Introduction
Influenza A Virus
Influenza viruses are enveloped viruses with segmented, single‐stranded, negative‐sense RNA genomes. Every year, influenza epidemics cause numerous deaths and millions of hospitalizations, but the most frightening effects are seen when new strains of the virus emerge, causing worldwide outbreaks of infection. Recent reports of direct avian‐to‐human transmission of influenza make the prospect of a new pandemic particularly alarming. The replication of influenza virus has been studied in depth, and several antiviral compounds have been developed, but their long‐term efficacy is often limited by toxicity and the almost inevitable selection of drug‐resistant viral mutants.Influenza A virus strains are categorized according to two proteins found on the surface of the virus: hemagglutinin (H) and neuraminidase (N). All influenza A viruses contain hemagglutinin and neuraminidase, but the structure of these proteins differ from strain to strain due to rapid genetic mutation in the viral genome.
Influenza A virus strains are assigned an H number and an N number based on which forms of these two proteins the strain contains. There are 16 H and 9 N subtypes known in birds, but only H 1, 2 and 3, and N 1 and 2 are commonly found in humans.
Resveratrol
Resveratrol (RV; 3,5,4′‐trihydroxy‐trans‐stilbene) is a polyphenol that is synthesized by at least 72 plant species, including grapes (50–100 μg/g of RV) and other fruits, in response to physiological stimuli and environmental stress. Its health benefits include cardio‐ and neuroprotective effects and anticarcinogenic activity. Some researchers have reported that RV also inhibits the replication of herpes simplex virus and synergistically enhances the effects of known anti‐HIV drugs, but the mechanisms underlying these actions remain obscure. RV appears to be capable of interfering with several intracellular signaling pathways, including those activated by protein kinase C (PKC) and by mitogen‐activated protein kinases (MAPKs). It has documented antioxidant activity , and its cardioprotective effects have been related to its inhibition of lipid peroxidation and the oxidation of low‐density lipoproteins .
Discussion
There is increasing evidence that the oxidoreductive (redox) balance of cells is involved in viral infections and that certain antioxidant molecules exert potent antiviral activities in vitro and in vivo.According to a study by Dr Anna T. Palamara,on her paper>Inhibition of Influenza A Virus Replication by Resveratrol
Anna T. Palamara,1 Lucia Nencioni,1 Katia Aquilano,2 Giovanna De Chiara,3 Leyanis Hernandez,3 Federico Cozzolino,4 Maria R. Ciriolo,2 and Enrico Garaci3
They have previously demonstrated that RNA and DNA viruses can deplete host‐cell levels of the antioxidant glutathione (GSH) and that the administration of exogenous GSH inhibits viral replication in several experimental systems. These observations prompted them to investigate RV’s potential for inhibiting the replication of influenza virus and the possible mechanisms underlying these effects. They found that RV strongly inhibits the replication of influenza A virus in vitro but that this effect did not seem to be directly related to GSH‐mediated antioxidant activity. Instead, it appeared to involve the blockade of nuclear‐cytoplasmic translocation of viral ribonucleoproteins (vRNPs) and reduced expression of late viral proteins, and these effects were related to the inhibition of PKC activity and its dependent pathways. In in vivo studies, RV also improved survival and decreased pulmonary viral titers in influenza virus–infected mice.
Its is also shown that RV, a natural polyphenol whose concentration in red wine is 1.5–3.0 mg/L, can inhibit the in vitro and in vivo replication of influenza A virus without producing any significant toxicity. The drug’s effects involved blockade of the nuclear‐cytoplasmic translocation of vRNP complexes, decreased expression of late viral proteins, and an inhibition of cellular PKC activity and its dependent pathways.
Depletion of host‐cell GSH is a direct consequence of several viral infections, and various antioxidant substances display strong antiviral activities. RV has been characterized as a potent free‐radical scavenger, and it has reportedly increased GSH levels in different experimental models. Therefore, their in vitro findings of decreased GSH levels in uninfected cells treated with RV and its mild effect in restoring the GSH depletion provoked by viral infection were somewhat unexpected. However, natural phenols can produce in vivo antioxidant or pro‐oxidant effects, depending on their own oxidative status, which, in turn, reflects the specific redox potential in the microenvironment. Thus, although RV can quench reactive free radicals by donating hydrogen atoms, this process also generates phenoxyl radicals that can oxidize GSH to GS•. Moreover, the oxidation of the RV‐phenoxyl radical produces an RV‐quinone form, which can alkylate GSH and further diminish intracellular concentrations of free GSH. Our findings suggest that RV’s inhibition of PR8 replication involves mechanisms other than a GSH‐mediated modulation of the cell redox state, although they cannot exclude the possibility that the RV quinone is involved in the drug’s inhibition of virus growth.
RV had little effect on early viral protein expression, but it dose‐dependently inhibited the expression of M1 and HA. That mRNA for these late viral proteins was efficiently transcribed in the presence of RV suggests that the drug acts on posttranscriptional phases of the viral life cycle. This hypothesis was confirmed by immunofluorescence data that showed an RV‐induced blockade of the nucleocytoplasmic translocation of vRNPs. Inhibition of influenza virus replication, with decreased production of HA and M1 and nuclear retention of vRNPs, is also produced by the broad‐spectrum kinase inhibitor H7, and this similarity suggests that kinase inhibition might be involved in RV’s antiviral effects.
