Is Green Tea a Fad or a Real Health Boost?

In continuation of my updates on Green tea

Green tea is a popular health trend, with many people sipping in hopes of deriving benefits from the brew.

There's nothing wrong with that, dietitians say -- green tea is a healthy drink loaded with antioxidants. But the jury's still out on many of its purported health benefits.

"Clinical trials related to green tea are still in their early stages," said Nancy Farrell Allen, a registered dietitian nutritionist in Fredericksburg, Va. "I say drink it, enjoy it. It's not going to hurt, and it might have worthy benefits to it. But nutrition is a science, and it takes time for our understanding to evolve."

Green tea's potential health benefits derive from catechins, which are powerful antioxidant compounds known as flavonoids, said Chelsey Schneider, clinical nutrition supervisor at Mount Sinai Beth Israel Cancer Center in New York City.

One catechin in particular, known as EGCG, is found at higher levels in green tea than in either white or black tea, she said.

"This compound can be even stronger than vitamin C and E, which are very, very strong antioxidants," Schneider said. Antioxidants help prevent damage to cells.

Green, black and white tea all come from the same plant, said Allen, who is a spokeswoman for the Academy of Dietetics and Nutrition.

Green tea is made from the leaves of the mature plant, while white tea is made of leaves plucked early in development. Black tea is made from green tea leaves that are laid out and covered with a damp cloth, she said.

"They dry and blacken and ferment a little, giving black tea that darker, richer flavor," Allen said. But this process also reduces levels of catechins in black tea.

Weight loss has been associated with green tea, with experts suggesting that its mixture of caffeine and catechins can enhance a person's metabolism and processing of fat, according to the University of California-Davis Department of Nutrition.

But it appears that folks have to drink a lot of green tea to get substantial weight loss benefits and carefully watch the rest of their diet, UC-Davis says.

Green tea also has been tied to heart health.

For example, green tea was shown to reduce "bad" LDL cholesterol in a 2018 study of more than 80,000 Chinese published in the Journal of the American Heart Association.

Evidence suggests catechins in green tea also could lower risk of heart attacks, help blood vessels relax and reduce inflammation, UC-Davis says.

Green tea even has been associated with a lower risk of some cancers.

The American Cancer Society says studies have linked green tea to a reduction in ovarian cancer risk. And UC-Davis said experimental models have shown that green tea might reduce risk of a variety of other cancers.

But a 2016 evidence review by the Cochrane Library concluded that there is "insufficient and conflicting evidence to give any firm recommendations regarding green tea consumption for cancer prevention."

Schneider said the research is limited. "Some small studies say green tea can maybe be preventative for certain cancers, like breast, ovarian, endometrial, pancreatic and oral cancers, but there aren't so many conclusive human trials that support that," she said.

Green tea also might help keep your brain younger. A 2014 study in the journal PLOS One found that Japanese who drank more green tea had significantly less decline in brain function, although researchers couldn't rule out the possibility that these folks might have other healthy habits that helped keep them mentally sharp.

One caveat with all of this research is that it tends to take place in Asian countries, where people drink much more green tea. There might be significant differences for Americans.

And the way you take your green tea could diminish any potential positive effects, Schneider added.

"A lot of people are adding processed white sugar to their green tea, which really makes something beautiful and healthy into something unhealthy," she said.

Adding milk or cream to your tea also might not be a good idea.

"There are some studies that say having milk in green tea can actually block the effects of you absorbing the antioxidant," Schneider said. "If it was me, I'd drink it straight up."

Walnuts could be key to happier state-of-mind in young healthy men

In continuation of my update on walnuts

College can be a stressful time for young adults as they figure out how to manage intense daily routines that include work, study and play. Eat well, exercise and get plenty of sleep is a familiar mantra to alleviate this stress, but now with the results of his latest study, UNM Nutrition Professor Peter Pribis is able to tell college students that walnuts could be a key to a happier state-of-mind. 

In this first intervention study in humans, Pribis measured the effect of walnut consumption on mood.

"In the past, studies on walnuts have shown beneficial effects on many health outcomes like heart disease, diabetes and obesity," said Pribis. "Our study was different because we focused on cognition, and in this controlled randomized trial (CRT) we measured mood outcomes in males and females."

