Aim Global Inc.
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- 2. Unit 301 & 320 3 rd Floor AIC-Burgundy EmpireTower ADBAve. Cor. Garnet Road Ortigas Center Pasig City Keeping Dreams Alive!! March 18, 2006 27-B TABACO ST. TAGBILARAN City
- 3. Engr. Francis Miguel VP for Finance Mr. Raymond Asperin VP for Sales Dr. Eduardo Cabantog President/CEO Board of Directors
- 5. Tie-up
- 7. What is a ORAC (Oxygen Radical Absorbance Capacity) ? The ORAC Scale on antioxidant capacity USDA researchers at Tufts University in Boston, Massachusetts , have developed a new laboratory test to measure the oxygen radical absorption capacity of different foods and natural substances. Known as the ORAC scale, it is one of the most sensitive and reliable methods for measuring antioxidant capacity. The first test of its kind, the ORAC (Oxygen Radical Absorbance Capacity) scale measures both the time and degree of free-radical inhibition. What are Antioxidants? Antioxidants are substances or nutrients in our food which can prevent the oxidative damage to our body. Phythonutrients act as antioxidants which help form the body's defense against free radical damage to cells . Antioxidants act as free radical scavengers and prevent and repair damage done by the free radicals
- 8. What is a free radical? Free radicals are produced when our cells create energy and when we are exposed to pollutants or toxins such as cigarette smoke, alcohol or pesticides. If allowed to go unquenched, free radicals can cause damage to the body's cells. The cells that line the arteries, the fat cells in the blood, the immune cells and so on can all be affected by free radicals. And because of this, free radical damage (or oxidation) has been linked to the formation of every degenerative disease known including cancer, cardiovascular disease, cataracts and the ageing process itself. This free radical damage cannot be prevented or cured by any drugs - in fact most drugs are sources of MORE free radicals in the body. Reference 2005 American Cancer Society ; D. Harmon, J. Gerontol
- 10. We need to eat at least 5 kinds of Fruits & Vegetables
- 19. R E S T O R L Y F L O N G E V I T Y F O R M U L A v 1-5
- 36. PERFECT WHITE
- 37. The World’s First Coffee-ceuticals!!!
- 40. The World’s First Choco-ceuticals!!!
- 42. Omega-3 EFA of DHA and EPA For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc. v 2.1
- 44. Eating fat from fish is healthy For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc. Reduces inflammation Prevents heart disease Supports eye/brain function Improves mood
- 45. Today’s problem: Eating the wrong fats For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc.
- 46. Trans Fat (the worst) For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc.
- 47. Saturated Fat (some good, some bad) For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc.
- 48. Unsaturated Fat (All good: omega-3 EFAs) For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc.
- 50. Cell Membranes made from EFAs For educational purposes only. Do not copy or distribute. ©2008 Nature’s Way Products, Inc. CELL cell membrane CELL MEMBRANE fatty acids
- 57. Heart disease begins when cholesterol, fatty material, and calcium build up in the arteries, Our Liver produce 2 type of Cholesterol Good & BAD Cholesterol .Cholesterol is a waxy fat like substance that travel throughout the body in the blood stream. Bad Cholesterol remain through the blood .High amount of Bad cholesterol will cause of abnormal blood circulation .
- 58. The plaque deposits harden and narrow the wall of the artery, reducing or stopping blood flow .
- 59. When plaque builds up , it causes a blood clot to form in the coronary artery. The blood clot blocks blood from flowing to the heart muscle, leading to a heart attack . In a worst-case scenario, sudden cardiac arrest or fatal can occur.
- 60. High blood pressure Or "hypertension." Blood pressure rises and falls throughout the day. An optimal blood pressure is less than 120/80 mmHg. When blood pressure stays high, greater than or equal to 140/90 mmHg, then it is considered high blood pressure. High blood pressure increases the risk for heart disease and stroke.
