The science of healthful aging: how to retain a sharp mind and an energetic body.

There is a misconception that as we age we are destined to lose our vitality and energy and become more prone to develop joint pain, memory problems and chronic diseases. This does not need to be the case. The key is how we treat our bodies during the aging process. When you combine a comprehensive healthy aging supplement plan with a whole foods diet, exercise, water, sleep, and stress management, you can age with the same level of energy and vitality you experienced in your youth.

The Akasha healthy Aging program includes cutting edge supplements proven to improve concentration as well as physical and mental energy by providing your brain and muscle cells with a recharge. These products go way beyond gingko to help you stay powerful in all respects. Scientific advances have been made in the ability to prevent brain, body and skin aging. This carefully chosen group of supplements takes advantage of the latest scientific research to help you look and feel younger.

THE MEDICAL SCIENCE BEHIND THIS PROGRAM: SUMMARY

By Dr. Myles Spar

Akasha's healthy aging package gives your body nutrients, anti-oxidants and herbs which are known to support a sharp mind and energetic body during the aging process. This program includes clinically proven, state of the art science based supplements.

One of the enemies of healthy aging is inflammation. Inflammation has been shown to be the culprit behind many of the neurological declines we associate with aging and is the primary factor leading to heart attacks and strokes.

Fish oil, an omega 3 fatty acids including EPA and DHA, is a potent anti-inflammatory modulator, therefore a high quality fish oil taken in dosages shown to decrease inflammation throughout the brain and body is essential for a healthy aging supplement program.

In addition the synergistic herbal formula,Infla-Regulator, has been added to help maintain the balance between certain enzymes within the body that regulate the inflammatory response.

CytoKind PRP represents the newest way to improve brain function, containing proline rich polypeptide complex (PRP) which boosts concentration and focus. For further nervous system support, we include

Cereguard providing powerful anti-oxidant protection for the brain and overall nervous system as well as acetyl-l-carnitine for energy, N-acetylcysteine for combating oxidative damage, grape seed extract for anti-aging benefit and a host of B vitamins for important neurologic support.

Coenzyme Q 10 is added as an essential cofactor to support cells all over the body for combating cellular damage related to aging.

Acai Super Berry Antioxidant offers even more antioxidant protection to the body with powerful ingredients such as Pomegranate and Green Tea Extract, which help minimize the aging process on a cellular level.

Doctor-recommended health practices during supplement program.

These supplements are helpful in and of themselves. However we recommend a healthy diet, exercise and stress management plan in order to achieve maximal benefit in terms of performance, feeling great and prevention of illness.

Your specific exercise recommendations depend on your overall health and baseline activity level, but in general at least 30 minutes of physical activity 5 or 6 days a week is recommended.

The optimal diet for most people is a variation of the anti-inflammatory diet. This diet has been shown to be anti-inflammatory and to lower the risk of heart disease and stroke. Your specific dietary recommendations depend on your unique medical issues.

Stress management is also important to overall health. We recommend a daily practice of some sort that helps you to lower the impact stress has on the body. This can be in the form of exercise, yoga, meditation, deep breathing, Tai chi, journeying, artwork or a hobby that you enjoy.

RELEVANT RESEARCH STUDIES: HEALTHY AGING PROGRAM INGREDIENTS:

Cereguard:

1. Wald, D et al. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis.

British Journal of Medicine. 2002;325:1202

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC135491/

*Quick Summary of Study: Lower  serum homocysteine levels reduces the risk of cardiovascular disease.

Abstract

Objective

To assess whether the association of serum homocysteine concentration with ischaemic heart disease, deep vein thrombosis and pulmonary embolism, and stroke is causal and, if so, to quantify the effect of homocysteine reduction in preventing them.

Design

Meta-analyses of the above three diseases using (a) 72 studies in which the prevalence of a mutation in the MTHFR gene (which increases homocysteine) was determined in cases (n=16b) 20 prospective studies (3820 participants) of serum homocysteine and disease risk.

Main outcome measures

Odds ratios of the three diseases for a 5 μmol/l increase in serum homocysteine concentration.

Results

There were significant associations between homocysteine and the three diseases. The odds ratios for a 5 μmol/l increase in serum homocysteine were, for ischaemic heart disease, 1.42 (95% confidence interval 1.11 to 1.84) in the genetic studies and 1.32 (1.19 to 1.45) in the prospective studies; for deep vein thrombosis with or without pulmonary embolism, 1.60 (1.15 to 2.22) in the genetic studies (there were no prospective studies); and, for stroke, 1.65 (0.66 to 4.13) in the genetic studies and 1.59 (1.29 to 1.96) in the prospective studies.

Conclusions

The genetic studies and the prospective studies do not share the same potential sources of error, but both yield similar highly significant results—strong evidence that the association between homocysteine and cardiovascular disease is causal. On this basis, lowering homocysteine concentrations by 3 μmol/l from current levels (achievable by increasing folic acid intake) would reduce the risk of ischaemic heart disease by 16% (11% to 20%), deep vein thrombosis by 25% (8% to 38%), and stroke by 24% (15% to 33%).