Influenza A virus infection causes the activation of various MAPK pathways , including the p38MAPK and JNK pathways (which are thought to play roles in the inflammatory and apoptotic responses and the Raf/MEK/ERK cascade. Blockade of the latter pathway with the ERK inhibitor U0126 results in nuclear retention of vRNPs and diminished virus production but has no effect on the expression of late viral protein. Phosphorylation events also seem to play crucial roles in other steps of the influenza virus life cycle, such as cell penetration and budding.
The influenza A virus has 6 phosphorylated proteins, including NP . That both H7 and U0126 block the export of vRNPs to the cytosol strongly suggests that a phosphorylation event is required for efficient nuclear export of NP, but the specific kinase responsible for this event has not been identified .Pleschka et al reported that NP phosphorylation is not directly affected by the ERK inhibitor U0126 and suggested that vRNP export might even depend on the phosphorylation of a cellular factor.
RV reportedly interferes with signaling cascades by modulating the activities of kinases and other enzymes—for example, the inhibition of PKC activity. It also exerts modulatory effects on MAPK pathways as a consequence of the inhibition of PKC activity. In the present study, RV efficiently inhibited the PR8‐ and TPA‐induced phosphorylation of PKD, a downstream effector of PKC, as well as that of p38MAPK and JNK. That ERK activation was not affected by RV is consistent with previous observations and suggests that (1) different PKC isoenzymes can be involved in the activation of different MAPK pathways and (2) the functional outcome is both isoenzyme and cell‐type specific. Their data strongly suggest that RV’s antiviral effects are related to the inhibition of PKC activity and its dependent pathways. Studies are already under way to identify the cellular and/or viral substrates of RV‐inhibited kinases and their specific roles in the PR8 life cycle.
RV’s in vitro antiviral effects were mirrored in a murine model of influenza. Treatment of PR8‐infected mice markedly improved their survival, decreased pulmonary virus titers, and caused no significant toxicity. The latter finding is consistent with the results of previous in vivo studies, including some in which RV was administered at doses higher than the ones that they have used . Different mechanisms might underlie the in vivo efficacy of RV documented in their study. RV inhibits several cell‐signaling pathways that are involved in the inflammatory airway damage that is characteristic of influenza disease. This finding raises the possibility that the survival benefits of RV observed in their study involved a dual mechanism: inhibition of both viral replication and NF‐κB–induced inflammation. Studies under way in their laboratory of inflammatory‐cytokine levels in PR8‐infected mice treated with RV should shed more light on this hypothesis.
All currently approved anti‐influenza drugs target essential viral functions and/or structures, and the major drawback of this approach is that the virus will eventually adapt to the selective pressure exerted by the drug . Inactivation of host‐cell functions that are essential for virus replication, which seems to be the mechanism of RV’s anti‐influenza activity, offers 2 important advantages: not only it is more difficult for the virus to adapt to, but it can also be expected to affect viral replication independently of the invader’s type, strain, and antigenic properties. For these reasons, RV merits further investigation as a potential weapon for combating the growing threat of influenza.
Saturday, June 27, 2009
Tuesday, May 5, 2009
Swine Flu versus Lifepak *Transmission of disease
Transmission
Transmission between pigs
Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US.Antibodies to the virus are also common in pigs in other countries.
Transmission to humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur.
Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa.This study among others forms the basis of a recommendation that peole whose jobs involve handling poultry and swine be the focus of increased public health surveilance.
Interaction with avian H5N1 in pigs
Pigs are unusual as they can be infected with influenza strains that usually infect three different species: pigs, birds and humans.This makes pigs a host where influenza viruses might exchange genes, producing new and dangerous strains.Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains.H3N2 evolved from H2N2 by antigenic shift.In August 2004, researchers in China found H5N1 in pigs.
Transmission between pigs
Influenza is quite common in pigs, with about half of breeding pigs having been exposed to the virus in the US.Antibodies to the virus are also common in pigs in other countries.
Transmission to humans
People who work with poultry and swine, especially people with intense exposures, are at increased risk of zoonotic infection with influenza virus endemic in these animals, and constitute a population of human hosts in which zoonosis and reassortment can co-occur.
Transmission of influenza from swine to humans who work with swine was documented in a small surveillance study performed in 2004 at the University of Iowa.This study among others forms the basis of a recommendation that peole whose jobs involve handling poultry and swine be the focus of increased public health surveilance.
Interaction with avian H5N1 in pigs
Pigs are unusual as they can be infected with influenza strains that usually infect three different species: pigs, birds and humans.This makes pigs a host where influenza viruses might exchange genes, producing new and dangerous strains.Avian influenza virus H3N2 is endemic in pigs in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains.H3N2 evolved from H2N2 by antigenic shift.In August 2004, researchers in China found H5N1 in pigs.
Swine Flu versus Lifepak *introduction/History
Swine influenza (also called swine flu, hog flu, and pig flu) refers to influenza caused by those strains of influenza virus, called swine influenza virus (SIV), that usually infect pigs.
Transmission of swine influenza virus from pigs to humans is not common and properly cooked pork poses no risk of infection. When transmitted, the virus does not always cause human influenza and often the only sign of infection is the presence of antibodies in the blood, detectable only by laboratory tests. When transmission results in influenza in a human, it is called zoonotic swine flu.