The participants of the study were 64 students between the ages of 18-25. They represented most ethnic groups: Caucasian, African American, Hispanic and Asian.

The participants were asked to eat three slices of banana bread every day for sixteen weeks--eight weeks of banana bread with walnuts and eight weeks of banana bread without walnuts. The nuts were finely ground into the dough so the two banana breads were similar in taste and appearance. While eating banana bread with walnuts the participants consumed half a cup of walnuts daily.

The mood of the students was measured at the end of each eight-week period.

"We used a validated questionnaire called Profiles of Mood States (POMS)," says Pribis. "It is one of the most widely used and accepted mood scales in studies on cognition. The test has six mood domains: tension, depression, anger, fatigue, vigor, confusion and also provides a Total Mood Disturbance score (TMD). The lower the TMD score the better the mood."

In this double-blind, randomized, placebo controlled, cross-over feeding trial with walnuts for eight weeks, Pribis observed a significant improvement in mood in young, healthy males.

"There was a meaningful, 28 percent improvement of mood in young men," said Pribis. "However we did not observe any improvement of mood in females. Why this is we do not know."

There are several nutrients in walnuts that could be responsible for the improved mood like alpha-Linolenic acid, vitamin E, folate, polyphenols or melatonin. However, this was a whole food study, so in the end it was the synergy and interaction of all the nutrients in the walnuts combined.

For Pribis, the lesson learned from this food study is clear, "Eat more walnuts. This is an easy intervention. They're not only good for your mood, but overall health as well. The recommended amount is one handful per day."

With this knowledge in hand--and hopefully walnuts in the other--young men can happily tackle life's daily stress.

Ref: http://news.unm.edu/news/the-key-to-a-better-mood-for-young-men-is-a-nut




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Metabolite of oral DMF drug for multiple sclerosis appears to slow onset of Parkinson's disease

In continuation of my update on dimethylfumarate 

The metabolite of a drug that is helping patients battle multiple sclerosis appears to significantly slow the onset of Parkinson's disease, researchers say.

The oral drug, dimethylfumarate, or DMF, and its metabolite, monomethylfumarate, or MMF, both increase activity of Nrf2, a protein that helps protect the body from oxidative stress and inflammation, hallmarks of both diseases, said Dr. Bobby Thomas, neuroscientist in the Department of Pharmacology and Toxicology at the Medical College of Georgia at Augusta University.

 dimethylfumarate  monomethylfumarate, 

But the new study provides the first evidence that the metabolite, which is essentially the active portion of the parent drug, more directly targets Nrf2, potentially reducing known side effects of the parent drug that include flushing, diarrhea, nausea, vomiting, abdominal pain and the brain infection encephalopathy, said Thomas, corresponding author of the study in The Journal of Neuroscience.

Particularly, the gastrointestinal side effects can exacerbate some problems patients with Parkinson's already experience, said Dr. John Morgan, neurologist, neuroscientist and Parkinson's disease specialist in the MCG Department of Neurology. In addition to destroying neurons in the brain that produce dopamine, a neurotransmitter that enables movement and learning, Parkinson's causes nerve cell death in the gastrointestinal tract and related problems such as severe constipation.

"Nrf2 is a natural protective mechanism we have for oxidative stress," Thomas said. The fact that multiple sclerosis and Parkinson's have in common evidence of declining activity of the Nrf2 pathway has generated interest in the drug for Parkinson's and other neurodegenerative diseases.

DMF was approved for multiple sclerosis three years ago by the Food and Drug Administration. While its metabolite MMF is not quite as potent as the parent drug in increasing Nrf2 activity, the new study indicates that its action is sufficient to dramatically slow the loss of dopamine-producing neurons as well as the parent drug, in an animal model of Parkinson's.

In their model, mice given the neurotoxin MPTP experience a dramatic loss of dopamine-producing neurons, losing about half within a handful of days, and rapidly develop Parkinson's-like symptoms. Patients, on the other hand, slowly develop symptoms over many years. By the time they seek medical care, patients may have lost 30-50 percent of their dopaminergic neurons, said Morgan, a study coauthor. "Presentation is after the disease is kind of out of the gate."