2.  Homocysteine Lowering Trialists' Collaboration. Lowering blood homocysteine with folic acid based supplements: meta-analysis of randomised trials. Homocysteine Lowering Trialists' Collaboration. BMJ. 1998;316(7135):894-898
   

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC28491/?tool=pubmed

*Quick Summary of Study: Folic acid,B-12 and B-6 were found to reduce serum levels of homocysteine.

Abstract

Objective: To determine the size of reduction in homocysteine concentrations produced by dietary supplementation with folic acid and with vitamins B-12 or B-6.

Design: Meta-analysis of randomised controlled trials that assessed the effects of folic acid based supplements on blood homocysteine concentrations. Multivariate regression analysis was used to determine the effects on homocysteine concentrations of different doses of folic acid and of the addition of vitamin B-12 or B-6.

Subjects: Individual data on 1114 people included in 12 trials.

Findings: The proportional and absolute reductions in blood homocysteine produced by folic acid supplements were greater at higher pretreatment blood homocysteine concentrations (P<0.001) and at lower pretreatment blood folate concentrations (P<0.001). After standardisation to pretreatment blood concentrations of homocysteine of 12

Conclusions: Typically in Western populations, daily supplementation with both 0.5-5 mg folic acid and about 0.5

3. Al-Majed AA, Sayed-Ahmed MM, Al-Omar FA, Al-Yahya AA, Aleisa AM, Al-Shabanah OA (August 2006). "Carnitine esters prevent oxidative stress damage and energy depletion following transient forebrain ischaemia in the rat hippocampus".  2006; 33 (8): 725-733.
   

http://www.ncbi.nlm.nih.gov/pubmed?term=16895547

*Quick Summary of Study: Animal study shows that Acetyl-L-carnitine can help keep neurons intake against induced ischaemia neural damge.

Abstract

1. The present study investigated whether propionyl-L-carnitine (PLC) has neuroprotective effects, similar to those reported for acetyl-L-carnitine (AC), against transient forebrain ischaemia-induced neuronal damage and biochemical derangement in the rat hippocampal CA1 region. 2. In total, 105 adult male Wistar albino rats were divided into seven groups of 15 animals each. The first three groups were injected i.p. with normal saline, AC (300 mg/kg) or PLC (300 mg/kg) for 7 successive days. The next three groups were injected i.p. with the same doses of normal saline, AC or PLC immediately after the induction of 10 min forebrain ischaemia and i.p. injections were continued for 7 successive days. Rats in the seventh group were subjected to sham-operated ischaemia and injected with normal saline for 7 successive days. 3. Seven days after treatment, animals were killed and their brains isolated for histopathological examination and biochemical studies. 4. Forebrain ischaemia resulted in a significant decrease in the number of intact neurons (77%), ATP concentration (51%) and glutathione content (32%), whereas there was a significant increase in the production of thiobarbituric acid-reactive substances (TBARS; 71%) and total nitrate/nitrite (NOx; 260%) in hippocampal tissues. 5. Administration of either AC or PLC attenuated forebrain ischaemia-induced neuronal damage, manifested by a greater number of intact neurons, ATP and glutathione, as well as a decrease in TBARS and NOx in hippocampal tissues. 6. Results from the present study suggest, for the first time, that PLC attenuates forebrain ischaemia-induced neuronal injury, oxidative stress and energy depletion in the hippocampal CA1 region. Propionyl-L-carnitine has neuroprotective effects similar to AC and could have a potential use in the treatment of neurodegenerative diseases. 7. The results of the present study will open up new perspectives for the use of PLC in the treatment of neurodegenerative diseases associated with, or secondary to, myocardial ischaemia-reperfusion injury and chronic circulatory failure.

4. Haleagrahara N, Julian V, Chakravarthi S. N-acetylcysteine Offers Cardioprotection by Decreasing Cardiac Lipid Hydroperoxides and 8-Isoprostane Level in Isoproterenol-Induced Cardiotoxicity in Rats. Cardiovasc Toxicol. 2011 Jul 28.

http://www.ncbi.nlm.nih.gov/pubmed/21796404

*Quick Summary of Study: Animal study shows that NAC can improve antioxidant enzymes levels and reduce  the negative effects caused by induced cardiovascular toxicity.

