CONFIRMED: Quercetin-tocotrienols combination combats cancer

Image: CONFIRMED: Quercetin-tocotrienols combination combats cancer

The battle against cancer is heading into new territory, as scientists explore the healing ability of substances that support the body’s cells, instead of killing them off. Researchers from the Italian National Institute of Health and Science on Aging (INRCA) have made a breakthrough discovery for preventing the spread of malignant tumors. A natural plant-based combination, including quercetin and tocotrienols, effectively targets aging cells that cause chronic inflammation and cancer. This dynamic, anti-cancer duo causes stubborn cancer cells to die off and simultaneously promotes the growth of normal cells.

This dynamic duo heals the body at the cellular level by triggering a die-off sequence within aging and malignant cells. If old, decrepit cells become inefficient at performing cellular division, new cells cannot be created. If these senile cells refuse to die off, a condition called cellular senescence sets in. This causes an accumulation of aged cells that emit pro-inflammatory chemicals into the body. This process promotes aging in the body and increases cancer risk. Quercetin and tocotrienols help to remove aging cells so healthy cells have space to flourish.

Moreover, quercetin and tocotrienols identify malignant cancer cells and speed up their cellular senescence. This dynamic duo effectively target unwanted cancer cells and speed up their death, preventing cancer cell replication. The two natural substances remove inflammatory, aging cells and stop malignant cells from growing. This combination is a highly intelligent form of medicine that deciphers dangerous cells and manipulates cellular senescence so that the body can heal itself. The combination can be employed as an adjunct therapy for cancers of many origins. This combination can be used to prevent cancer from taking hold and stop early cancers in their tracks.

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Anti-cancer intelligence of tocotrienols

Tocotrienols are an anti-inflammatory type of vitamin E that can be found in wheat germ, barley, oat, rye, cranberries, blueberries, kiwi, plum, coconut, and some nuts. It is also isolated in supplement form. Research confirms that this form of vitamin E can reverse cell cycle arrest and reduce DNA damage, especially for treatment of breast cancer, pancreatic cancer, and melanoma. However, assimilation of tocotrienols in the human intestine is poor because they are lipophilic in nature (they dissolve in lipids and fats). Researchers must find ways to increase the bio-availability of tocotrienols to increase this vitamin’s therapeutic effects. Intestinal absorption depends upon the secretion of bile and transporters such as ?-tocopherol transfer protein (?-TTP); therefore, assimilation of tocotrienols occurs more readily with food. Nutritionists recommend a daily dose of 150 mg of tocotrienols. One should expect to see therapeutic benefits with supplementation after ninety days.

The healing nature of quercetin

Quercetin is a plant-based flavonoid and antioxidant that helps plants defend against disease. When quercetin is combined with tocotrienols, synergy is created; together these natural substances slow the aging process, prolong the life of healthy cells, and induce apoptosis of malignant cancer cells. Because of its anti-inflammatory properties, quercetin can benefit seasonal allergies, asthma, bronchitis, and congestion. Quercetin is commonly found in apples, tea, onions, nuts, berries, cauliflower and cabbage and can be isolated and consumed in the form of a supplement. To rid the body of aging cells, nutritionists recommend a daily dose of quercetin (500 to 800 mg) for up to three consecutive months, followed by a maintenance dose of 150 mg a day. It is best to consult a healthcare professional, as many medications can adversely interact with the body when healing substances are introduced.

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Critical step in DNA repair, cellular aging pinpointed

The body’s ability to repair DNA damage declines with age, which causes gradual cell demise, overall bodily degeneration and greater susceptibility to cancer. Now, research reveals a critical step in a molecular chain of events that allows cells to mend their broken DNA.

The body’s ability to repair DNA damage declines with age, which causes gradual cell demise, overall bodily degeneration and greater susceptibility to cancer.

DNA repair is essential for cell vitality, cell survival and cancer prevention, yet cells’ ability to patch up damaged DNA declines with age for reasons not fully understood.

Now, research led by scientists at Harvard Medical School reveals a critical step in a molecular chain of events that allows cells to mend their broken DNA.

The findings, published March 24 in Science, offer a critical insight into how and why the body’s ability to fix DNA dwindles over time and point to a previously unknown role for the signaling molecule NAD as a key regulator of protein-to-protein interactions in DNA repair. NAD, identified a century ago, is already known for its role as a controller of cell-damaging oxidation.

Additionally, experiments conducted in mice show that treatment with the NAD precursor NMN mitigates age-related DNA damage and wards off DNA damage from radiation exposure.