To accommodate the very compressed timeline in their model and the fact that several daily doses are needed before the drug starts to work, the researchers first gave the mice either the drug or metabolite the day before they started the toxin.

Dopamine-producing neurons are located in a darker-pigmented central portion of the brain called the substantia nigra. Even in the absence of disease, making dopamine is a stressful job for these neurons that makes them generally more fragile and actually results in oxidative stress even in a healthy scenario, Morgan said. To make a difficult situation worse, increased oxidative stress can make dopamine toxic to neurons, he said.

To increase Nrf2 activity, the parent drug DMF also appears to first make bad matters worse. DMF increases oxidative stress by depleting the natural antioxidant, glutathione, and reduces the power of cell powerhouses, called mitochondria, by limiting their ability to use oxygen and glucose to make energy leading to reduced viability of dopamine-producing cells, Thomas said.

The metabolite MMF appears to more directly activate Nrf2, and actually increases glutathione and improves mitochondrial function, brain cell studies showed. While the parent drug ultimately produces a higher Nrf2 activation, the researchers found the MMF effect was sufficient to stop the dramatic neuron loss in the animal model.

Both DMF and MMF slowed neuron loss to a more normal level, and the neurons that survived continued to make dopamine. Inflammation and oxidative stress levels also were significantly reduced, the researchers said.

As a next step, they are working toward a clinical trial of MMF in patients with early Parkinson's disease. Although the metabolite could be easily formulated for humans, it has not yet been done, Thomas notes.

"If we can catch them early enough, maybe we can slow the disease," Morgan said. "If it can help give five to eight more years of improved quality of life that would be great for our patients."

Clinical studies of the drug in Parkinson's are being planned in the United Kingdom and additional analogues of its metabolite, which could be used clinically and which the researchers think ultimately will be the best option for patients, are under development.

Oxidative stress is a byproduct of the body's use of oxygen. Free radicals, generated by oxygen use, are unstable molecules that can interfere with usual cell function and are believed to contribute to a wide range of conditions from normal aging to Alzheimer's disease. Simply giving antioxidants, such as vitamin E, which work more like scavengers to scarf up free radicals, has not worked in combating neurodegenerative disease, Thomas said. He's optimistic that directly targeting Nrf2 will be effective in at least slowing the disease, but there remains a need for clinically safe Nrf2 activators.

Activity of the Nrf2 pathway tends to slowly decline with age. Exercise upregulates Nrf2, and Morgan regularly encourages his patients to be as active as possible. A small group of patients with Parkinson's in Europe has a concentrated activation of Nrf2 that at least delays their disease onset. Parkinson's tends to be diagnosed in the mid-to-late 50s and early 60s and is more common in men.

One concern with chronically elevating anti-oxidant and anti-inflammatory molecules with drugs like DMF and MMF is creating some of the same problems that immunosuppressive drugs given to organ transplant patients create. Chronic suppression of the immune response makes patients more susceptible to invaders like cancers and infections.

Ref : http://www.jneurosci.org/content/36/23/6332.short?sid=e7a934c5-6996-4fff-bfa9-f2c600507e1f

Metabolite of oral DMF drug for multiple sclerosis appears to slow onset of Parkinson's disease

Walnuts may improve your colon health: Eating walnuts changes the gut microbiome and reduces cancer growth, study shows

In continuation of my update on walnuts  

A team of researchers from UConn Health and The Jackson Laboratory for Genomic Medicine found that mice that ate 7-10.5 percent of their total calories as walnuts developed fewer colon cancers. The effect was most pronounced in male mice, which had 2.3 times fewer tumors when fed walnuts as part of a diet similar to the typical American's. That's equivalent to a human eating about an ounce of walnuts a day.

"Our results show for the first time that walnut consumption may reduce colon tumor development," said Principal Investigator Dr. Daniel W. Rosenberg of UConn Health. "There is accumulating evidence that eating walnuts may offer a variety of benefits related to health issues like cancer. This study shows that walnuts may also act as a probiotic to make the colon healthy, which in turn offers protection against colon tumors."

Walnuts are packed with compounds known to be important nutritionally. They have the most polyunsaturated fatty acids of all the commonly eaten tree nuts, as well as the highest ratio of omega-3 to omega-6 fatty acids, and high levels of a form of Vitamin E with anti-cancer properties.