Abstract

This study investigated the cardioprotective effect of N-acetylcysteine (NAC) on isoproterenol (ISO)-induced cardiotoxicity in rats. Male Sprague-Dawley rats were divided into control, NAC alone (100 mg/kg BW orally for 14 days), ISO-control (85 mg/kg BW), and ISO with NAC (for 14 days). Serum creatine kinase-MB and Lactate dehydrogenase were measured. From the heart homogenate lipid hydroperoxides (LPO), superoxide dismutase (SOD), total glutathione (GSH), and 8-isoprostane (IP) were measured. Histopathological examination of the heart was also carried out. There was a significant increase (P < 0.05) in LPO and IP levels in ISO-control group and NAC treatment reduced these changes. Antioxidant enzyme, SOD and GSH, level decreased significantly (P < 0.05) in ISO-control group, and treatment with NAC was able to reverse these changes significantly (P < 0.05). Histopathologically, ISO-control group showed morphological changes suggestive of cardiotoxicity with large areas of coagulative necrosis, with diffused interstitial edema. NAC treatment successfully reduced these histopathological changes. In conclusion, the study proves that NAC has a strong cardioprotective effect against isoproterenol-induced cardiac changes. NAC decreases isoproterenol-induced LPO and IP levels in the heart tissue and prevented free radicals-induced damage to the myocardium

Cytokind PRP

1. Leszek J, Inglot D, Janusz M, Lisowski J, Krukowska K, Georgiades A, Colostrinin®: a Proline-Rich Polypeptide (PRP) ComplexIsolated from Ovine Colostrum for Treatment of Alzheimer’s Disease. A Double-Blind, Placebo-Controlled Study. AITE .1999 47:377-385.

2. Gibson L. G., Douraghi-Zadeh D., Siddiqui A., Pasrons B.R., Austen M.B., Neurodegeneration Unit, Basic Medical Sciences, St. George's Hospital Medical School, London (2009).

3.  Shankar GM, Li S, Mehta TH, Garcia-Munoz A, Shepardson NE, Smith I, Brett FM, Farrell MA, Rowan MJ, Lemere CA, Regan CM, Walsh DM, Sabatini BL, Selkoe DJ (August 2008). "Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory". Nat. Med. 14 (8): 837–42.

*Quick Summary of Study:  Amyloid- beta protein dimers can impair synapse structure and function as shown in animal studies with rats induced with Alzheimer’s disease.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772133/?tool=pmcentrez

Abstract

Alzheimer’s disease (AD) constitutes a rising threat to public health. Despite extensive research in cellular and animal models, identifying the pathogenic agent present in the human brain and showing that it confers key features of AD have not been achieved. We extracted soluble amyloid β–protein (Aβ) oligomers directly from the cerebral cortex of typical AD subjects. The oligomers potently inhibited long term potentiation (LTP), enhanced long term depression (LTD), and reduced dendritic spine density in normal rodent hippocampus. Soluble Aβ from AD brain also disrupted the memory of a learned behavior in normal rats. These various effects were specifically attributable to Aβ dimers. Mechanistically, metabotropic glutamate receptors (mGluR) were required for LTD enhancement and NMDA receptors (NMDAR) for spine loss. Co-administering antibodies to the Aβ N-terminus prevented the LTP and LTD deficits, whereas antibodies to the mid-region or C-terminus were less effective. Insoluble amyloid plaque cores from AD cortex did not impair LTP unless they were first solubilized to release Aβ dimers, suggesting that plaque cores are largely inactive but sequester Aβ dimers that are synaptotoxic. We conclude that soluble Aβ oligomers extracted from AD brains potently impair synapse structure and function and that dimers are the smallest synaptotoxic species.

4. Leszek J, Inglot AD, Janusz M, Byczkiewicz F, Kiejna A, Georgiades J, Lisowski J. Colostrinin proline-rich polypeptide complex from ovine colostrum--a long-term study of its efficacy in Alzheimer's disease. Med Sci Monit. 2002 Oct;8(10)

*Quick Summary of Study: Proline rich polypeptides were found to be helpful in stabilizing the health of individuals with Alzheimer’s disease.

http://www.ncbi.nlm.nih.gov/pubmed/12388930

Abstract

BACKGROUND:

Colostrinin, a proline-rich polypeptide complex (PRP) isolated from ovine colostrum, with immunoregulatory and procognitive properties, has shown positive effects in the treatment of Alzheimer's disease (AD). The aim of the present study was to evaluate the effects of long-term Colostrinin treatment of AD patients.

MATERIAL/METHODS:

The patients were taking Colostrinin tablets (containing 100 mg of PRP complex) every other day for three weeks, followed by a 2-week hiatus to avoid the development of hyporeactivity. This mode of application, '3+2 weeks,' was used consistently throughout the trial. The efficacy of treatment was assessed by the MMSE scale, and each patient was evaluated at 4-month intervals. 33 patients were treated for 16 months. However, 13 patients from this group had already been treated with Colostrinin for 12 months during placebo-controlled studies, and thus participated in the trial for a total of 28 months.

RESULTS:

The results we obtained showed that Colostrinin induced slight but statistically significant improvement or stabilization of the health status of the patients in the trial. The adverse reactions observed, if any, were remarkably mild, including anxiety, logorrhea, and insomnia, and subsided spontaneously within a short period of time (3-4 days).

CONCLUSIONS:

Colostrinin is a very promising preparation which can be used to retard the development of AD.

Fish Oil

1. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002; 106(21):2747-2757.

http://circ.ahajournals.org/content/106/21/2747.long

*Quick Summary of Study: Fish oil was found to have beneficial effects against cardiovascular disease.