In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.
The 2009 flu outbreak in humans, known as "swine flu", is due to a new strain of influenza A virus subtype H1N1 that contained genes most closely related to swine influenza.The origin of this new strain is unknown, however, and the World Organization for Animal Health (OIE) reports that this strain has not been isolated in pigs. This strain can be transmitted from human to human,and causes the normal symptoms of influenza.
History
Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930.
1918 pandemic in humans
The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs,thus may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that, in this case, pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918, after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and swine suggests that the 1918 outbreak in humans followed a reassortment event within a mammal, the exact origin of the 1918 strain remains elusive.
1976 U.S. outbreak
Main article: 1976 swine flu outbreak
On February 5, 1976, in the United States an army recruit at Fort Dix said he felt tired and weak. He died the next day and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced that the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1). It was detected only from January 19 to February 9 and did not spread beyond Fort Dix.
President Ford receives swine flu vaccination
This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic.
1988 zoonosis
In September 1988, a swine flu virus killed one woman in Wisconsin, and infected at least hundreds of others. 32-year old Barbara Ann Wieners was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at the Walworth County Fair. Barbara died eight days later, though doctors were able to induce labor and deliver a healthy daughter before she passed away. Her husband recovered from his symptoms.
Influenza-like illnesses were reportedly widespread among the pigs at the farm they had visited, and 76% of the swine exhibitors there tested positive for antibody to SIV, but no serious illnesses were detected among this group. Additional studies suggested between one and three health care personnel who had contact with the patient developed mild influenza-like illnesses with antibody evidence of swine flu infection.However, there was no community outbreak.
1998 US outbreak in swine
In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found that this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains.
2007 Philippine outbreak in swine
On August 20, 2007 Department of Agriculture officers investigated the outbreak (epizootic) of swine flu in Nueva Ecija and Central Luzon, Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera. On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and 5 regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga, even if these tested negative for the swine flu virus.
Transmission of swine influenza virus from pigs to humans is not common and properly cooked pork poses no risk of infection. When transmitted, the virus does not always cause human influenza and often the only sign of infection is the presence of antibodies in the blood, detectable only by laboratory tests. When transmission results in influenza in a human, it is called zoonotic swine flu.
In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general, namely chills, fever, sore throat, muscle pains, severe headache, coughing, weakness and general discomfort.
The 2009 flu outbreak in humans, known as "swine flu", is due to a new strain of influenza A virus subtype H1N1 that contained genes most closely related to swine influenza.The origin of this new strain is unknown, however, and the World Organization for Animal Health (OIE) reports that this strain has not been isolated in pigs. This strain can be transmitted from human to human,and causes the normal symptoms of influenza.
History
Swine influenza was first proposed to be a disease related to human influenza during the 1918 flu pandemic, when pigs became sick at the same time as humans. The first identification of an influenza virus as a cause of disease in pigs occurred about ten years later, in 1930.
1918 pandemic in humans
The 1918 flu pandemic in humans was associated with H1N1 and influenza appearing in pigs,thus may reflect a zoonosis either from swine to humans, or from humans to swine. Although it is not certain in which direction the virus was transferred, some evidence suggests that, in this case, pigs caught the disease from humans. For instance, swine influenza was only noted as a new disease of pigs in 1918, after the first large outbreaks of influenza amongst people. Although a recent phylogenetic analysis of more recent strains of influenza in humans, birds, and swine suggests that the 1918 outbreak in humans followed a reassortment event within a mammal, the exact origin of the 1918 strain remains elusive.
1976 U.S. outbreak
Main article: 1976 swine flu outbreak
On February 5, 1976, in the United States an army recruit at Fort Dix said he felt tired and weak. He died the next day and four of his fellow soldiers were later hospitalized. Two weeks after his death, health officials announced that the cause of death was a new strain of swine flu. The strain, a variant of H1N1, is known as A/New Jersey/1976 (H1N1). It was detected only from January 19 to February 9 and did not spread beyond Fort Dix.
President Ford receives swine flu vaccination
This new strain appeared to be closely related to the strain involved in the 1918 flu pandemic.
1988 zoonosis
In September 1988, a swine flu virus killed one woman in Wisconsin, and infected at least hundreds of others. 32-year old Barbara Ann Wieners was eight months pregnant when she and her husband, Ed, became ill after visiting the hog barn at the Walworth County Fair. Barbara died eight days later, though doctors were able to induce labor and deliver a healthy daughter before she passed away. Her husband recovered from his symptoms.
Influenza-like illnesses were reportedly widespread among the pigs at the farm they had visited, and 76% of the swine exhibitors there tested positive for antibody to SIV, but no serious illnesses were detected among this group. Additional studies suggested between one and three health care personnel who had contact with the patient developed mild influenza-like illnesses with antibody evidence of swine flu infection.However, there was no community outbreak.
1998 US outbreak in swine
In 1998, swine flu was found in pigs in four U.S. states. Within a year, it had spread through pig populations across the United States. Scientists found that this virus had originated in pigs as a recombinant form of flu strains from birds and humans. This outbreak confirmed that pigs can serve as a crucible where novel influenza viruses emerge as a result of the reassortment of genes from different strains.