The scientists caution that the effects of many therapeutic substances are often profoundly different in mice and humans owing to critical differences in biology. However, if affirmed in further animal studies and in humans, the findings can help pave the way to therapies that prevent DNA damage associated with aging and with cancer treatments that involve radiation exposure and some types of chemotherapy, which along with killing tumors can cause considerable DNA damage in healthy cells. Human trials with NMN are expected to begin within six months, the researchers said.

“Our results unveil a key mechanism in cellular degeneration and aging but beyond that they point to a therapeutic avenue to halt and reverse age-related and radiation-induced DNA damage,” said senior author David Sinclair, professor in the Department of Genetics at HMS and professor at the University of New South Wales School of Medicine in Sydney, Australia.

A previous study led by Sinclair showed that NMN reversed muscle aging in mice.

A plot with many characters

The investigators started by looking at a cast of proteins and molecules suspected to play a part in the cellular aging process. Some of them were well-known characters, others more enigmatic figures.

The researchers already knew that NAD, which declines steadily with age, boosts the activity of the SIRT1 protein, which delays aging and extends life in yeast, flies and mice. Both SIRT1 and PARP1, a protein known to control DNA repair, consume NAD in their work.

Another protein DBC1, one of the most abundant proteins in humans and found across life forms from bacteria to plants and animals, was a far murkier presence. Because DBC1 was previously shown to inhibit vitality-boosting SIRT1, the researchers suspected DBC1 may also somehow interact with PARP1, given the similar roles PARP1 and SIRT1 play.

“We thought if there is a connection between SIRT1 and DBC1, on one hand, and between SIRT1 and PARP1 on the other, then maybe PARP1 and DBC1 were also engaged in some sort of intracellular game,” said Jun Li, first author on the study and a research fellow in the Department of Genetics at HMS.

They were.

To get a better sense of the chemical relationship among the three proteins, the scientists measured the molecular markers of protein-to-protein interaction inside human kidney cells. DBC1 and PARP1 bound powerfully to each other. However, when NAD levels increased, that bond was disrupted. The more NAD present inside cells, the fewer molecular bonds PARP1 and DBC1 could form. When researchers inhibited NAD, the number of PARP1-DBC1 bonds went up. In other words, when NAD is plentiful, it prevents DBC1 from binding to PARP1 and meddling with its ability to mend damaged DNA.

What this suggests, the researchers said, is that as NAD declines with age, fewer and fewer NAD molecules are around to stop the harmful interaction between DBC1 and PARP1. The result: DNA breaks go unrepaired and, as these breaks accumulate over time, precipitate cell damage, cell mutations, cell death and loss of organ function.

Averting mischief

Next, to understand how exactly NAD prevents DBC1 from binding to PARP1, the team homed in on a region of DBC1 known as NHD, a pocket-like structure found in some 80,000 proteins across life forms and species whose function has eluded scientists. The team’s experiments showed that NHD is an NAD binding site and that in DBC1, NAD blocks this specific region to prevent DBC1 from locking in with PARP1 and interfering with DNA repair.

And, Sinclair added, since NHD is so common across species, the finding suggests that by binding to it, NAD may play a similar role averting harmful protein interactions across many species to control DNA repair and other cell survival processes.

To determine how the proteins interacted beyond the lab dish and in living organisms, the researchers treated young and old mice with the NAD precursor NMN, which makes up half of an NAD molecule. NAD is too large to cross the cell membrane, but NMN can easily slip across it. Once inside the cell, NMN binds to another NMN molecule to form NAD.

As expected, old mice had lower levels of NAD in their livers, lower levels of PARP1 and a greater number of PARP1 with DBC1 stuck to their backs.

However, after receiving NMN with their drinking water for a week, old mice showed marked differences both in NAD levels and PARP1 activity. NAD levels in the livers of old mice shot up to levels similar to those seen in younger mice. The cells of mice treated with NMN also showed increased PARP1 activity and fewer PARP1 and DBC1 molecules binding together. The animals also showed a decline in molecular markers that signal DNA damage.

In a final step, scientists exposed mice to DNA-damaging radiation. Cells of animals pre-treated with NMN showed lower levels of DNA damage. Such mice also didn’t exhibit the typical radiation-induced aberrations in blood counts, such as altered white cell counts and changes in lymphocyte and hemoglobin levels. The protective effect was seen even in mice treated with NMN after radiation exposure.

Taken together, the results shed light on the mechanism behind cellular demise induced by DNA damage. They also suggest that restoring NAD levels by NMN treatment should be explored further as a possible therapy to avert the unwanted side effects of environmental radiation, as well as radiation exposure from cancer treatments.