Abstract

Since the first AHA Science Advisory “Fish Consumption, Fish Oil, Lipids, and Coronary Heart Disease,”1 important new findings, including evidence from randomized controlled trials (RCTs), have been reported about the beneficial effects of omega-3 (or n-3) fatty acids on cardiovascular disease (CVD) in patients with preexisting CVD as well as in healthy individuals.2 New information about how omega-3 fatty acids affect cardiac function (including antiarrhythmic effects), hemodynamics (cardiac mechanics), and arterial endothelial function have helped clarify potential mechanisms of action. The present Statement will address distinctions between plant-derived (α-linolenic acid, C18:3n-3) and marine-derived (eicosapentaenoic acid, C20:5n-3 [EPA] and docosahexaenoic acid, C22:6n-3 [DHA]) omega-3 fatty acids. (Unless otherwise noted, the term omega-3 fatty acids will refer to the latter.) Evidence from epidemiological studies and RCTs will be reviewed, and recommendations reflecting the current state of knowledge will be made with regard to both fish consumption and omega-3 fatty acid (plant- and marine-derived) supplementation. This will be done in the context of recent guidance issued by the US Environmental Protection Agency and the Food and Drug Administration (FDA) about the presence of environmental contaminants in certain species of fish.

2. Hu FB, Bronner L, Willett WC, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA. 2002; 287: 1815–182.

http://jama.ama-assn.org/content/287/14/1815.full

*Quick Summary of Study: Fish oil consumption in women was found to reduce the risk of coronary heart disease.

Abstract

Context  Higher consumption of fish and omega-3 fatty acids has been associated with a lower risk of coronary heart disease (CHD) in men, but limited data are available regarding women.

Objective  To examine the association between fish and long-chain omega-3 fatty acid consumption and risk of CHD in women.

Design, Setting, and Participants  Dietary consumption and follow-up data from 84 688 female nurses enrolled in the Nurses' Health Study, aged 34 to 59 years and free from cardiovascular disease and cancer at baseline in 1980, were compared from validated questionnaires completed in 1980, 1984, 1986, 1990, and 1994.

Main Outcome Measures  Incident nonfatal myocardial infarction and CHD deaths.

Results  During 16 years of follow-up, there were 1513 incident cases of CHD (484 CHD deaths and 1029 nonfatal myocardial infarctions). Compared with women who rarely ate fish (<1 per month), those with a higher intake of fish had a lower risk of CHD. After adjustment for age, smoking, and other cardiovascular risk factors, the multivariable relative risks (RRs) of CHD were 0.79 (95% confidence interval [CI], 0.64-0.97) for fish consumption 1 to 3 times per month, 0.71 (95% CI, 0.58-0.87) for once per week, 0.69 (95% CI, 0.55-0.88) for 2 to 4 times per week, and 0.66 (95% CI, 0.50-0.89) for 5 or more times per week (P for trend = .001). Similarly, women with a higher intake of omega-3 fatty acids had a lower risk of CHD, with multivariable RRs of 1.0, 0.93, 0.78, 0.68, and 0.67 (P<.001 for trend) across quintiles of intake. For fish intake and omega-3 fatty acids, the inverse association appeared to be stronger for CHD deaths (multivariate RR for fish consumption 5 times per week, 0.55 [95% CI, 0.33-0.90] for CHD deaths vs 0.73 [0.51-1.04]) than for nonfatal myocardial infarction.

Conclusion  Among women, higher consumption of fish and omega-3 fatty acids is associated with a lower risk of CHD, particularly CHD deaths.

3. Hu FB, Stampfer MJ, Manson JE, et al. Dietary intake of alpha-linolenic acid and risk of ischemic heart disease among women. Am J Clin Nutr.1999;69:890-897.
   

http://www.ajcn.org/content/69/5/890.full

*Quick Summary of Study: Omega 3 consumption was shown to provide protection against ischemic heart disease.

Abstracts

Background: Experimental studies in laboratory animals and humans suggest that α-linolenic acid (18:3n-3) may reduce the risk of arrhythmia.

Objective: The objective was to examine the association between dietary intake of α-linolenic acid and risk of fatal ischemic heart disease (IHD).

Design: This was a prospective cohort study. The intake of α-linolenic acid was derived from a 116-item food-frequency questionnaire completed in 1984 by 76283 women without previously diagnosed cancer or cardiovascular disease.

Results: During 10 y of follow-up, we documented 232 cases of fatal IHD and 597 cases of nonfatal myocardial infarction. After adjustment for age, standard coronary risk factors, and dietary intake of linoleic acid and other nutrients, a higher intake of α-linolenic acid was associated with a lower relative risk (RR) of fatal IHD; the RRs from the lowest to highest quintiles were 1.0, 0.99, 0.90, 0.67, and 0.55 (95% CI: 0.32, 0.94; P for trend = 0.01). For nonfatal myocardial infarction there was only a modest, nonsignificant trend toward a reduced risk when extreme quintiles were compared (RR: 0.85; 95% CI: 0.61, 1.19; P for trend = 0.50). A higher intake of oil and vinegar salad dressing, an important source of α-linolenic acid, was associated with reduced risk of fatal IHD when women who consumed this food ≥5–6 times/wk were compared with those who rarely consumed this food (RR: 0.46; 95% CI: 0.27, 0.76; P for trend = 0.001).