- 62. Daisy papaya soap This is an organic/hypoallergenic product that has no harmful chemical ingredients and its safe for children to use. Papaya enzyme has anti bacterial properties that effectively remove body odor. It is clinically proven to lighten skin pigmentation and other skin blemishes such as pimple scars, freckles and melasma caused by excessive sun exposure. Regular use of Daisy Papaya Soap will help rejuvenate skin damage for a healty, glowing and flawless result.
- 64. WE DID IT AGAIN! The Most Outstanding Mega-Nutritional Supplement (National) has been awarded Mega -Nutritionals Global Award For Marketing Excellence (Symbol of Agora Excellence) Mega -Nutritionals Global Award For Marketing Excellence The Most Outstanding Wellness Technology Awarded as
- 66. = Php7,980
- 67. = Php7,980 1) 2) 25% Life Time Discounts on All Products
- 68. = Php7,980 1) 2) 25% Life Time Discounts on All Products 3) Free Web Page www.aimglobalinc.com
- 69. = Php7,980 1) 2) 25% Life Time Discounts on All Products 3) Free Web Page www.aimglobalinc.com 4) ATM Card
- 70. = Php7,980 1) 2) 25% Life Time Discounts on All Products 3) Free Web Page www.aimglobalinc.com 4) ATM Card 5) Business Kit + Free Trainings
- 71. = Php7,980 1) 50,000 UMA 10,000 MMR 10,000 BE 2) 25% Life Time Discounts on All Products 3) Free Web Page www.aimglobalinc.com 4) ATM Card 6) 200,000 PAI 5) Business Kit + Free Trainings
- 72. = Php7,980 1) 10,000 MMA + 10,000BE 2) 25% Life Time Discounts on All Products 3) Free Web Page www.aimglobalinc.com 4) ATM Card 5) Business Kit + Free Trainings 6) 200,000 PAI + 10,000 MR 7) Free Medical Check-Up
- 73. = Php7,980 Tie-up Clinics:
- 74. = Php7,980 8) Free Scholarship Program
- 75. Tuition Fee: 30,000/ SEM 15,000 X 2 SEM 50% (half scholarship) TRANSFERABLE NO ENTRANCE EXAM NO MAINTAINING GRADE 30,000 X 4 years = P 120,000 worth BIG DISCOUNT !
- 76. School Alliance AMA Computer College
- 80. COMMON PARADIGM WORK wages bills ? loan loan
- 81. WORK wages savings ASSET PARADIGM for Success part-time business profits bills investments, more business %%%%
- 82. 3 BUSINESS S Y STEMS: Franchise NETWORK MARKETING (Personal Franchise) BUILDING YOUR A S SET S
- 84. BUSINESS S Y STEMS: TRADITIONAL BUSINESS AIM GLOBAL BUSINESS Capital Shop+Rental+Permit+Bills CUSTOMERS Sales Big Investment low income MEMBERSHIP ONLINE www.aimglobalinc.com “ K ” system Big Profit sales + Commision Small investment BIG income
- 88. Formula: 1 LEFT + 1 RIGHT = P 1,500 People who will join you will be divided into two groups 3. Matching Sales Bonus
- 89. YOU LEFT SALES FORCE RIGHT SALES FORCE 2,500 1,000 1,500 + Harry Ron Marketing Support = PHP1,500.00 3. Matching Sales Bonus
- 90. YOU LEFT SALES FORCE RIGHT SALES FORCE Ron Patrick Fred John Mitch 1,500 1,500 1,500 Sales Matching Bonus 2,500 + 4,500 = 7,000 in just a month Harry Walter 1,200 SV 1,200 SV 1,200 SV 1,500 PLACEMENT Slim and Trim Choleduz Alive! DTC GLOBAL PACKAGE = GLOBAL PACKAGE PRODUCT = GLOBAL PACKAGE PRODUCT = PRODUCT 1,500
- 91. YOU LEFT SALES FORCE RIGHT SALES FORCE 16 pax / day 16 pax / day 16 pairs / day maximum pay out per account x 1,500 = 24, 000 / day 18 pax 2 pax 20 pax 4 pax flush out!!!
