDL, high density lipoproteins; LDL, low density lipoproteins; ICAM, inter‐cellular adhesion molecule 1; VCAM, vascular cell adhesion molecule 1; iNOS, inducible nitric oxide synthase; eNOS, endothelial nitric oxide synthase.…”

“…It is 13 years since the first paper reported the initial in vitro and in vivo evidence of cancer chemopreventative activity of RSV [5]. The abundance of research providing promising data brings this phytochemical to the era of clinical testing [6–8]. This review will summarize the pharmacology of RSV, as evidenced in the first published clinical observations, and discuss its clinical relevance.…”