In December 2016, a collaborative project between the Sinclair Lab and Liberty Biosecurity became a national winner in NASA’s iTech competition for their concept of using NAD-boosting molecules as a potential treatment in cosmic radiation exposure during space missions.

Trio wins Nobel Chemistry Prize for DNA repair work.

Sweden’s Tomas Lindahl, Paul Modrich of the US and Aziz Sancar, a Turkish-American, won the 2015 Nobel Chemistry Prize today for work on how cells repair damaged DNA.

The three opened a dazzling frontier in medicine by unveiling how the body repairs DNA mutations that can cause sickness and contribute to ageing, the Nobel jury said.

“Their systematic work has made a decisive contribution to the understanding of how the living cell functions, as well as providing knowledge about the molecular causes of several hereditary diseases and about mechanisms behind both cancer development and ageing,” the panel said.

DNA – deoxyribonucleic acid – is the chemical code for making and sustaining life.
When cells divide, molecular machines seek to replicate the code perfectly, but random slipups in their work can cause the daughter cells to die or malfunction. DNA can also be damaged by strong sunlight and other environmental factors.

But there is a swarm of proteins – a molecular repair kit – designed to monitor the process. It proof-reads the code and repairs damage.

The three were lauded for mapping these processes, starting with Lindahl, who identified so-called repair enzymes – the basics in the toolbox.

Sancar, born in Savur, Turkey, discovered the mechanisms used by cells to fix damage by ultraviolet radiation. Modrich laid bare a complex DNA-mending process called mismatch repair.

“The basic research carried out by the 2015 Nobel laureates in chemistry has not only deepened our knowledge of how we function, but could also lead to the development of lifesaving treatments,” the Nobel committee said.

The three share the prize sum of eight million Swedish kronor (around USD 950,000 or 855,000 euros).

The Nobel awards week continues with the announcements for the two most closely-watched prizes: tomorrow the winner of the literature prize will be announced, followed by the peace prize on Friday.

The economics prize will wrap up this year’s Nobel season on Monday, October 12.
The laureates will receive their prizes at formal ceremonies in Stockholm and Oslo on December 10, the anniversary of the 1896 death of prize creator Alfred Nobel, a Swedish philanthropist and scientist.

Senescence and aging: the critical roles of p53.

p53 functions as a transcription factor involved in cell-cycle control, DNA repair, apoptosis and cellular stress responses. However, besides inducing cell growth arrest and apoptosis, p53 activation also modulates cellular senescence and organismal aging. Senescence is an irreversible cell-cycle arrest that has a crucial role both in aging and as a robust physiological antitumor response, which counteracts oncogenic insults. Therefore, via the regulation of senescence, p53 contributes to tumor growth suppression, in a manner strictly dependent by its expression and cellular context. In this review, we focus on the recent advances on the contribution of p53 to cellular senescence and its implication for cancer therapy, and we will discuss p53’s impact on animal lifespan. Moreover, we describe p53-mediated regulation of several physiological pathways that could mediate its role in both senescence and aging.


Source: Oncogene

Various modes of cell death induced by DNA damage.

The consequences of DNA damage depend on the cell type and the severity of the damage. Mild DNA damage can be repaired with or without cell-cycle arrest. More severe and irreparable DNA injury leads to the appearance of cells that carry mutations or causes a shift towards induction of the senescence or cell death programs. Although for many years it was argued that DNA damage kills cells via apoptosis or necrosis, technical and methodological progress during the last few years has helped to reveal that this injury might also activate death by autophagy or mitotic catastrophe, which may then be followed by apoptosis or necrosis. The molecular basis underlying the decision-making process is currently the subject of intense investigation. Here, we review current knowledge about the response to DNA damage and subsequent signaling, with particular attention to cell death induction and the molecular switches between different cell death modalities following damage.


Glioblastoma: bridging the gap with gene therapy.