- 92. Your Potential Maximum Earning for 1 Year What if ?... Matching Bonus Month Distributors Earnings 1-month 2 2,500.00 2-month 4 3,000.00 3-month 8 6,000.00 4-month 16 12,000.00 5-month 32 24,000.00 6-month 64 48,000.00 7-month 128 96,000.00 8-month 256 240,000.00 9-month 512 384,000.00 10-month 1,024 720,000.00 11-month 2,048 720,000.00 12-month 4,096 720,000.00 2,963,500
- 93. 5 Sales Pair Php 7,500 PAY OUT: EVERYDAY product benefits SEC / DTI PYRAMIDING P
- 94. Ways To Earn: YOUR GROUP MAY STOP FROM SHARING THE OPPORTUNITY, BUT THEY WILL NEVER STOP FROM USING THE PRODUCTS. BECAUSE OF THIS, YOUR MONTHLY INCOME IS ASSURED. Php 1,688 Minimum Sales Activity Requirement per Month. Unilevel Sales Bonus 4
- 95. Mitch John Patrick Harry 2nd 3rd 4th 5th 6th 7th 8th 9th 10th 1st 4. Unilevel Sales Bonus 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 5% of Product SV 10% of Product SV With Dynamic Compression Dynamic Compression ensures that qualified Distributors will earn bonuses on all levels without breakage to the company and without encumbrance due to inactive or non-performing Distributors within the earning levels (10 levels). Unilevel Structure This is paid to qualified Distributors based on the genealogical structure formed using the Direct Sponsor information of each Distributor Account.
- 96. Income Assumption & Projection Level Distributor Percent Earnings 1 2 10% 1,012.08 2 4 5% 1,012.08 3 8 5% 2,025.06 4 16 5% 4,051.20 5 32 5% 8,102.04 6 64 5% 16,204.08 7 128 5% 32,409.06 8 256 5% 64,819.02 9 512 5% 129,638.04 10 1,024 5% 259,276.08 2,046 518,047.02 Sponsor only (2) direct distributor Each of one buying 6 Boxes of ALIVE or Global Re-order Your Potential Income per Month UNI-LEVEL SALES COMMISION
- 97. Income Assumption & Projection Level Distributor Percent Earnings 1 2 10% 80.00 2 4 5% 80.00 3 8 5% 160.00 4 16 5% 320.00 5 32 5% 640.00 6 64 5% 1,280.00 7 128 5% 2,560.00 8 256 5% 5,120.00 9 512 5% 10,240.00 10 1,024 5% 20,480.00 2,046 40,960.00 Sponsor only (2) direct distributor Each of one buying two boxes of ALIVE 30 vcaps Your Potential Income per Month UNI-LEVEL SALES COMMISION
- 98. Stair Step Plan (Overriding Commission) Distributor Silver Executive Gold Executive Global Ambassador +10% +20% +30% +10% +20% +10% Up to infinity or next same/higher rank Earn the Difference based on Title/Rank +10% +20% +30% Requirement : 10 GPs 1000 GPs 100 GPs Accumulation of group re-orders 0% NO DEMOTION NO TIME FRAME NO PASS UP GROUP SALES POINTS 2000 GPs
- 99. All expenses paid w/ nature's way and AIM Global visa assistance
- 100. 6. Royalty Income DISTRIBUTOR DISTRIBUTOR 2% of Breakaway Group Product SV 1st Generation 2nd Generation 3rd Generation 4th Generation 5th Generation 2% of Breakaway Group Product SV 2% of Breakaway Group Product SV 2% of Breakaway Group Product SV 2% of Breakaway Group Product SV GLOBAL AMBASSADOR GLOBAL AMBASSADOR GLOBAL AMBASSADOR GLOBAL AMBASSADOR GLOBAL AMBASSADOR DISTRIBUTOR DISTRIBUTOR DISTRIBUTOR DISTRIBUTOR GLOBAL AMBASSADOR
- 103. YOU A B C D LEFT RIGHT 500 500 500 500 1,500 1,500 1 HEAD = P7,980 3 HEADS = P23,940 Direct Sales Bonus = P2,000 Group Sales Bonus = P3,000 P5,000 Products = P6.750 Payback = P11,750 Maximum Earnings per/day = P24,000 Per month = P720,000 YOU (1) LEFT RIGHT YOU (2) YOU (3) A B C D 500 500 500 500 500 500 1,500 1,500 1,500 1,500 1,500 Direct Sales Bonus = P3,000 Group Sales Bonus = P7,500 P10,500 Products = P20,250 Payback = P30,750 Maximum Earnings per/day = P72,000 Per month= P2,160,000 Assuming you have four (4) friends who want to join in your group
- 104. YOU A B C D LEFT RIGHT 500 500 500 500 1,500 1,500 1 HEAD = P7,980 Direct Sales Bonus = P2,000 Group Sales Bonus = P3,000 P5,000 Products = P6.750 Payback = P11,750 Maximum Earnings per/day = P24,000 Per month = P720,000
- 105. 3 HEADS = P23,940 YOU (1) LEFT RIGHT YOU (2) YOU (3) A B C D 500 500 500 500 500 500 1,500 1,500 1,500 1,500 1,500 Direct Sales Bonus = P3,000 Group Sales Bonus = P7,500 P10,500 Products = P20,250 Payback = P30,750 Maximum Earnings per/day = P72,000 Per month= P2,160,000 Assuming you have four (4) friends who want to join in your group