Conclusions: This study supports the hypothesis that a higher intake of α-linolenic acid is protective against fatal IHD. Higher consumption of foods such as oil-based salad dressing that provide polyunsaturated fats, including α-linolenic acid, may reduce the risk of fatal IHD.

Key Words: Ischemic heart disease • diet • α-linolenic acid • risk • Nurses' Health Study • trans fatty acids • women

4. Wang C, Harris W, Chung M, Lichtenstein A, Balk E, Kupelnick B, Jordan H La J.  N-3 Fatty acids from fish or fish-oil supplements, but not –linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review. Am J Clin Nutr. July 2006; 84(1): 5-17.

*Quick Summary of Study: Fish oil supplementation was found to have lower rates of cardiovascular disease among those individuals.

http://www.ajcn.org/content/84/1/5.full.pdf+html

Abstract

Studies on the relation between dietary n–3 fatty acids (FAs) and cardiovascular disease vary in quality, and the results are inconsistent. A systematic review of the literature on the effects of n–3 FAs (consumed as fish or fish oils rich in eicosapentaenoic acid and docosahexaenoic acid or as α-linolenic acid) on cardiovascular disease outcomes and adverse events was conducted. Studies from MEDLINE and other sources that were of ≥1 y in duration and that reported estimates of fish or n–3 FA intakes and cardiovascular disease outcomes were included. Secondary prevention was addressed in 14 randomized controlled trials (RCTs) of fish-oil supplements or of diets high in n–3 FAs and in 1 prospective cohort study. Most trials reported that fish oil significantly reduced all-cause mortality, myocardial infarction, cardiac and sudden death, or stroke. Primary prevention of cardiovascular disease was reported in 1 RCT, in 25 prospective cohort studies, and in 7 case-control studies. No significant effect on overall deaths was reported in 3 RCTs that evaluated the effects of fish oil in patients with implantable cardioverter defibrillators. Most cohort studies reported that fish consumption was associated with lower rates of all-cause mortality and adverse cardiac outcomes. The effects on stroke were inconsistent. Evidence suggests that increased consumption of n–3 FAs from fish or fish-oil supplements, but not of α-linolenic acid, reduces the rates of all-cause mortality, cardiac and sudden death, and possibly stroke. The evidence for the benefits of fish oil is stronger in secondary- than in primary-prevention settings. Adverse effects appear to be minor.

Super Berry Green Tea Plus

1.  Bagchi D, Sen CK, Ray SD, et al. (Feb-Mar 2003). "Molecular mechanisms of cardioprotection by a novel grape seed proanthocyanidin extract". Mutat Res. 523-524: 87–97.

*Quick Summary of Study: Grape Seed extract was shown to decrease oxidation of LDLs, high levels of which can contribute to cardiovascular disease.

http://www.ncbi.nlm.nih.gov/pubmed/12628506

Abstract

Free radicals and oxidative stress play a crucial role in the pathophysiology of a broad spectrum of cardiovascular diseases including congestive heart failure, valvular heart disease, cardiomyopathy, hypertrophy, atherosclerosis and ischemic heart disease. We have demonstrated that IH636 grape seed proanthocyanidin extract (GSPE) provides superior antioxidant efficacy as compared to Vitamins C, E and beta-carotene. A series of studies were conducted using GSPE to demonstrate its cardioprotective ability in animals and humans. GSPE supplementation improved cardiac functional assessment including post-ischemic left ventricular function, reduced myocardial infarct size, reduced ventricular fibrillation (VF) and tachycardia, decreased the amount of reactive oxygen species (ROS) as detected by ESR spectroscopy and reduced malondialdehyde (MDA) formation in the heart perfusate. Cardiomyocyte apoptosis detected by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining. In concert, the proapoptotic signals mediated by JNK-l and c-fos proteins were also reduced suggesting that the novel cardioprotective properties of GSPE may be at least partially attributed to its ability to block anti-death signaling mediated through the proapoptotic transcription factors and genes such as JNK-1 and c-JUN. In a separate study, GSPE pretreatment significantly inhibited doxorubicin-induced cardiotoxicity as demonstrated by reduced serum creatine kinase (CK) activity, DNA damage and histopathological changes in the cardiac tissue of mice. Concentration-dependent efficacy of GSPE was also assessed in a hamster atherosclerosis model. Approximately 49 and 63% reduction in foam cells, a biomarker of early stage atherosclerosis, were observed following supplementation of 50 and 100 mg GSPE/kg body weight, respectively. A human clinical trial was conducted on hypercholesterolemic subjects. GSPE supplementation significantly reduced oxidized LDL, a biomarker of cardiovascular diseases. Finally, a cDNA microarray study demonstrated significant inhibition of inducible endothelial CD36 expression, a novel cardioregulatory gene, by GSPE. These results demonstrate that GSPE may serve as a potential therapeutic tool in promoting cardiovascular health via a number of novel mechanisms.