But walnuts are not merely the sum of their chemical parts, and it may be as a whole food that they pack the most significant anti-cancer punch against colon cancer, the third most common cancer in the world. Other studies have shown walnuts have promise warding off diseases connected to diet and lifestyle, including heart disease, diabetes and neurological disorders.

Rosenberg, a cancer researcher and professor of medicine at UConn Health and Dr. Masako Nakanishi, a research associate in the Center for Molecular Medicine at UConn Health tested the cancer prevention qualities of walnuts on mice fed two different diets. One group of mice ate a standard lab mouse chow, while the other group ate a chow that captured the nutritional profile of the typical American diet. Subsets of both groups were supplemented with walnuts.

Interestingly, male mice fed the Western diet fortified with 10.5 percent walnuts showed the greatest decrease in colon tumors compared with mice fed no walnuts.

To figure out why walnuts were beneficial, the UConn Health team collaborated with Dr. George Weinstock and colleagues at The Jackson Laboratory. Weinstock's lab took fecal samples from the mice and analyzed the communities of bacteria living in their digestive tracts. They found that walnut consumption tended to push the gut microbiome toward an ecology that was potentially protective against cancer. It's not clear exactly how this works, but there are clues. For example, previous research has shown that some gut bacteria digest fiber into compounds with anti-inflammatory properties that may reduce tumor initiation. The microbiome analyses also reflected interesting differences between male and female. Males on walnut-free diets tended to have less-diverse gut flora than females. Adding walnuts to the diets of male mice brought their microbiomes closer to those of female mice on either of the diets. Whether this change contributes to the protection seen in male mice remains to be determined.

Because the studies were done only in mice, more testing needs to be done in humans before walnuts can be unequivocally recommended as a cancer-prevention agent. Rosenberg's group is working with a nutritionist and surveying human colonoscopy patients about their diets as part of a longer term study in humans.

However, Rosenberg isn't waiting for the final word. Even right now, he says, "I try to eat walnuts every day."

Revolutionary drug explained by scientists: Scientists figured out how the world's first drug that protects the cell mitochondria from damage by aggressive oxygen can work

Recently, Russian researchers, led by Prof. Vladimir P. Skulachev, managed to create an antioxidant drug that selectively accumulates within mitochondria and protects them from oxidative damage. Under the trade name "Visomitin" the drug was approved for treatment of such eye diseases as cataracts and dry eye. Prof. Armen Mulkidjanian of the Faculty of Bioengineering and Bioinformatics of the Lomonosov Moscow State University and the University of Osnabrück, Germany, and his colleagues have explained why very small doses of synthetic antioxidants such as "Visomitin" could give a pronounced therapeutic effect, despite the presence of large quantities of natural mitochondrial antioxidants.

 Visomitin

Mitochondria are intracellular structures that conduct respiration. Respiration, however, is accompanied by formation of reactive oxygen species (ROS) as by-products. The ROS are capable of damaging the mitochondria. Damaged mitochondria produce even more ROS, which can destroy cells and tissues, so that nature has special mechanisms, such as mitophagy and apoptosis, for elimination of damaged mitochondria and cells. These mechanisms are triggered after a signal of a disorder passes through the double membrane surrounding the mitochondria. Several laboratories have shown that it is possible to avoid the decay of cells and tissues by preventing the oxidation of a particular component of the mitochondrial membrane -- cardiolipin, because the oxidized molecules of cardiolipin are exactly the triggers of the signal chain.

The group of Prof. Vladimir Skulachev, the Dean of the Faculty of Bioengineering and Bioinformatics and the Director of the Belozersky Institute of Physical and Chemical Biology, (the Lomonosov Moscow State University), has developed a line of mitochondria-targeted antioxidants, the so-called SkQ-ions, specifically protecting the molecules of mitochondrial cardiolipin from oxidation. In animal trials, the SkQ-ions cured inflammatory eye diseases, helped to overcome the ischemia-simulating conditions, and even reduced the manifestation of senescence. Although similarly acting drugs have been developed and studied in the US and UK laboratories, the Russian group was the first to get an approval for their drug -- as eye drops. The researchers hope that SkQ-based drugs, in the form of pills and injections, after their certification, would help to attenuate the pathological symptoms that accompany strokes, heart attacks and serious traumas.