- 106. 7 HEADS = P55,860 YOU (1) LEFT RIGHT YOU (2) YOU (3) 4 5 6 7 500 500 500 500 500 500 1,500 1,500 1,500 1,500 1,500 1 st phase Direct Sales Bonus = P3,000 Group Sales Bonus = P7,500 P10,500 Products = P47,250 Payback = P57,750 7 heads projection 1 2 3 4 5 6 7 8 Maximum potential Earnings = P5,040,000 2nd Phase Total 22,000.00 Direct Refer. [email_address] 4,000.00 01 4 pairs 6,000.00 02 2 pairs 3,000.00 03 2 pairs 3,000.00 04 1 pair 1,500.00 05 1 pair 1,500.00 06 1 pair 1,500.00 07 1 pair 1,500.00
- 107. Retail Sales Profit (RSP) X 10 = SRP DP PROFIT 10 ORDERS / MONTH 1,125 844 281 2,810
- 108. Retail Sales Profit (RSP) X 10 = SRP DP PROFIT 10 ORDERS / MONTH 1,900 1,425 475 4,750
- 109. Retail Sales Profit (RSP) X 10 = SRP DP PROFIT 10 ORDERS / MONTH 320 240 80 800
- 110. Retail Sales Profit (RSP) X 10 = SRP DP PROFIT 10 ORDERS / MONTH 400 300 100 1,000
- 111. Retail Sales Profit (RSP) X 10 = CHOLEDUZ SRP DP PROFIT 10 ORDERS / MONTH 800 600 200 2,000
- 112. Retail Sales Profit (RSP) X 10 = SLIM AND TRIM SRP DP PROFIT 10 ORDERS / MONTH 1,125 844 281 2,810
Hinweis der Redaktion
- “ Mitochondria are also important sources of ROS in the vasculature, especially in aging ( 66 ). In the present study, we show that cigarette smoke exposure also increases mitochondrial O2 – production in endothelial cells ( Fig. 4 ). It has also been shown that cigarette smoke constituents impair mitochondrial function and elicit mitochondrial oxidative stress in other cell types as well ( 6 , 29 , 30 , 33 , 36 , 37 , 55 ). In this regard, a recent study demonstrated that acrolein, a major toxicant in cigarette smoke, causes oxidative mitochondrial damage ( 36 ). A higher level of oxidative mitochondrial DNA damage has been observed in smokers ( 7 , 37 , 39 ). These data support the hypothesis that cigarette smoke-induced mitochondrial damage and dysfunction may contribute an increased risk for cardiovascular disease in smokers. It is significant that in our study resveratrol substantially reduced mitochondrial oxidative stress in CSE-treated endothelial cells ( Fig. 4 ), perhaps due to the previously demonstrated effects of resveratrol on cellular antioxidant enzymes ( 63 ). Because of efficient scavenging of O2 – by high levels of SOD in mitochondria, it is likely that mitochondria-derived O2 – is a minor factor in impairing endothelial vasomotor function in cigarette smokers. There are several lines of evidence supporting the view that O2 – in the mitochondria is dismutated to H2O2, which easily penetrates the mitochondrial membranes. Accordingly, our laboratory has shown that cellular H2O2 levels are increased in CSE-treated endothelial cells ( 46 ), which are significantly reduced by resveratrol treatment. “ Moreover, SIRT1 overexpression also mimicked the anti-inflammatory action of resveratrol ( Fig. 7 ). Atherosclerosis is a chronic inflammatory disease, and pathological and epidemiological evidence suggest that proinflammatory cytokines play a central role orchestrating the pathological processes underlying the development of the atherosclerotic plaque. Thus our findings are of great significance, showing that resveratrol can abrogate the development of a proatherogenic microenvironment in the vascular wall induced by cigarette smoke-related oxidative stress. Relevant to the present discussion are the observations that resveratrol also attenuated oxidative stress-induced expression of iNOS and ICAM in arteries of aged F344 rats as well ( 66 ). We have good reason to believe that the aforementioned anti-inflammatory and antioxidant effects of resveratrol will contribute to the ability of chronic resveratrol treatment to delay vascular aging. ” ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)” “ Because in humans cardiovascular aging is responsible for the largest portion of age-related morbidity and mortality, it is particularly important to elucidate whether resveratrol exerts antiaging effects in the cardiovascular system ( 2 ). Cardiovascular aging is characterized by oxidative stress, inflammation [i.e., NF- B