2. University of California, Davis - Health System (2006, March 27). Study Shows Grape Seed Extract May Be Effective In Reducing Blood Pressure. ScienceDaily. Retrieved August 11, 2011, from http://www.sciencedaily.com

3. Vitseva O, Varghese S Chakrabarti S; Folts J, Freedman J. Grape Seed and Skin Extracts Inhibit Platelet Function and Release of Reactive Oxygen Intermediates. Journal of Cardiovascular Pharmacology. October 2005. 46(4): 445-451.

*Quick Summary of Study: Grape seeds were shown to reduce inflammation and oxidative stress on platelets during in vitro studies.

http://journals.lww.com/cardiovascularpharm/Fulltext/2005/10000/Grape_Seed_and_Skin_Extracts_Inhibit_Platelet.7.aspx

Abstract

Red wine and purple grape juice contain polymeric flavonoids with antioxidant properties believed to be protective against cardiovascular events but the alcohol and sugar content of these beverages has curtailed their medicinal use. Acute cardiac events are also associated with enhanced inflammation and thrombosis. In this study, the extracts from grape skins or seeds were examined for their anti-inflammatory properties and effect on platelet release of reactive oxygen intermediates. Incubation of platelets with seed or skin extract led to a decrease in platelet aggregation from 68.8 ± 19.8% to 45 ± 3.6% for seeds and to 27 ± 7.2% for skin, respectively (P < 0.05). Platelet incubation with grape skin or seed extracts led to a marked decrease in superoxide release from 73 ± 6.2 to 2 ± 3.4 for grape seeds and to 0.33 ± 0.57 for grape skin (chemilum. units; P < 0.05) as well as a significant increase in radical-scavenging activity, decrease in reactive oxygen species release by confocal microscopy, and enhanced platelet NO was measured using an NO-sensitive microelectrode. These effects were dose dependent for both grape extracts. Coincubation with seeds and skins led to additive inhibition of platelet aggregation, enhanced NO release, and prevented superoxide production. Incubation with seed or skin extracts led to an immediate attenuation of release of the inflammatory mediator, soluble CD40 ligand. Thus, the extracts from purple grape skins and seeds inhibit platelet function and platelet-dependent inflammatory responses at pharmacologically relevant concentrations. These findings suggest potentially beneficial platelet-dependent antithrombotic and anti-inflammatory properties of purple grape-derived flavonoids.

Inflacalm

1. Rani MP, Padmakumari KP, Sankarikutty B, Cherian OL, Nisha VM, Raghu KG. Inhibitory potential of ginger extracts against enzymes linked to type 2 diabetes, inflammation and induced oxidative stress. Int J Food Sci Nutr. 2001 Mar; 62(2): 106-110

*Quick Summary of Study: Ginger extracts were shown to inhibit key enzymes within the inflammatory cascade.

http://www.ncbi.nlm.nih.gov/pubmed/20874376

Abstract

Ginger (Zingiber officinale Roscoe) continues to be used as an important cooking spice and herbal medicine around the world. Gingerols, the major pungent components of ginger, are known to improve diabetes, including the effect of enhancement against insulin sensitivity. In the current study, ginger sequentially extracted with different solvents-namely, hexane, ethyl acetate, methanol, 70% methanol-water and water-were screened to determine the variations in phenolic-linked active constituents. The potential of these extracts to inhibit key enzymes relevant to type 2 diabetes and inflammation was studied. Phenolic compounds-namely, gingerols and shoagols-were quantified using high-performance liquid chromatography. Ethyl acetate extract showed higher activity compared with other extracts. These studies indicate that ginger has very good potential for α-glucosidase and α-amylase inhibition relevant for type 2 diabetes management and cyclooxygenase inhibition for inflammation.

2. Lampe J. Spicing up a vegetarian diet: chemopreventive effects of phytochemicals. American Journal of Clinical Nutrition. 2003 Sept; 78(3): 5795-5835.

http://www.ajcn.org/content/78/3/579S.full?sid=c228e88a-5e38-45b4-bbf4-517ddf15213a

*Quick Summary of Study: This article explores the beneficial effects of phytochemicals form herbs and other common spices on human health.