2007 Philippine outbreak in swine
On August 20, 2007 Department of Agriculture officers investigated the outbreak (epizootic) of swine flu in Nueva Ecija and Central Luzon, Philippines. The mortality rate is less than 10% for swine flu, unless there are complications like hog cholera. On July 27, 2007, the Philippine National Meat Inspection Service (NMIS) raised a hog cholera "red alert" warning over Metro Manila and 5 regions of Luzon after the disease spread to backyard pig farms in Bulacan and Pampanga, even if these tested negative for the swine flu virus.
Sunday, February 8, 2009
Skin Carotenoid Score
Your Skin Carotenoid Score is a measurement of the presence of carotenoid antioxidants in your skin. Carotenoids are powerful antioxidants found in abundance in certain fruits and vegetables. Carotenoids neutralize damaging free radical molecules and are absorbed in human plasma and tissue, providing an excellent indicator of a person’s antioxidant level. Unlike other methods of measuring antioxidants (which fluctuate throughout the day), your Skin Carotenoid Score shows the stable level of carotenoid antioxidants in your skin - providing you with a more accurate and reliable biomarker of your antioxidant level. (The scoring system is based on data gathered from more than 1,300 individuals with a variety of diets.) Your Skin Carotenoid Score will help you determine whether you are consuming an adequate amount of antioxidant-containing nutrients. Unlike other biomarkers that you may be familiar with, your Skin Carotenoid Score does not predict disease or pre-condition of disease.
How can I improve my score?
You can begin by making a daily commitment to supplement your diet with LifePak or LifePak Nano and g3, the premium Pharmanex antioxidant/vitamin/mineral supplements. You can track your subsequent Skin Carotenoid Scores to determine if your score is improving.This proprietary supplement contains comprehensive levels of antioxidants, bone nutrients, cardio nutrients, and B vitamins for vitality and general wellness*. A doubleblind clinical study showed that control groups that regularly consumed LifePak® had dramatically higher antioxidant levels than control groups that did not.† Using LifePak® and tracking your Skin Carotenoid Score over time will provide you with personal evidence of the antioxidant benefits demonstrated in the LifePak® clinical study.You won't find comparable clinical evidence and testing programs with any other supplement available today.
In addition to taking LifePak®, you can improve your score by consuming five or more servings of fruits and vegetables each day that are rich in carotenoid antioxidants, as recommended by the USDA, the American Dietetics Association, and other health organizations. Be aware, however, that individual responses to dietary intake of carotenoid antioxidants may vary due to biological differences in the ability to absorb dietary carotenoids. Lifestyles that include eating foods fried in saturated oils, exposure to pollution, exposure to cigarette smoke, and prolonged sun exposure may negatively influence your antioxidant defense levels. Changes you make to your diet or lifestyle activities - in an effort to improve your score - will take about 30 to 60 days before they are reflected in your Skin Carotenoid Score.
Sunday, January 25, 2009
Alpha lipoic acid
What is Alpha Lipoic Acid?
Other names: lipoic acid, thioctic acid, ALA
Alpha lipoic acid is a fatty acid found naturally inside every cell in the body. It's needed by the body to produce the energy for our body's normal functions. Alpha lipoic acid converts glucose (blood sugar) into energy.Function;
Reasons For Use
Lipoic Acid is the only antioxidant that is fat- and water-soluble. This property has made it a perfect electron transporter for both oxidized ascorbic acid (water-soluble) and vitamin E (fat-soluble); it is easily absorbed and transported across cell membranes. Whereas many antioxidants only provide protection outside of cells, ALA is broken down inside cells to dihydrolipoic acid - an even more potent antioxidant. It also regenerates other antioxidants like vitamin C, vitamin E and glutathione
Food sources
Lipoic acid is found in a variety of foods, notably kidney, heart and liver meats as well as spinach, broccoli and potatoes.
Alpha lipoic acid is also an antioxidant, a substance that neutralizes potentially harmful chemicals called free radicals. What makes alpha lipoic acid unique is that it functions in water and fat, unlike the more common antioxidants vitamins C and E, and it appears to be able to recycle antioxidants such as vitamin C and glutathione after they have been used up. Glutathione is an important antioxidant that helps the body eliminate potentially harmful substances. Alpha lipoic acid increases the formation of glutathione.
Alpha lipoic acid is made by the body and can be found in very small amounts in foods such as spinach, broccoli, peas, Brewer's yeast, brussel sprouts, rice bran, and organ meats. Alpha lipoic acid supplements are available in capsule form at health food stores, some drugstores, and online. For maximum absorption, the supplements should be taken on an empty stomach.
Why People Use Alpha Lipoic Acid
# Peripheral Neuropathy
Peripheral neuropathy can be caused by injury, nutritional deficiencies, chemotherapy or by conditions such as diabetes, Lyme disease, alcoholism, shingles, thyroid disease, and kidney failure. Symptoms can include pain, burning, numbness, tingling, weakness, and itching.
Alpha lipoic acid is thought to work as an antioxidant in both water and fatty tissue, enabling it to enter all parts of the nerve cell and protect it from damage.
Preliminary studies suggest that alpha lipoic acid may help. In one of the largest studies on the use of alpha lipoic acid, 181 people took 600 mg, 1200 mg or 1800 mg of alpha lipoic acid a day or a placebo. After 5 weeks, alpha lipoic acid improved symptoms. The dose that was best tolerated while still providing benefit was 600 mg once daily.