Adult glioblastoma is the most common primary brain tumour. It is characterised by substantial morbidity and mortality despite multimodal therapy with surgical resection and adjuvant radiochemotherapy as standard care.1 The poor prognosis is largely due to the disease’s high frequency of recurrence, which is indicative of its intrinsic invasive properties into the peritumoral zone.2 Consequently, an unmet need exists to improve local control of glioblastoma beyond the margin of resection and to explore new treatment options targeted peritumouraly. Local therapies that can be applied during surgery are therefore well-suited to bridge the gap between initial surgical resection and subsequent radiochemotherapy. In The Lancet Oncology, Manfred Westphal and colleagues3 explore the use of so-called suicide gene therapy to address this treatment gap, describing the results of a randomised, open-label phase 3 trial (ASPECT) for the treatment of operable high-grade glioblastoma. This trial was based on previous phase 1 and phase 2 trials4—6 and relies on local injection into the resection cavity of a replication-deficient adenoviral vector encoding a herpes simplex virus thymidine kinase (HSV-tk) gene to selectively eliminate any residual glioblastoma cells. The HSV-TK catalyses the conversion of a non-toxic ganciclovir prodrug into a toxic nucleotide analogue that is incorporated into the DNA of dividing cancer cells, prompting apoptosis. This approach overcomes the typical inaccessibility of glioblastoma tumour, and brain-infiltrating, cells to most systemic therapies. Moreover, preclinical studies indicate that both the HSV-tk gene-modified cells and adjacent, non-modified dividing cells are eliminated through a so-called bystander effect that enhances the overall anti-tumour effect. This bystander effect is probably mediated by intercellular trafficking of the toxic ganciclovir metabolites through gap junctions or immune mechanisms.78 Another advantage is that normal neurons do not proliferate and are therefore resistant to the ganciclovir metabolites, which improves the tumour selectivity of this treatment strategy.

The specific objective of the ASPECT trial was to determine whether ganciclovir with adenoviral HSV-tk gene therapy was better than standard care, with time to death or re-intervention as the composite primary endpoint. After the ASPECT trial had begun, temozolomide emerged as a new and effective treatment for glioblastoma and was included in both the treatment and control groups. Consequently, this invalidated the initial statistical analysis strategy. A post-hoc multivariate statistical analysis based on a Cox’s proportional hazards model was therefore needed for the composite primary endpoint, which took into consideration the use of temozolomide as a time-dependent covariate. The methylation status of the MGMTpromoter is a prognostic factor and was therefore also taken into account as a covariate in the Cox analysis. MGMT encodes a DNA-repair enzyme that removes alkyl groups from DNA. High levels of MGMT activity in glioblastoma annihilate the therapeutic effect of alkylating agents, including temozolomide, creating a temozolomide-resistant phenotype. Conversely, epigenetic silencing of the MGMT gene by promoter methylation in glioblastoma cells is associated with loss of MGMTexpression, diminished DNA-repair activity, and increased sensitivity to temozolomide. Consequently, patients with glioblastoma containing a methylated MGMT promoter benefit from temozolomide, whereas the drug has no therapeutic effect in those with an unmethylated MGMT promoter.9

In the multivariate statistical analysis of the ASPECT trial, patients in the experimental group had a favourable outcome in terms of the primary composite endpoint—time to death or re-intervention—compared with those in the standard care group (hazard ratio 1·53, 95% CI 1·13—2·07; p=0·006). One of the intriguing findings of this trial is that a post-hoc subgroup analysis showed an even more pronounced effect in a subgroup of patients with an unmethylated MGMT promoter (hazard ratio 1·72, 1·15—2·56; p=0·008). Hemiparesis, hyponatraemia, and seizures were more common in the experimental group and were mainly transient. Despite the statistically significant effect on the composite primary endpoint, the difference in overall survival between gene therapy and standard care was not statistically significant. Nevertheless, there seemed to be improved overall survival in the experimental group versus the control group in a subgroup of patients with non-methylatedMGMT, although this difference was not statistically significant. This finding needs substantiation in larger trials. The investigators recorded no between-group difference in tumour sizes at the time of re-intervention, suggesting that the time to re-intervene was not biased in favour of the treatment group.

Findings from the ASPECT trial raise several interesting hypotheses and questions. Most importantly, the post-hoc multivariate analysis suggests that patients with a glioblastoma containing an unmethylated MGMT promoter might benefit most from the proposed gene therapy strategy. This difference in regards to methylation status might ultimately create new perspectives for the treatment of patients who do not benefit from temozolomide treatment. Methylation status of the MGMTpromoter was not prespecified at the time of treatment, ruling out a possible treatment bias. Post-hoc analysis also showed that the effect of the treatment seemed to be greater in patients with a higher baseline titre of adenovirus-specific neutralising antibodies, suggesting a possible immunological bystander effect resulting from previous infection with wild-type adenovirus.8 Further studies are needed to address these different hypotheses. Findings from the ASPECT trial also indicate a need to develop new approaches that augment transduction efficiency, improve vector spread within the residual tumour tissue, and enhance bystander effects. The continuous development of these multipronged strategies represent the new for patients and their families.

Source: Lancet


8 Summer Beverages to Avoid.


Story at-a-glance

  • Many of the most popular “summer” drinks come with a hefty downside, like exorbitant amounts of sugar or artificial sweeteners
  • Summer drinks better off avoided include regular and diet soda, wine coolers, beer, lemonade, sports and energy drinks, and frozen coffees
  • Carbonated water with mint leaves, fresh green vegetable juice, coconut water, iced green tea and iced dark-roast organic coffee are examples of delicious summer beverages that give your health a boost

A tall, cool beverage goes hand-in-hand with a hot summer day, but many of the most popular “summer” drinks come with a hefty downside, like exorbitant amounts of sugar.