Abstract

Thousands of chemical structures have been identified in plant foods. Many are found in spices. Typically, spices are the dried aromatic parts of plants—generally the seeds, berries, roots, pods, and sometimes leaves—that mainly, but not invariably, grow in hot countries. Given the wide range of botanical species and plant parts from which spices are derived, they can contribute significant variety and complexity to the human diet. In the past, the medicinal uses of spices and herbs were often indistinguishable from their culinary uses, and for good reason: people have recognized for centuries both the inherent value, as well as the potential toxicity, of phytochemicals in relation to human health. Plants have the capacity to synthesize a diverse array of chemicals, and understanding how phytochemicals function in plants may further our understanding of the mechanisms by which they benefit humans. In plants, these compounds function to attract beneficial and repel harmful organisms, serve as photoprotectants, and respond to environmental changes. In humans, they can have complementary and overlapping actions, including antioxidant effects, modulation of detoxification enzymes, stimulation of the immune system, reduction of inflammation, modulation of steroid metabolism, and antibacterial and antiviral effects. Embracing a cuisine rich in spice, as well as in fruit and vegetables, may further enhance the chemopreventive capacity of one’s diet.

3. Gagnier JJ, van Tulder MW, Berman B, Bombardier C. Herbal medicine for low back pain: a Cochrane review. Spine. 2007 Jan 1; 78(3): 82-92.

*Quick Summary of Study: This article explains the role that phytochemicals can have on the immune system, digestion and the inflammatory response.

http://www.ncbi.nlm.nih.gov/pubmed/17202897

Abstract

Thousands of chemical structures have been identified in plant foods. Many are found in spices. Typically, spices are the dried aromatic parts of plants—generally the seeds, berries, roots, pods, and sometimes leaves—that mainly, but not invariably, grow in hot countries. Given the wide range of botanical species and plant parts from which spices are derived, they can contribute significant variety and complexity to the human diet. In the past, the medicinal uses of spices and herbs were often indistinguishable from their culinary uses, and for good reason: people have recognized for centuries both the inherent value, as well as the potential toxicity, of phytochemicals in relation to human health. Plants have the capacity to synthesize a diverse array of chemicals, and understanding how phytochemicals function in plants may further our understanding of the mechanisms by which they benefit humans. In plants, these compounds function to attract beneficial and repel harmful organisms, serve as photoprotectants, and respond to environmental changes. In humans, they can have complementary and overlapping actions, including antioxidant effects, modulation of detoxification enzymes, stimulation of the immune system, reduction of inflammation, modulation of steroid metabolism, and antibacterial and antiviral effects. Embracing a cuisine rich in spice, as well as in fruit and vegetables, may further enhance the chemopreventive capacity of one’s diet.

4. Meng CQ. Atherosclerosis is an inflammatory disorder after all. Curr Top Med Chem. 2006; 6(2): 93-102.
   

http://www.ncbi.nlm.nih.gov/pubmed/16454761

*Quick Summary of Study: This report explores the role that inflammation has on major diseases such as atherosclerosis.

Abstract

Inflammation has been increasingly recognized as an important player in the pathophysiology of numerous human disorders. Accumulating evidence has led to the conclusion that atherosclerosis is an inflammatory disease, although it was believed to be a disorder of high cholesterol levels in the bloodstream for over a century. Cholesterol does contribute to the pathogenesis of atherosclerosis, but through inflammatory mechanisms. Statins lower cholesterol levels and hence reduce inflammation in the vasculature and prevent heart disease. Statins may also exert anti-inflammatory effects through mechanisms independent of cholesterol lowering. Adhesion molecules, cytokines, oxidative stress, etc. appear to contribute to the inflammatory state of atherosclerosis and therapeutic approaches directed toward these markers or targets have the potential to be effective in reducing inflammation and treating atherosclerosis.

Charo IF, Taub R. Anti-inflammatory therapeutics for the treatment of atherosclerosis. Nat Rev Drug Discov. 2011 May; 10(5):365-376.

http://www.ncbi.nlm.nih.gov/pubmed/21532566

*Quick Summary of Study: This article explains how inflammation is the underlining cause in the pathogenesis of  Atherosclerosis and how therapies should target reducing inflammation as a viable means of treatment.

Abstract

Atherosclerosis is the primary cause of heart disease and stroke and is thus the underlying pathology of the leading causes of death in the western world. Although risk can be reduced by lowering lipid levels, the equally important contribution of inflammation to the development of cardiovascular disease is not adequately addressed by existing therapies. Here, we summarize the evidence supporting a role for inflammation in the pathogenesis of atherosclerosis, discuss agents that are currently in the clinic and provide a perspective on the challenges faced in the development of drugs that target vascular inflammation.

CoQ10

1. Deichmann R, Larie C, Andrews S. Coenzyme Q10 and Statin-Induced Mitochondrial Dysfunction. Ochner J. 2010 Spring; 10(2)
   

16-21

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096178/?tool=pubmed

*Quick Summary of Study: Statin drugs reduce the synthesis of coenzyme Q10 which may lead to statin-induced myopathic

Abstract

Coenzyme Q10 is an important factor in mitochondrial respiration. Primary and secondary deficiencies of coenzyme Q10 result in a number of neurologic and myopathic syndromes. Hydroxyl-methylglutaryl coenzyme A reductase inhibitors or statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of coenzyme Q10. The statin medications routinely result in lower coenzyme Q10 levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies. However, coenzyme Q10 supplements have not been shown to routinely improve muscle function. Additional research in this area is warranted and discussed in this review.