Armen Mulkidjanian and his collaborators have managed to suggest answers to some intriguing questions. Specifically, it was not clear why cardiolipin, of all the components of the membrane, it specifically oxidized. Molecules of cardiolipin, while making only 10-20% of total membrane lipids, are specifically targeted by ROS and, after getting oxidized, trigger the self-destruction of cells. Secondly, it was not clear why the natural antioxidants, namely coenzyme Q (ubiquinol) and vitamin E (alpha-tocopherol), which are present in mitochondrial membranes in large quantities, fail in the case of cardiolipin. It remained a mystery why these substances could not protect cardiolipin from oxidation, whereas artificial, mitochondria-targeted antioxidants, designed either by the Skulachev's group in Moscow, or by their counterparts in the US and the UK, perfectly coped with this task, in spite of very small doses of the administered drugs.

Armen Mulkidjanian says that the goal of the study was set by Prof. Skulachev.

'Prof. Skulachev asked our group in Germany to tackle these puzzles,' says Armen Mulkidjanian. 'Most of the work was carried out by the post-graduate students and the employees of the Moscow University, who worked in Russia and in Germany, so that their contribution was decisive. As to the research, we have developed an experimental system to investigate quantitatively the oxidation of the cardiolipin membranes and the ability of various antioxidants to prevent it. It turned out that the SkQ-ions and the molecules of coenzyme Q protected the cardiolipin membranes from oxidation equally well, whereas vitamin E performed much worse'.

To understand why cardiolipin molecules are the main target of the ROS, the researchers compared the experimental data with their previous results and the structures of respiratory enzymes. A fraction of cardiolipin molecules is occluded within respiratory protein complexes, just those that generate ROS. 'These molecules should be the first to be oxidized,' Mulkidjanian says.

The bulky, water-insoluble molecule of coenzyme Q cannot get to these "hidden" cardiolipin molecules, as opposed to small, agile molecules of artificial antioxidants, which, as shown in the study, are capable of protecting cardiolipin molecules from oxidation by accessing them both from the membrane and from the aqueous phase.

"The essence of our work is that we have proposed a mechanism that explains how very low doses of mitochondria-targeted antioxidants could provide a distinct therapeutic effect, even being applied over large amounts of natural antioxidants, which were ineffective in this case. The mechanism should be valid for the whole class of similar drugs. We hope that our findings would help to develop new drugs,' says Armen Mulkidjanian.

Revolutionary drug explained by scientists: Scientists figured out how the world's first drug that protects the cell mitochondria from damage by aggressive oxygen can work: An international team now clarifies the molecular mechanism of a drug created in Russia and designed to prevent the damaging of cell mitochondria by reactive oxygen species.

Researchers identifiy elusive anti-cancer property of vitamin E

Researchers identifiy elusive anti-cancer property of vitamin E

Can Brightly Colored Fruits, Veggies Protect Against ALS? - Drugs.com MedNews

Researchers from Harvard School of Public Health have,  found that increasing consumption of carotenoids, particularly beta-carotene and lutein, might reduce the risk for this progressive neurological disease, which attacks nerve cells in the brain and spinal cord.

Carrots, yams and mangoes are rich in beta-carotenes, and spinach, collard greens and egg yolks are good sources of lutein. The study found, however, that diets rich in the antioxidants lycopene, beta-cryptoxanthin and vitamin C do not apparently reduce the risk for ALS, which causes the muscles to waste away and eventually results in paralysis.

"ALS is a devastating degenerative disease that generally develops between the ages of 40 and 70, and affects more men than women," senior study author Dr. Alberto Ascherio, a professor of epidemiology and nutrition at Harvard School of Public Health, said in a journal news release. "Understanding the impact of food consumption on ALS development is important."

Analyzing information on more than 1 million people, the researchers identified nearly 1,100 cases of ALS. The researchers found that increased overall carotenoid intake -- especially among those who ate diets rich in beta-carotene and lutein -- seemed to be linked to a lower risk for the devastating condition. 

Those who ate more carotenoids daily also were more likely to exercise, have an advanced degree, have increased vitamin C intake and take vitamin C and E supplements.