It’s alarmingly easy to sip and slurp your way through hundreds of grams of excess sugar just by enjoying a cool drink once or twice a day – and that’s only the start.

There are plenty of options to quench your thirst and even satisfy your sweet tooth that will actually support your health at the same time (I’ll get to those later), so there’s no reason to sabotage your health (and your waistline) with these dietary disasters.

8 Top Summer Beverages to Avoid

1. Soda (Regular or Diet)

Drinking soda is in many ways as bad as smoking. Most sodas contain far too much sugar, or even worse, artificial sweeteners.

For instance, the chemical aspartame, often used as a sugar substitute in diet soda, has over 92 different side effects associated with its consumption including brain tumors, birth defects, diabetes, emotional disorders and epilepsy/seizures. Plus, each sip of soda exposes you to:

  • Phosphoric acid, which can interfere with your body’s ability to use calcium, leading to osteoporosis or softening of your teeth and bones.
  • Benzene. While the federal limit for benzene in drinking water is 5 parts per billion (ppb), researchers have found benzene levels as high as 79 ppb in some soft drinks, and of 100 brands tested, most had at least some detectable level of benzene present. Benzene is a known carcinogen.
  • Artificial food colors, including caramel coloring, which has been identified as carcinogenic. The artificial brown coloring is made by reacting corn sugar with ammonia and sulfites under high pressures and at high temperatures.
  • Sodium benzoate, a common preservative found in many soft drinks, which can cause DNA damage. This could eventually lead to diseases such as cirrhosis of the liver and Parkinson’s.

2. Wine Coolers

Wine coolers are alcoholic beverages made to taste much more like fruit juice than alcohol, which is why they’re a popular drink of choice on a warm summer day. But in order to make them taste sweet, manufacturers typically add fruit juice and sugar to the wine, which is usually the cheapest available grade. Some “wine” coolers aren’t even made from wine but the far cheaper “malt” instead.

These coolers can also contain artificial food colors, artificial flavors and even artificial sweeteners like aspartame. And, of course, they also contain alcohol, which is very similar to fructose both in its addictive properties and the kind of damage it can do to your health.

While I don’t recommend drinking alcohol (it is a neurotoxin that can poison your brain as well as disrupt your hormonal balance), if you’re going to have an alcoholic beverage, a glass of red or white wine is far preferable to a heavily (or artificially) sweetened wine cooler.

3. Beer

The “usual” problems associated with beer – its alcohol content and hefty amount of empty calories – are only the tip of the iceberg for why you should limit your consumption. It turns out that the yeast and all that’s used to make beer work together to make beer another powerful uric acid trigger.

Uric acid is a normal waste product found in your blood. High levels of uric acid are normally associated with gout, but it has been known for a long time that people with high blood pressure or kidney disease, and those who are overweight, often have high uric acid levels as well. It used to be thought that the uric acid was secondary in these conditions, and not the cause.

But research by Dr. Richard Johnson indicates that it could be a lead player in the development of these conditions, rather than just a supporting actor, when its levels in your body reach 5.5 mg per dl or higher. At this level, uric acid is associated with an increased risk for developing high blood pressure, as well as diabetes, obesity and kidney disease.

The classic “beer belly syndrome” is actually quite similar to metabolic syndrome, and includes abdominal obesity, hypertriglyceridemia (high triglycerides), high blood pressure, and even insulin resistance, so minimizing or eliminating beer consumption is also something to definitely consider when you’re watching your weight and trying to improve your health.

4. Lemonade and Fruit Juices

For many, nothing says “summer” like a cold glass of lemonade, but this, and other fruit juices, is usually just another source of sugar you’re better off without.

Lemonade is typically a concoction of sugar or high fructose corn syrup, water, and flavorings. It may or may not contain small amounts of actual lemon juice. In terms of its impact on your health, lemonade and fruit juice will act much like soda, exposing you to excessive amounts of fructose that will increase your risk of weight gain and chronic degenerative diseases. Lemonade is simply soda’s evil twin in disguise! However, if you make fresh lemonade or limeade then it is fine because these are the lowest fruits in fructose. Just be sure if you use a sweetener that you stick to stevia and avoid sugar and artificial sweeteners.