activation, endothelial activation, inflammatory cytokine expression, and upregulation of inducible nitric oxide (NO) synthase (iNOS)], disruption of endogenous tissue-protective mechanisms ( 27 ), and an increased rate of apoptotic cell death, which lead to an age-dependent deterioration of cardiovascular functions [recently reviewed elsewhere ( 19 , 61 , 64 )]. In this regard, recent in vitro studies from this and other laboratories have shown that resveratrol in vitro can attenuate cellular oxidative stress, inhibits endothelial activation and monocyte adhesion ( 20 , 28 , 42 ), protects endothelial cells from oxidative stress-induced apoptosis ( 63 ), and attenuates proinflammatory gene expression by the inhibition of NF- B activation in coronary arterial endothelial cells (CAECs) ( 20 ). Importantly, resveratrol is being considered as a therapeutic for humans for a variety of indications ( 10 ). To gain a better insight into the antiaging effects of resveratrol, in a series of studies we are currently characterizing the in vivo cytoprotective, antioxidant, and anti-inflammatory vascular effects of resveratrol in models of accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)” It is significant that in our study resveratrol substantially reduced mitochondrial oxidative stress in CSE-treated endothelial cells
- Because in humans cardiovascular aging is responsible for the largest portion of age-related morbidity and mortality, it is particularly important to elucidate whether resveratrol exerts antiaging effects in the cardiovascular system ( 2 ). Cardiovascular aging is characterized by oxidative stress, inflammation [i.e., NF- B activation, endothelial activation, inflammatory cytokine expression, and upregulation of inducible nitric oxide (NO) synthase (iNOS)], disruption of endogenous tissue-protective mechanisms ( 27 ), and an increased rate of apoptotic cell death, which lead to an age-dependent deterioration of cardiovascular functions [recently reviewed elsewhere ( 19 , 61 , 64 )]. In this regard, recent in vitro studies from this and other laboratories have shown that resveratrol in vitro can attenuate cellular oxidative stress, inhibits endothelial activation and monocyte adhesion ( 20 , 28 , 42 ), protects endothelial cells from oxidative stress-induced apoptosis ( 63 ), and attenuates proinflammatory gene expression by the inhibition of NF- B activation in coronary arterial endothelial cells (CAECs) ( 20 ). Importantly, resveratrol is being considered as a therapeutic for humans for a variety of indications ( 10 ). To gain a better insight into the antiaging effects of resveratrol, in a series of studies we are currently characterizing the in vivo cytoprotective, antioxidant, and anti-inflammatory vascular effects of resveratrol in models of accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- Resveratrol is present in: Foods, including peanuts, blueberries, lingonberries, sparkleberries, cranberries, deerberries, partridgeberries, and bilberries Plants, including knotweed, eucalyptus, spruce, pine, and lily Found in most abundance in skin of grapes used to make red wine It Increases mitochondria* Powerful antioxidant Activates siRT1 enzyme (sirtuin class enzyme)* Because in humans cardiovascular aging is responsible for the largest portion of age-related morbidity and mortality, it is particularly important to elucidate whether resveratrol exerts antiaging effects in the cardiovascular system ( 2 ). Cardiovascular aging is characterized by oxidative stress, inflammation [i.e., NF- B activation, endothelial activation, inflammatory cytokine expression, and upregulation of inducible nitric oxide (NO) synthase (iNOS)], disruption of endogenous tissue-protective mechanisms ( 27 ), and an increased rate of apoptotic cell death, which lead to an age-dependent deterioration of cardiovascular functions [recently reviewed elsewhere ( 19 , 61 , 64 )]. In this regard, recent in vitro studies from this and other laboratories have shown that resveratrol in vitro can attenuate cellular oxidative stress, inhibits endothelial activation