# Brain Function
Alpha lipoic acid can cross the blood-brain barrier, a wall of tiny vessels and structural cells, and pass easily into the brain. It is thought to protect brain and nerve tissue by preventing free radical damage.
# Age-Related Conditions
As an antioxidant, alpha lipoic acid can neutralize free radicals which can damage cells. Free radical damage is thought to contribute to aging and chronic illness.
# Other Conditions
Alpha lipoic acid has also been suggested for cataracts, glaucoma, multiple sclerosis, burning mouth syndrome, Alzheimer's disease and stroke, but large, well-designed studies are needed to see if it's effective for these conditions.
for more information in depth reagarding Alpha lipoic acid do visit the website below:
http://lpi.oregonstate.edu/infocenter/othernuts/la/#intro
Saturday, January 24, 2009
Resveratrol: Clinical and Anti-Aging Benefits
Resveratrol: Clinical and Anti-Aging Benefits
Resveratrol (3,5,4’-trihydroxy-trans-stilbene) (Fig. 1) is a compound found in the skins of red fruits, grapes, seeds, berries (especially, mulberries), peanuts, red wine, various herbs, and propolis (a natural honeybee product). Resveratrol occurs in two forms — cis and trans resveratrol — but it is the trans isomer that is biologically active. This article reviews resveratrol’s history, mechanisms, dosage and broad range of clinical uses and anti-aging potential.
The Resveratrol Story
Resveratrol was first identified in the early 1980s as the principal active ingredient in the dried roots of Polygonum cuspidatum. As a traditional Japanese and Chinese medicine, Polygonum extracts have been used to treat a wide range of afflictions, including fungal infections, various skin inflammations, and liver and cardiovascular diseases.1
In the early 1990s, scientists were attempting to unravel the “French paradox”—i.e., the surprisingly low incidence of cardiovascular disease observed in France among people consuming a rich, high-fat diet.2 Researchers proposed that the “paradox” may be due to the routine consumption by the French of resveratrol-rich red wine.
Studies that subsequently compared alcohol consumption to the risk of death from coronary heart disease (CHD) revealed that those with the lowest risk drank red wine, while those who preferred other alcoholic beverages had the highest risk.3 Scientists also discovered that when healthy subjects were given pure alcohol or red wine for 15 days, pure alcohol increased platelet aggregation (a cause of heart attack and stroke-producing blood clots); however, red wine decreased platelet aggregation while elevating HDL-cholesterol (“good” cholesterol).
As scientists began to appreciate the cardiovascular benefits conferred by red wine polyphenols—especially, resveratrol—a blockbuster article in the prestigious journal Science electrified the scientific community with the finding that “Resveratrol inhibits cellular events associated with tumor initiation, promotion and progression.” In other words, resveratrol blocks all three mechanisms of cancer formation!4 But resveratrol’s effects don’t stop there.
Mechanisms and Potential Clinical Uses of Resveratrol
Cardio-Protective Effects
* Resveratrol has been shown to protect the cardiovascular system by multiple mechanisms. Among these are:
* protecting against ischemia-reperfusion injury (see next paragraph)
* promoting vasorelaxation (i.e., protect against vasospasm)
* protecting and maintaining the smooth, single cell-thick lining of the arteries (endothelium), which produces substances that influence arterial dilation
* inhibiting the oxidation of low-density lipoprotein (LDL)5,6
* suppressing platelet aggregation.7
“Ischemia-reperfusion injury” refers to the extensive damage to tissues when blood flow is restored following a temporary loss of circulation. Such a situation occurs due to spasm of an artery, or temporary blockage of blood flow by a thrombus (blood clot), followed by resumption of blood flow.
The ischemia-reperfusion mechanism is the cause of extensive tissue damage in strokes, transient ischemic attacks (TIAs—mini strokes) and heart attacks. Resveratrol has been demonstrated to protect against ischemia-reperfusion injury not only in the heart,5,8 but also in the ovaries9 and spine.10
In these studies, resveratrol administration resulted in a number of beneficial effects, including:
* decreased cardiac arrhythmias
* reduced cardiac infarct size
* increased NO (nitric oxide) release
* decreased plasma levels of lactate dehydrogenase (LDH) and creatine kinase (CK) (indicators of tissue damage)
* decreased levels of malondial-dehyde and xanthine oxidase (indicators of oxidative stress)
* increased glutathione (a protective antioxidant).
Anti-Cancer
Cancer is one of the leading causes of death in the United States, second only to heart disease. The prognosis for patients with metastatic carcinoma of the lung, colon, breast, or prostate undergoing conventional therapeutic and surgical approaches remains dismal.
An ideal natural anti-cancer substance should have certain properties: little or no toxic effects in normal and healthy cells; high efficacy against multiple sites; capability of oral consumption; known mechanism of action; and low cost.11 Resveratrol appears to meet all these criteria.