5. Sweetened Teas

Sweet tea is another popular summer beverage, and one that’s often confused as “healthy” because of the tea. While teacan be a good source of antioxidants, sweetened tea is another source of extra sugar that will decimate your health. While the actual sugar content of sweetened teas obviously varies, it’s not unusual to find sweet tea recipes that contain 22 percent sugar, which is twice the amount in a can of soda.1

In the Southern US, sweet tea is not an occasional treat, it’s more of a daily staple, making the health risks even steeper.

6. Energy Drinks

The US energy drink market is expected to reach nearly $20 billion in 2013, which is close to a 160 percent increase from 2008.2 While many choose them for the quick energy boost they provide, consuming large quantities of caffeine in energy drinks can have serious health consequences, especially in children and teens, including caffeine toxicity, stroke, anxiety, arrhythmia, and in some rare cases death. Drinking energy drinks has also been compared to “bathing” teeth in acid because of their impact on your tooth enamel.3

If a lack of energy and fatigue state is compelling you to drink energy drinks, please realize that this is likely a result of certain lifestyle choices, such as not enough healthy food, processed foods and sugar, and not enough exercise and sleep, plus an overload of stress. Increasing your energy levels, then, is as easy as remedying these factors.

7. Sports Drinks

Sports drinks are especially popular in the summer months, when many believe they are necessary to restore your electrolyte balance during exercise or other outdoor activities. They basically “work” because they contain high amounts of sodium (processed salt), which is meant to replenish the electrolytes you lose while sweating. But only a very small portion of exercisers work out hard enough that a sports drink might be necessary; typically they aren’t even necessary during amarathon, let alone during most regular workouts.4

Additionally, the leading brands of sports drinks on the market typically contain as much as two-thirds the sugar of sodas and more sodium. They also often contain high-fructose corn syrup (HFCS) or artificial sweeteners (they can lead to impaired kidney function, depression, headaches, infertility, brain tumors, and a long list of other serious health problems), artificial flavors and food coloring, which has been connected to a variety of health problems, including allergic reactions, hyperactivity, decreased IQ in children, and numerous forms of cancer.

Also, sports drinks are up to 30 times more erosive to your teeth than water. And brushing your teeth won’t help because the citric acid in the sports drink will soften your tooth enamel so much it could be damaged by brushing.

8. Frappes and Other Frozen/Iced Coffees

An iced coffee sounds innocent enough, until you start adding in the copious amounts of sweeteners (sugar, HFCS and artificial sweeteners may all apply) and flavorings that turn ordinary coffee into a treat that more closely resembles a hyped up milkshake. Some leading coffee drinks from restaurants like Dunkin’ Donuts and Seattle’s Best contain 100 grams of sugar or more, which is more than 2.5 times the amount of sugar an adult man should consume in a day!5

Delicious and Refreshing Summer Drinks That BOOST Your Health

I know what you’re thinking… you’re not going to give up the simple pleasure of enjoying a cool, tasty beverage on a hot summer day. And I should hope not! But you needn’t assume that sugar-laden soda, lemonade, sweet tea or frappes are your only options. By thinking outside the box, you can satisfy your craving for a delicious cool beverage in a way that will actually support instead of hinder your health.

Instead Of … Choose …
Soda Sparkling mineral water… spruce it up with fresh lemon or lime juice, a drop or two of natural peppermint extract, liquid stevia, cucumber slices or a few crushed mint leaves.

If you’re adventurous, there are mint-flavored chlorophyll drops on the market that can be added to a glass of water. Chlorophyll may help flush toxins out of your blood and improves your breath.

Wine Coolers A small glass of white or red wine, ideally organic and biodynamic, on occasion.
Beer Try adding whole gingerroot to chilled carbonated water for a spicy alternative.
Lemonade or Fruit Juice Here’s a recipe for a refreshing homemade fruit drink that’s actually good for you. You can even throw in frozen berries instead of ice cubes.
Another tasty option is to blend some homemade kefir with frozen blueberries, raspberries or any fruit you enjoy. Kefir is a fermented milk beverage that contains beneficial bacteria that give your immune system a boost, among many other health benefits.

To make kefir all you need is one-half packet of kefir starter granules in a quart of raw milk, which you leave at room temperature overnight.

Sweetened Tea Iced green tea is a great pick-me-up that’s high in antioxidants. Although green tea contains caffeine, it also contains a naturally calming amino acid called L-theanine, which balances out caffeine’s adverse effects.

If you want it sweet, you can add natural liquid stevia, which is an herb that has no downsides for your health.

Another option is Tulsi tea (aka Holy Basil), which has a naturally delicious taste – slightly sweet and a bit spicy.

Energy Drinks For the ultimate refreshing vitamin-rich energy drink, make up some green juice from fresh, organic veggies like spinach, parsley, cucumbers and celery.