and monocyte adhesion ( 20 , 28 , 42 ), protects endothelial cells from oxidative stress-induced apoptosis ( 63 ), and attenuates proinflammatory gene expression by the inhibition of NF- B activation in coronary arterial endothelial cells (CAECs) ( 20 ). Importantly, resveratrol is being considered as a therapeutic for humans for a variety of indications ( 10 ). To gain a better insight into the antiaging effects of resveratrol, in a series of studies we are currently characterizing the in vivo cytoprotective, antioxidant, and anti-inflammatory vascular effects of resveratrol in models of accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF- ) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF- B activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008) Increasing SIRT1 has been found to protect cells against amyloid-beta-induced ROS production and DNA damage, thereby reducing apoptotic death in vitro
- The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF- ) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF- B activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- Category Info: Sales of $96,989 (SPINS Dollars) 66% growth over last year (2007) Product Specs: Japanese Knotweed std. to 50% Total Resveratrol Grape Seed 95% Polyphenols Red Wine Extract 30% Polyphenols Label Claim: Antioxidant 37.5 mg resveratrol per capsule SRP $19.99 USD 60 count, Vcap® Traditional Use: Japanese Knotweed – heart, liver and blood vessels Resveratrol/ Red Wine – French paradox: French eat diets high in fat & cholesterol but have low incidence of heart disease – believed due to red wine consumption.
- In an animal model study conducted at Harvard Medical School and National Institute on Aging: (additional points) Had increased mitochondria production Resveratrol found to have a positive impact on obesity: Reduced levels of inflammatory compounds (interleukins 6 & 8) (Interleukins associated with development of obesity-related disorders, such as diabetes and atherosclerosis) Increased level of adiponectin, decreases risk of heart attack Our studies show that resveratrol exerts anti-inflammatory, antioxidant, and antiproliferative effects in the pulmonary arteries, which may contribute to the prevention of pulmonary hypertension. (AHA Hypertension July 13, 2009) The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF- ) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF- B activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- Statements on obesity were extrapolated from PCP presentation given by Dr. Holley Lucille. No references where found for these therein. Brain Res Rev. 2006 Sep;52(2):316-26. Links “ Resveratrol--a boon for treating Alzheimer's disease? Anekonda TS . Neurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, 97006, USA. anekondt@ohsu.edu Resveratrol, a red wine polyphenol, is known to protect against cardiovascular diseases and cancers, as well as to promote antiaging effects in numerous organisms. It also modulates pathomechanisms of debilitating neurological disorders, such as strokes, ischemia, and Huntington's disease. The role of resveratrol in Alzheimer's disease is still unclear, although some recent studies on red wine bioactive compounds suggest that resveratrol modulates multiple mechanisms of Alzheimer's disease pathology. Emerging literature indicates that mechanisms of aging and Alzheimer's disease are intricately linked and that these mechanisms can be modulated by both calorie restriction regimens and calorie restriction mimetics, the prime mediator of which is the SIRT1 protein, a human homologue of yeast silent information regulator (Sir)-2, and a member of NAD+-dependent histone deacetylases. Calorie restriction regimens and calorie restriction-mimetics trigger sirtuins in a wide variety of organisms, ranging from bacteria to mouse. In a mouse model of Huntington's disease, resveratrol-induced SIRT1 was found to protect neurons against ployQ toxicity and in Wallerian degeneration slow mice, resveratrol was found to protect the degeneration of neurons from axotomy, suggesting that resveratrol