The researchers pointed out, however, that long-term vitamin C supplements did not lower people's risk for this degenerative disease.

"Our findings suggest that consuming carotenoid-rich foods may help prevent or delay the onset of ALS," Ascherio concluded. "Further food-based analyses are needed to examine the impact of dietary nutrients on ALS."

 Ref : http://onlinelibrary.wiley.com/doi/10.1002/ana.23820/abstract

Can Brightly Colored Fruits, Veggies Protect Against ALS? - Drugs.com MedNews

Beta carotene may protect people with common genetic risk factor for type-2 diabetes

Stanford University School of Medicine investigators have found that for people harboring a genetic predisposition that is prevalent among Americans, beta carotene, which the body converts to a close cousin of vitamin A, may lower the risk for the most common form of diabetes, while gamma tocopherol, the major form of vitamin E in the American diet, may increase risk for the disease. 

Beta carotene may protect people with common genetic risk factor for type-2 diabetes

Does Vitamin E Prevent or Promote Cancer?

In continuation of my update on Vitamin-E

The cancer preventive activity of vitamin E has been suggested by many epidemiologic studies. However, several recent large-scale human trials with α-tocopherol, the most commonly recognized and used form of vitamin E, failed to show a cancer preventive effect. The recently finished follow-up of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) even showed higher prostate cancer incidence in subjects who took α-tocopherol supplementation. The scientific community and the general public are faced with a question: “Does vitamin E prevent or promote cancer?” Researchers lead by Dr. Chung S. Yang, Director of the center did experiments in animal models and tried to conclude about  the cancer preventive activity of γ- and δ-tocopherols as well as a naturally occurring mixture of tocopherols, and the lack of cancer preventive activity by α-tocopherol. 

On the basis of these results as well as information from the literature, we suggest that vitamin E, as ingested in the diet or in supplements that are rich in γ- and δ-tocopherols, is cancer preventive; whereas supplementation with high doses of α-tocopherol is not.

Ref : http://cancerpreventionresearch.aacrjournals.org/content/early/2012/04/14/1940-6207.CAPR-12-0045.abstract?sid=5d446d6b-8eb0-426f-b86a-378f60ad7d15

Tocotrienol could help reduce stroke damage

In continuation of my update on the benefits of  Vitamin  E

Tocotrienol could help reduce stroke damage

ProstaCaid (33-ingredient comprehensive polyherbal preparation) against prostate cancer......

We have seen  many benefits of natural products rich in  Quercetin,   Epigallocatechin gallate (EGCG) and many other polyphenol antioxidant from natural products like green tea, broccoli peaches and plums. Interestingly, now researchers from  Columbia University have come up with an interesting finding, i.e., ProstaCaid is a 33-ingredient comprehensive polyherbal preparation with supplements of vitamin C, vitamin D3, zinc, selenium, quercitin, 3,3′-diinodolymethane (DIM), and lycopene was able to stop abnormal cell growth and induce apoptosis (programmed cell death) in both hormone sensitive and hormone resistant prostate cancer cell lines at unusually low concentrations, which makes the findings more significant...

Herbal extracts include the extracts from turmeric root, saw palmetto berry, grape skin, pomegranate, pumpkin seed, pygeum bark, sarsaparilla root, green tea, and Japanese knotweed. Hence, it is rich in natural polyphenols, including quercetin, resveratrol, epigallocatechin gallate (EGCG), and ellagic acid, which have previously demonstrated anticancer potential. The unique formula contains 3 medicinal mushrooms grown on an herbal-enhanced medium. The mushrooms included are Phellinus linteus, Ganoderma lucidum, and Coriolus versicolor, each with known anticancer properties.

Researchers claim that, ProstaCaid was designed based on constituents that exhibit antiprolifetaive, antioxidant, and apoptotic activities; however, its efficacy and the mechanisms of action are yet to be examined. Researchers looked at the effectiveness of the preparation in suppressing several types of prostate cancer cell lines in culture and attempt to delineate the mechanism of action for justification in pursuing animal to determine efficicacy invivo.