Add a pinch of sea salt and some lemon juice for a very refreshing beverage that is heavy on nutrition and virtually guaranteed to give you lasting energy.

Sports Drinks Try coconut water, which is a powerhouse of natural electrolytes, vitamins, minerals, trace elements, amino acids, enzymes, antioxidants and phytonutrients, and is low in sugar but pleasantly sweet.

It’s great for post-exercise rehydration, but also has anti-inflammatory properties, protects your heart and urinary tract, is a digestive tonic, improves your skin and eyes, supports good immune function, and can even help balance your blood glucose and insulin levels.

Look for a brand that has no additives, or purchase a young coconut and drain the coconut water yourself.

Frappes and Frozen Coffee Drinks Organic dark-roast coffee served over ice (without additives like milk or sugar) is refreshing and may even lower your risk for type 2 diabetes, Parkinson’s disease, dementia, stroke, and cancers of the liver, kidney and prostate.

When consumed in this healthful manner, coffeemay even lower your blood glucose level and increase the metabolic activity and/or numbers of beneficial Bifidobacteria in your gastrointestinal tract.




Why is cancer so common?.


Hundreds of thousands of people are diagnosed with cancer every year in the UK. It is not one disease; there are over 200 different types, each with its own symptoms, methods of diagnosis and treatment.

What is cancer?

Cancer starts when cells in our bodies start to reproduce out of control, forming new, abnormal cells. These abnormal cells form lumps, known as tumours.

If the cells from tumours cannot spread, then the tumours are benign. They are not cancerous and can usually be removed.

If the cells are able to invade nearby healthy tissue and organs, or spread around the body through the blood or lymphatic system causing further tumours to grow, then the tumours are malignant or cancerous. These cancer cells are likely to spread if the tumour is not treated.

What causes cancer?

Every cell in our body contains DNA. It carries our genetic code and contains the instructions for all the cell’s actions.

If the DNA inside cells is damaged, these instructions go wrong. In fact damage to the DNA or “mutations” as they are known, constantly occur in our cells as they divide and reproduce. Most of the time, the cells recognise that a mutation has occurred and repair the DNA, or self-destruct and die.

When a number of mutations have occurred in the DNA of a cell, control of cell growth may be lost and the cells do not die. Instead they start to follow abnormal instructions that make them reproduce and grow, producing more and more of these mutated cells – this is the start of a cancer.

Many factors such as smoking or too much exposure to the sun can also trigger DNA damage – leading to a faster accumulation of the mutations which lead to cancer.

A family history of cancer can also increase chances of getting the disease, because it usually means that person starts their life already having inherited some of the DNA mutations that take them down the path to cancer.

Even when in remission, those who have had the disease have a higher risk of it developing again. In most cases however, the exact cause or sequence of events by which cancer develops, is not yet known

A recent study has found that there are more than 80 genetic markers (i.e. mutated genes) that can increase the risk of developing breast, prostate or ovarian cancer, for example. Scientists believe the results could soon lead to widespread use of DNA profiling for these cancers, though individual genetic testing for those likely to be at increased risk – such as when there is a strong family history of a type of cancer – is already in use.

Why is it so deadly?

Cancer cells are able to invade other parts of the body, where they settle and grow to form new tumours known as secondary deposits – the original site is known as the primary tumour. The cells spread by getting into the blood or lymph vessels and travelling around the body.

For example, if bowel cancer has spread through the wall of the bowel itself, it can start growing on the bladder. If cells enter the bloodstream they can travel to distant organs, such as the lungs or brain. Over time, the tumours will then replace normal tissue.

The process of cancer cells spreading is called metastasis. Once a cancer has started to spread, the chances of a cure often begin to fall, as it becomes more difficult to treat for a variety of reasons.

Cancer harms the body in a number of ways. The size of the tumour can interfere with nearby organs or ducts that carry important chemicals. For example, a tumour on the pancreas can grow to block the bile duct, leading to the patient developing obstructive jaundice. A brain tumour can push on important parts of the brain, causing blackouts, fits and other serious health problems. There may also be more widespread problems such as loss of appetite and increased energy use with loss of weight, or changes in the body’s clotting system leading to deep vein thrombosis.

Why is it so hard to stop?

Cancer is an extremely complex condition. Each type of cancer is biologically different from any other type. For example, skin cancer is biologically different from the blood cancer called lymphoma, of which there are then many different types.

That is then coupled with genetic differences between individuals and the often random nature of the DNA mutations that cause cancer.

All this makes it difficult to identify the way the particular cancer cells are behaving and how they are likely to spread or damage the body. Without a full understanding of the physiology of the cancer, effective treatments are hard to develop.