may possess therapeutic value to neuronal degeneration. This paper mainly focuses on the role of resveratrol in modulating AD pathomechanisms. ( Brain Research Reviews Volume 52, Issue 2 , September 2006, Pages 316-326).” Adiponectin: A protein hormone that modulates glucose regulation and fatty acid catabolism en.wiktionary.org/wiki/adiponectin a hormone produced by fat cells that promotes sensitivity to insulin. In an animal model study conducted at Harvard Medical School and National Institute on Aging: (additional points) Had increased mitochondria production Resveratrol found to have a positive impact on obesity: Reduced levels of inflammatory compounds (interleukins 6 & 8) (Interleukins associated with development of obesity-related disorders, such as diabetes and atherosclerosis) Increased level of adiponectin, decreases risk of heart attack Our studies show that resveratrol exerts anti-inflammatory, antioxidant, and antiproliferative effects in the pulmonary arteries, which may contribute to the prevention of pulmonary hypertension. (AHA Hypertension July 13, 2009) The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF- ) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF- B activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- Carotid arteries are the major arteries in the neck that supply blood to the brain. Our studies show that resveratrol exerts anti-inflammatory, antioxidant, and antiproliferative effects in the pulmonary arteries, which may contribute to the prevention of pulmonary hypertension. (AHA Hypertension July 13, 2009) Prevents cigarette smoke stress ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008) “ The fourth important finding of our study is that cigarette smoking can induce apoptosis in endothelial cells, which was prevented by resveratrol treatment ( Fig. 8 ). Resveratrol was also effective in preventing CSE-induced apoptosis in CAECs in vitro ( Fig. 8 ). Moreover, our laboratory has recently shown that resveratrol, in a physiologically relevant concentration range, also prevents endothelial apoptosis induced by H2O2, TNF- , and oxidized LDL ( 63 ). Present and previous findings of our laboratory ( 63 ) suggest that antiapoptotic effects of resveratrol are mediated by a SIRT1-dependent pathway ( Fig. 8 ), which likely involves the induction of H2O2 scavenging mechanisms (e.g., glutathione peroxidase) ( 63 ). There is accumulating evidence that increased endothelial cell apoptosis may initiate atherosclerosis, whereas at later phases of atherogenesis, the increased rate of apoptosis of endothelial cells, vascular smooth muscle cells, and macrophages was observed in vulnerable lesions and at sites of plaque rupture ( 14 ). Because in humans cigarette smoke constituents, TNF- , and oxLDL are physiologically relevant stimuli of apoptosis, which play an important role in the development of coronary artery disease, it is likely that the antiapoptotic action of resveratrol/SIRT1 will contribute to their cardioprotective effects in vivo. “ The fifth interesting finding of our present study is that soluble cigarette smoke constituents can induce significant oxidative DNA damage in endothelial cells ( Fig. 9 ). “ The dietary polyphenolic compound resveratrol, by activating the protein deacetylase enzyme silent information regulator 2/sirtuin 1 (SIRT1), prolongs life span in evolutionarily distant organisms and may mimic the cytoprotective effects of dietary restriction. The present study was designed to elucidate the effects of resveratrol on cigarette smoke-induced vascular oxidative stress and inflammation, which is a clinically highly relevant model of accelerated vascular aging. Cigarette smoke exposure of rats impaired the acetylcholine-induced relaxation of carotid arteries, which could be prevented by resveratrol treatment. Smoking and in vitro treatment with cigarette smoke extract (CSE) increased reactive oxygen species production in rat arteries and cultured coronary arterial endothelial cells (CAECs), respectively, which was attenuated by resveratrol treatment. The smoking-induced upregulation of