1. Crane F. Biochemical Functions of Coenzyme Q10.  J Am Coll Nutr. December 2011; 20(6): 591-598.

http://www.jacn.org/content/20/6/591.long

*Quick Summary of Study: Coenzyme Q10, which is made naturally in the body, has two main functions which include helping with ATP production in the mitochondria and undergoing oxidation/reduction reactions in cell memebranes.

Abstract

Coenzyme Q is well defined as a crucial component of the oxidative phosphorylation process in mitochondria which converts the energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis. New roles for coenzyme Q in other cellular functions are only becoming recognized. The new aspects have developed from the recognition that coenzyme Q can undergo oxidation/reduction reactions in other cell membranes such as lysosomes, Golgi or plasma membranes. In mitochondria and lysosomes, coenzyme Q undergoes reduction/oxidation cycles during which it transfers protons across the membrane to form a proton gradient. The presence of high concentrations of quinol in all membranes provides a basis for antioxidant action either by direct reaction with radicals or by regeneration of tocopherol and ascorbate. Evidence for a function in redox control of cell signaling and gene expression is developing from studies on coenzyme Q stimulation of cell growth, inhibition of apoptosis, control of thiol groups, formation of hydrogen peroxide and control of membrane channels. Deficiency of coenzyme Q has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase inhibitors (statins) or for unknown reasons in ageing and cancer. Correction of deficiency requires supplementation with higher levels of coenzyme Q than are available in the diet.

1. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.

http://www.ncbi.nlm.nih.gov/pubmed?term=1637852

*Quick Summary of Study: Oral supplementation of CoQ10 may increase resistance to LDL oxidation.

Abstract

Ubiquinol-10 (CoQH2, the reduced form of coenzyme Q10) is a potent antioxidant present in human low-density lipoprotein (LDL). Supplementation of humans with ubiquinone-10 (CoQ, the oxidized coenzyme) increased the concentrations of CoQH2 in plasma and in all of its lipoproteins. Intake of a single oral dose of 100 or 200 mg CoQ increased the total plasma coenzyme content by 80 or 150%, respectively, within 6 h. Long-term supplementation (three times 100 mg CoQ/day) resulted in 4-fold enrichment of CoQH2 in plasma and LDL with the latter containing 2.8 CoQH2 molecules per LDL particle (on day 11). Approx. 80% of the coenzyme was present as CoQH2 and the CoQH2/CoQ ratio was unaffected by supplementation, indicating that the redox state of coenzyme Q10 is tightly controlled in the blood. Oxidation of LDL containing various [CoQH2] by a mild, steady flux of aqueous peroxyl radicals resulted immediately in very slow formation of lipid hydroperoxides. However, in each case the rate of lipid oxidation increased markedly with the disappearance of 80-90% CoQH2. Moreover, the cumulative radical dose required to reach this 'break point' in lipid oxidation was proportional to the amount of CoQH2 incorporated in vivo into the LDL. Thus, oral supplementation with CoQ increases CoQH2 in the plasma and all lipoproteins thereby increasing the resistance of LDL to radical oxidation.

4. Mabuchi H, Higashikata T, Kawashiri M, Katsuda S, Mizuno M, Nohara A, Inazu A, Koizumi J, Kobayashi J.Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients. J Atheroscler Thromb. 2005;12(2):111-9.

http://www.jstage.jst.go.jp/article/jat/12/2/111/_pdf

*Quick Summary of Study: Statin drugs act as a HMG-CoA reductase inhibitor that leads to not only the reduction of cholesterol synthesis but also the reduction of serum CoQ10 levels which may have associated risks.

Abstract

Reduction of serum cholesterol levels with statin therapy decreases the risk of coronary heart disease. Inhibition of HMG-CoA reductase by statin results in decreased synthesis of cholesterol and other products downstream of mevalonate, which may produce adverse effects in statin therapy. We studied the reductions of serum ubiquinol-10 and ubiquinone-10 levels in hypercholesterolemic patients treated with atorvastatin. Fourteen patients were treated with 10 mg/day of atorvastatin, and serum lipid, ubiquinol-10 and ubiquinone-10 levels were measured before and after 8 weeks of treatment. Serum total cholesterol and LDL-cholesterol levels decreased significantly. All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels, and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 +/- 0.21 to 0.46 +/- 0.10 microg/ml (p < 0.0001), and from 0.10 +/- 0.06 to 0.06 +/- 0.02 microg/ml (p = 0.0008), respectively. Percent reductions of ubiquinol-10 and those of total cholesterol showed a positive correlation (r = 0.627, p = 0.0165). As atorvastatin reduces serum ubiquinol-10 as well as serum cholesterol levels in all patients, it is imperative that physicians are forewarned about the risks associated with ubiquinol-10 depletion.