Resveratrol
In Vitro (Cellular) Studies
Following the previously mentioned discovery of resveratrol’s ability to block all three stages of carcinogenesis, a number of cellular (in vitro) and animal (in vivo) studies were conducted to evaluate resveratrol’s anti-cancer effects on a number of tumor types. Resveratrol’s cancer fighting effects include the ability to inhibit cell proliferation and induce necrosis (cell death) and apoptosis (“cell suicide” of abnormal cells). These anti-cancer effects of resveratrol were confirmed in in vitro studies in virtually every type of human cancer on which it was tested, including:
* breast12,13
* cervix14
* ovary15
* esophagus16
* prostate17-19
* lung20-21
* neuroblastoma (NB) (an aggressive childhood cancer of the peripheral nervous system)22
* melanoma (a highly virulent form of skin cancer)23,24
* leukemia.25
In addition, resveratrol sensitizes cancer cells to enhance the effects of anti-cancer drugs, making them more effective against the target cells while reducing their toxic side effects to healthy cells.26
In Vivo (Animal) Studies
Skin Cancer: In Taiwan, a team of Chinese scientists demonstrated that resveratrol-fed mice treated topically with an agent known to cause skin cancer caused a delay in tumor formation, with fewer tumors per mouse compared to control animals.27
Hepatoma:One of the most virulent forms of cancer is that of the liver. In Asia, hepatoma is among the most common of abdominal tumors, although it is rarely found as a primary tumor in the U.S. Scientists in Japan and China treated rats implanted with hepatoma cells with resveratrol. Resveratrol, by itself, suppressed tumor growth and reduced metastases in two studies.6,28 When used in conjunction with the anti-cancer drug 5-FU, resveratrol enhanced the efficacy of the drug and reduced its toxicity.29
Glioma: In animals implanted subcutaneously with gliomas (a type of brain tumor), resveratrol exerted significant antitumor effects, including slower tumor growth rate, longer animal survival time, and higher animal survival rate. The scientists concluded that resveratrol should be considered a possible treatment strategy for gliomas.30
Endocrine Normalizer
Resveratrol also acts as an estrogen receptor sensitizer (i.e., estrogen receptor agonist).31,32 This means that resveratrol will help maintain normal levels of estrogen, and that what estrogen is available will work more efficiently, with fewer estrogenic side effects.
In addition, scientists at the City of Hope in Duarte, California, recently provided evidence that resveratrol is also a potent aromatase inhibitor.33,34 Aromatase is the enzyme that converts testosterone to estrogen. Men who supplement their regimens with testosterone or testosterone precursors to normalize hormone levels (as well as bodybuilders who use testosterone and anabolic steroids) risk their testosterone also elevating their estrogen levels.
One effective way to prevent testosterone from elevating estrogen levels is to use the highly effective (and very expensive) prescription drug, Arimidex®, in a dose of about 1 mg two times per week. However, resveratrol may offer a far less expensive, natural solution to the problem of estrogen excess in men, as well as for women who require aromatase inhibitors in the treatment of cancer.
Other Potential Mechanisms / Clinical Uses
In addition to its unparalleled potential as a cardioprotectant and anti-cancer agent, resveratrol has a number of other beneficial effects including:
* anti-inflammatory35,36
* anti-infective against fungi37 and viruses (herpes simplex)38
* neuroprotective,39-43 including protection from noise-induced hearing loss.44
Anti-Aging / Life-Extension Potential of Resveratrol
Caloric restriction has been shown repeatedly to be one of the most effective means of slowing the rate of aging and extending lifespan. Severely reducing food intake of laboratory mice can increase their lifespan to the human equivalent of 162 years. Experiments demonstrate similar gains in maximum lifespan in virtually every organism in which caloric restriction has been tested. Nevertheless, despite the potential increase in lifespan that could be gained with caloric restriction, few humans willingly choose to live in a constant state of semi-starvation for even a few days, let alone 162 years.
Although the mechanism for the anti-aging effect of caloric restriction has remained elusive, scientists recently identified a class of regulatory “longevity genes”—that are shared by almost all living organisms—which they believe may be at least partially responsible for the effect of caloric restriction. These genes function to enhance survival during times of stress, such as during drought or famine, and have been designated as sirtuins (derived from the term silent information regulator proteins). Once triggered by environmental cues, the longevity genes “switch on” and induce defensive changes at the cellular level, such as slowing metabolism and enhancing cellular respiration to help the body adapt.45
The human sirtuin, SIRT-1, for example, has been shown to suppress the p53 enzyme system that helps to inhibit tumor growth and trigger cell death (apoptosis). By suppressing p53 activity, SIRT-1 prevents premature aging and apoptosis that is induced when cellular DNA is damaged or stressed, thus giving cells an opportunity to repair the damage. A second sirtuin found in yeast, SIR2, has also been shown to become activated when placed under stress. SIR2 increases DNA stability and speeds cellular repairs, while increasing total cell lifespan.46
Intrigued by the positive health benefits of caloric restriction, a research team from Harvard University began to search for other methods of modulating sirtuin activity without resorting to starvation. The researchers discovered that several plant metabolites acted as sirtuin-activating compounds (STACs), and that the most potent activator of sirtuins was resveratrol.
To test the ability of resveratrol to activate sirtuins in living creatures, the Harvard researchers selected yeast, a single-celled organism that is closely related to animals, including humans. The research team hypothesized that if resveratrol was effective in triggering sirtuin production, it would closely reflect the protein’s role in lifespan extension, at least for yeast. Their study found that even small doses of resveratrol helped yeast cells live as much as 60 to 80 percent longer, as measured by the number of generations. Yeast treated with resveratrol lived for an average of 38 generations, as compared to only 19 generations for untreated yeast47 (Fig. 2).