inflammatory markers (ICAM-1, inducible nitric oxide synthase, IL-6, and TNF- ) in rat arteries was also abrogated by resveratrol treatment. Resveratrol also inhibited CSE-induced NF- B activation and inflammatory gene expression in CAECs. In CAECs, the aforementioned protective effects of resveratrol were abolished by knockdown of SIRT1, whereas the overexpression of SIRT1 mimicked the effects of resveratrol. Resveratrol treatment of rats protected aortic endothelial cells against cigarette smoking-induced apoptotic cell death. Resveratrol also exerted antiapoptotic effects in CSE-treated CAECs, which could be abrogated by knockdown of SIRT1. Resveratrol treatment also attenuated CSE-induced DNA damage in CAECs (comet assay). Thus resveratrol and SIRT1 exert antioxidant, anti-inflammatory, and antiapoptotic effects, which protect the endothelial cells against the adverse effects of cigarette smoking-induced oxidative stress. The vasoprotective effects of resveratrol will likely contribute to its antiaging action in mammals and may be especially beneficial in pathophysiological conditions associated with accelerated vascular aging. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)” “ It is significant that SIRT1 also appears to regulate cigarette smoke-induced proinflammatory mediator release via the inhibition of NF- B in macrophages in vitro and in rat lungs in vivo ( 69 ). It is also logical to hypothesize that the SIRT1-mediated antioxidant action of resveratrol (e.g., scavenging of H2O2) contributes to its inhibitory effects on NF- B activation ( 38 ). This view is in line with our recent results showing that resveratrol effectively inhibits H2O2-induced NF- B activation in endothelial cells ( 20 ). ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)”
- Resveratrol is known to be easily absorbed from the digestive track, and per os resveratrol treatment was shown to induce substantial gene expression changes in a number of organs ( 9 , 10 ). After per os (by mouth) administration, the plasma concentration of resveratrol increases to the micromolar range. In the circulation, in addition to the free form of resveratrol, trans-resveratrol-3-sulfate, trans-resveratrol-4'-sulfate, trans-resveratrol-3,5-disulfate, trans-resveratrol-3,4'-disulfate, trans-resveratrol-3,4',5-trisulfate, trans-resveratrol-3-O-β-D-glucuronide, and resveratrol aglycone are also present, which likely retain much of the bioactivity of resveratrol. The findings that resveratrol consumption resulted in marked improvements in endothelial function and phenotype (similar to the observed direct in vitro effects of resveratrol) strongly suggest that resveratrol reaches the vascular cells in effective concentrations. ( Am J Physiol Heart Circ Physiol 294: H2721-H2735, 2008. April 18, 2008)
- Good for mothers, infants, children and adults Cognitive performance—function and speed Vision Brain development and function particularly in infancy and childhood After giving birth, the mother is often left depleted of omega-3s Baby blues Diet during pregnancy plays an important role in determining EFA status Additional EFAs are required during pregnancy, especially during 3 rd trimester Proper development of mammary glands, placenta, uterus and fetal brain and nervous system are most dependent on EFAs Fetal needs of DHA are greatest during 3 rd trimester during brain cell development phase If mother is deficient in EFAs the fetus will not be receiving adequate supply After giving birth it takes up to 4 years to replace the DHA lost during pregnancy Ongoing research shows that women with low levels of DHA may be at an increased risk of developing postpartum depression 15-20% of women who give birth in the US develop postpartum depression Countries with the highest fish consumption such as Japan, Hong Kong, Sweden and Chile had the lowest levels of postpartum depression Marine-source EFA’s Sourced in cold, deep waters Off the coast of Chile Molecular Distillation processing Types of fish used contain high amounts of EPA/DHA anchovy, sardine, mackerel, tuna PCBs & Heavy Metals testing