Researchers conclude that, the anticancer activity of ProstaCaid may be ascribed to its polyphenolic flavonoids and curcuminoids derived from various herbs as well as other supplements, such as DIM. The preparation contains supplements such as quercetin (15%), Curcuma longa root extract complex with enhanced bioavailability (BCM-95; 20%), DIM (3%), and resveratrol (0.2%). Some of these components have shown a strong doseand time-dependent growth inhibition and apoptotic death in prostate cancer cells; 25 mM of quercetin inhibited about 50% PC3 cell growth for 72 hours. At 24 hours, 50 mM and 100 mM quercetin induced G2/M arrest and apoptosis, manifested by the decrease in G2/M-related protiens.

Researchers summarise  that,    ProstaCaid has anti-cancer activities in both AD and AI prostate cancer cells at very low concentrations (25 mg/mL). It also suggests that ProstaCaid inhibits cell growth and survival, at least through the inhibition of AKT and MAPK signaling. The effect on AI cell lines is especially of importance as there is presently no curative therapy for hormone refractory prostate cancer.

Researchers postulate that ProstaCaid may affect activity of Cdc2/cyclin B1 kinase by reducing this complex formation. Cdc2 could be dephosphorylated by Cdc25C and become inactive or be phosphorylated by protein kinase, such as Wee1, and then converted into an inactive form. They also suggest that more studies are needed in the future to test it and to define its upstream events in PC3 cells.

Ref : Jun Yan and Aaron E. Katz, Integr Cancer Ther 2010 9: 186

The Secret of Lowering Cholesterol Through Diet...

I am really happy to share an interesting and important article  'the secret of lowering cholesterol through diet' by  Deborah Land, who has written this article exclusively for the readers of  my blog.......

The Secret of Lowering Cholesterol Through Diet

a. The Myth of Cholesterol - the Bad and the Good:

Most people think that cholesterol is always bad, but there are actually two types of cholesterol. LDL is  considered the "bad" cholesterol, and HDL is considered the "good" cholesterol. If there is too much LDL in our bloodstream, it will form plaque on our arteries. Over time, this narrows our arteries and can eventually block blood flow completely. Dietary cholesterol actually isn't the primary reason for high cholesterol in the blood; it is high amounts of saturated fat and trans fat. To keep cholesterol low, you should eat unsaturated fats, eat fibrous foods, and exercise more.

b. Number Relevance in Cholesterol :
Every adult should have their cholesterol checked at least every 5 years. When you get a cholesterol test, you'll usually get back four different results. Here are the 4 categories and the healthy range you want to be in.

Total Cholesterol - less than 200 mg/dL (5.2 mmol/L);
LDL Cholesterol - less than 100 mg/dL (2.6 mmol/L);
HDL Cholesterol - greater than 40 mg/dL (1.0 mmol/L) &
Triglycerides - less than 150 mg/dL (1.7 mmol/L).

If you are over or under the desired level on any category, it is usually indicative that a diet or exercise change is needed.

c. Heart Protection and Vitamin E:
Vitamin E, an important vitamin, is sourced in vegetable oils, nuts and leafy vegetables. Vitamin E can decrease your heart disease risk, but it will not prevent a heart attack.

d. Lowering Cholesterol with these Five Foods :
1. Oatmeal and Oat Bran: These contain a high amount of soluble fiber, which can lower LDL.
2. Fish: Fish is a great source of omega 3 fatty acids, which lowers LDL and raises HDL.
3. Nuts: Not only are nuts high in fiber, but they contain the healthy fats you need to keep LDL in check.
4. Plant Sterols: This is found in foods like margarine, salad dressing, orange juice, and functional cookies. 2  grams per day will lower your LDL by 10-15%.
5. Soy: This popular meat replacement can lower LDL by up to 3%.

e. Plant Sterols and Benefits to Health :
Foods such as VitaTops Muffin Tops, Benecol Spread, granola bars and fat free milk are rich sources of plant sterols. You can easily help your heart when you start eating foods packed with plant sterols and avoid eating foods that contain saturated fats. A saturated fat-filled diet is not canceled out by this. Exercising often as well as eating healthy food will keep your cholesterol in check.

About the Author - Deborah Land writes for Cholesterol Lowering Diet Blog  ,  her personal hobby blog focused on tips to eat healthy to prevent high cholesterol. I find the blog very informative, do visit for more details...