Additional experiments with human cells found that resveratrol enabled 30 percent of the treated human cells to survive gamma radiation compared to 10 percent of untreated cells. In the paper, the Harvard researchers also report that preliminary experiments with flies and worms are encouraging, and mouse studies are in the works.
One of the major impediments to faster progress in anti-aging research is the time required to prove that a substance has life-prolonging effects. Consequently, one of the major goals of biomedical gerontology is to develop a set of biomarkers that can be used to measure biological age to determine—in a reasonably short period—whether a substance has an age-retarding effect. Recently, two research teams have developed such biomarkers—one by scientists in Austria48 for use in the same yeast strain used by the Harvard research team described above, and another by researchers at the University of Connecticut for use in anti-aging studies with fruit flies.49 Interestingly, both of these research teams used their biomarkers to evaluate the anti-aging effects of resveratrol, and both confirmed that resveratrol was an effective anti-aging substance (at least, in yeast and fruit flies).
Bioavailability/Dosage/Safety
Resveratrol appears to be effective in the prevention and treatment of cancer in cells and experimental animals, and as a life-extending substance in yeast and fruit flies.
In a recent review article,51 researchers attempted to determine an equivalent human dosage to reproduce the apparent cancer “chemopreventive” benefits of resveratrol observed in in vitro and in vivo animal studies. The authors pointed out that most animal studies used what would be considered “massive” human doses, ranging from 10 to 500 mg/kg per day. That would equate directly to a daily human dose of about 700 to 35,000 mg per day! However animal doses can rarely be directly extrapolated to humans, due to differences in physiology and metabolic rates. Three more recent papers demonstrated “extraordinary in vivo [anti-cancer] potency” of resveratrol in rats, using much lower doses, ranging from 200 mcg/kg per day to 2 mg/kg per day.52-54 That is a doable range of about 14 to 140 times the amount of resveratrol consumed by our “average” daily wine drinker (i.e., a calculated human therapeutic dose ranging from about 10 to 100 mg of resveratrol per day).
The next question, pending human clinical studies, is what amount — if any — is a toxic dose of resveratrol? In a study designed to specifically evaluate potential toxicity of resveratrol, scientists from the National Cancer Institute conducted a four-week study of trans-resveratrol in rats, administered via gavage feeding (i.e., through a tube, directly into the stomach) at doses of 300, 1,000 and 3,000 mg per day. The 300-mg-per-day dosage resulted in absolutely no side effects whatsoever. The 1,000-mg-per-day dosage resulted in slight weight loss in female rats and slight elevation in white blood count in the
male rats.
However, the 3,000 mg per day dosage resulted in significant clinical signs of toxicity, as well as reduced body weight and food consumption. Other abnormalities caused by the 3,000 mg “mega dose” included55:
* elevated BUN (blood urea nitrogen)
* elevated creatinine
* elevated alkaline phosphatase
* elevated alanine aminotransferase
* elevated total bilirubin
* elevated albumin
* reduced hemoglobin
* reduced hematocrit
* reduced red cell counts
* increased white cell counts
* increased kidney weight
* increased incidence and severity of nephropathy (kidney damage)
It should be noted that no studies of resveratrol have ever used the high dosages seen in this study—and that the specific purpose of this study was to determine whether resveratrol was toxic at any dose. This study confirms that resveratrol is clearly one of the safest anti-cancer substances known.
Conclusion
The more we learn about resveratrol and its wide-ranging benefits in life-threatening diseases, the better it looks in terms of its preventive and therapeutic benefits—and overwhelming record of safety. Although optimum dosages of resveratrol for humans have not been definitively determined, based on our present state of knowledge, reasonable dosages for humans appear to be in the range of 1 to 10 mg per day for preventive and anti-aging purposes, and 10 to 100 mg per day for therapeutic purposes, with the higher doses recommended as an adjunctive part of a comprehensive anti-cancer regimen.
Tuesday, January 20, 2009
Biophotonic scanner?
The term biophotonics denotes a combination of biology and photonics, with photonics being the science and technology of generation, manipulation, and detection of photons, quantum units of light.
(photon is an elementary particle (or fundamental particle is a particle not known to have substructure; that is, it is not known to be made up of smaller particles. If an elementary particle truly has no substructure, then it is one of the basic building blocks of the universe from which all other particles are made), the quantum of the electromagnetic field and the basic unit of light and all other forms of electromagnetic radiation. It is also the force carrier for the electromagnetic force)
Biophotonics has therefore become the established general term for all techniques that deal with the interaction between biological items and photons. This refers to emission, detection, absorption, reflection, modification, and creation of radiation from biomolecular, cells, tissues, organisms and biomaterials. Areas of application are life science, medicine, agriculture, and environmental science.
A biophoton (from the Greek βιο meaning "life" and φωτο meaning "light"), synonymous with ultraweak photon emission, low-level biological chemiluminescence, ultraweak bioluminescence, dark luminescence and other similar terms, is a photon of light emitted from a biological system and detected by biological probes as part of the general weak electromagnetic radiation of living biological cells. Biophotons and their study should not be confused with bioluminescence, a term generally reserved for higher intensity luciferin/luciferase systems.
Biophotonics is the study, research and applications of photons in their interactions within and on biological systems. Topics of research pertain more generally to basic questions of biophysics and related subjects - for example, the regulation of biological functions, cell growth and differentiation, connections to so-called delayed luminescence, and spectral emissions in supermolecular processes in living tissues, etc.
Still lost to understand the word biophoton?
Biophotons are weak emissions of light radiated from the cells of all living things. A photon is a single particle of light. Plants, animals and humans generate up to 100 photons per second, per .15 square inches (1 sq. centimeter) of surface area. The light is too faint to be seen by the naked eye, but biophotons have been detected and verified using photomultiplier tubes.
According to a leading researcher of biophotons, German biophysicist Fritz-Albert Popp, light is constantly being absorbed and remitted by DNA molecules within each cell's nucleus. These biophotons create a dynamic, coherent web of light. A system that could be responsible for chemical reactions within the cells, cellular communication throughout the organism, and the overall regulation of the biological system, including embryonic development into a predetermined form.
The laser-like coherence of the biophoton field is a significant attribute, making it a prime candidate for exchanging information in a highly functional, efficient and cooperative fashion, lending credence to the idea that it may be the intelligence factor behind the biological processes. An aspect of, or cousin to consciousness, though this remains speculative.
Biophoton emissions will vary according to the functional state of the organism. If a disease such as cancer affects certain cells they will radiate a different photonic signature than healthy cells of the same type. In this way biophotons can be a noninvasive tool for assessing the state of health or vitality. Applications can extend far into other areas like testing food and water quality, checking for chemical or electromagnetic contamination, or agricultural testing for products that improve crop resistance to disease. Biophysicists in many European and Asian countries are currently engaged in such research.
The Bio-Scanner was developed at the University Of Utah, one of the top medical research facilities in the world. It uses a Nobel prize winning science, called Raman Spectroscopy, to scan into the first layer of skin cells and measure the number carotinoid anti-oxidants in the body. The carotinoid anti-oxidant, one of the most abundant anti-oxidants found in fruits and vegetables, is a benchmark for other important anti-oxidants that are needed for overall health and disease prevention.
(photon is an elementary particle (or fundamental particle is a particle not known to have substructure; that is, it is not known to be made up of smaller particles. If an elementary particle truly has no substructure, then it is one of the basic building blocks of the universe from which all other particles are made), the quantum of the electromagnetic field and the basic unit of light and all other forms of electromagnetic radiation. It is also the force carrier for the electromagnetic force)
Biophotonics has therefore become the established general term for all techniques that deal with the interaction between biological items and photons. This refers to emission, detection, absorption, reflection, modification, and creation of radiation from biomolecular, cells, tissues, organisms and biomaterials. Areas of application are life science, medicine, agriculture, and environmental science.
A biophoton (from the Greek βιο meaning "life" and φωτο meaning "light"), synonymous with ultraweak photon emission, low-level biological chemiluminescence, ultraweak bioluminescence, dark luminescence and other similar terms, is a photon of light emitted from a biological system and detected by biological probes as part of the general weak electromagnetic radiation of living biological cells. Biophotons and their study should not be confused with bioluminescence, a term generally reserved for higher intensity luciferin/luciferase systems.
Biophotonics is the study, research and applications of photons in their interactions within and on biological systems. Topics of research pertain more generally to basic questions of biophysics and related subjects - for example, the regulation of biological functions, cell growth and differentiation, connections to so-called delayed luminescence, and spectral emissions in supermolecular processes in living tissues, etc.
Still lost to understand the word biophoton?
Biophotons are weak emissions of light radiated from the cells of all living things. A photon is a single particle of light. Plants, animals and humans generate up to 100 photons per second, per .15 square inches (1 sq. centimeter) of surface area. The light is too faint to be seen by the naked eye, but biophotons have been detected and verified using photomultiplier tubes.
According to a leading researcher of biophotons, German biophysicist Fritz-Albert Popp, light is constantly being absorbed and remitted by DNA molecules within each cell's nucleus. These biophotons create a dynamic, coherent web of light. A system that could be responsible for chemical reactions within the cells, cellular communication throughout the organism, and the overall regulation of the biological system, including embryonic development into a predetermined form.
The laser-like coherence of the biophoton field is a significant attribute, making it a prime candidate for exchanging information in a highly functional, efficient and cooperative fashion, lending credence to the idea that it may be the intelligence factor behind the biological processes. An aspect of, or cousin to consciousness, though this remains speculative.
Biophoton emissions will vary according to the functional state of the organism. If a disease such as cancer affects certain cells they will radiate a different photonic signature than healthy cells of the same type. In this way biophotons can be a noninvasive tool for assessing the state of health or vitality. Applications can extend far into other areas like testing food and water quality, checking for chemical or electromagnetic contamination, or agricultural testing for products that improve crop resistance to disease. Biophysicists in many European and Asian countries are currently engaged in such research.
The Bio-Scanner was developed at the University Of Utah, one of the top medical research facilities in the world. It uses a Nobel prize winning science, called Raman Spectroscopy, to scan into the first layer of skin cells and measure the number carotinoid anti-oxidants in the body. The carotinoid anti-oxidant, one of the most abundant anti-oxidants found in fruits and vegetables, is a benchmark for other important anti-oxidants that are needed for overall health and disease prevention.
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