How common is cancer?

  • More than one in three people will develop some form of cancer during their lifetime
  • In 2010 324,579 people in the UK were diagnosed with cancer (excluding non-melanoma skin cancer).

Source: Cancer Research UK

Early surgery to remove tumours can work. But the cancer can return if any cells are left behind. It can also return if cells have broken away from the primary tumour and formed microscopic secondary tumours elsewhere in the body before an operation to remove the primary.

And because cancer cells are our own body’s cells, many treatments to destroy them also risk destroying our healthy cells.

One controversial theory of why cancer is so hard to stop is that it is rooted in the ancient traits of our genes.

Prof Paul Davies from Arizona State University believes cancer may use tried-and-tested genetic pathways going back a billion years to the dawn of multicellular life, when unregulated cell growth would have been an advantage.

He argues that this tendency was suppressed by later, more sophisticated genes, but lies dormant in all living organisms. Cancer occurs when something unlocks these ancient pathways.

Other scientists disagree, saying that these pathways would not have survived millions of years of evolution.

One thing is for sure – our genes hold the key to understanding cancer and how to treat it.

The future of cancer research

The field of cancer research is moving away from defining a cancer by where it is in the body, as one type of breast cancer can have more in common with an ovarian cancer than another cancer in the breast.

Instead scientists are looking deeper at what is going wrong inside cancerous cells – a tumour can have 100,000 genetic mutations and these alter over time.

By pinpointing the mutations that can cause certain cancers, doctors hope to personalise treatment – choosing the drug most likely to work on a particular type of tumour.

Scientists are creating targeted cancer therapies using their latest insights into cancer at a molecular level. These treatments block the growth of cancer by interfering with genetic switches and molecules specifically involved in tumour growth and progression.

Clinical trials using gene therapy are also underway. This experimental treatment involves adding genetic material into a person’s cells to fight or prevent disease.

Source: BBC



Does Diagnostic Radiation Increase Breast Cancer Risk in Women with BRCA Mutations?

European questionnaire-based study leaves the question unanswered.

Because ionizing radiation can damage DNA, diagnostic x-ray exposure in individuals with defects in DNA repair mechanisms (such as those associated with BRCA1 and BRCA2 mutations) could lead to excess risk for cancer. Investigators surveyed women with documented BRCA1/2 mutations in the Netherlands, France, and the U.K. to evaluate any association between radiation exposure and later development of breast cancer. Questionnaires were administered to BRCA1/2 carriers from 2006 to 2009 to elicit their recollections of the type and number of diagnostic procedures they had received in their lifetimes. Estimates of radiation doses to the breast during each type of diagnostic procedure (mammography, fluoroscopy, and computed tomography and conventional radiography of the chest or shoulder) were used to determine total cumulative dose. Cases that were diagnosed >5 years before completion of the study questionnaire were excluded to prevent survival bias.

Of the 1993 participants, 43% (mean age, 49.7) had received diagnoses of breast cancer. Self-reported exposure to any form of diagnostic radiation before age 30 was associated with significantly higher risk for breast cancer (hazard ratio, 1.90; 95% confidence interval, 1.20–3.00), and risk rose with increasing cumulative dose. A history of mammography before age 30 was associated with nonsignificantly increased risk for breast cancer (HR, 1.43; 95% CI, 0.85–2.40). No evidence of excess risk was found for diagnostic radiation exposure between ages 30 and 39.

Comment: As with other epidemiologic studies of diagnostic radiation and risk for breast cancer in BRCA1/2 mutation carriers, the results of this study are inconclusive. The retrospective questionnaire design is subject to recall bias, especially given that women were asked to recollect events occurring up to 30 years earlier. Moreover, no attempt was made to document the date and type of radiologic tests that were reported. Furthermore, estimates of cumulative radiation dose were hypothetical and subject to wide variation based on factors in individuals as well as facilities. Until further data are obtained, the National Comprehensive Cancer Network recommendation of screening with magnetic resonance imaging and mammography in BRCA mutation carriers beginning at age 25 should be followed.

Source: Journal Watch Oncology and Hematology




Cell-Specific Radiosensitization by Gold Nanoparticles at Megavoltage Radiation Energies

Gold nanoparticles (GNPs) have been shown to cause sensitization with kilovoltage (kV) radiation. Differences in the absorption coefficient between gold and soft tissue, as a function of photon energy, predict that maximum enhancement should occur in the kilovoltage (kV) range, with almost no enhancement at megavoltage (MV) energies. Recent studies have shown that GNPs are not biologically inert, causing oxidative stress and even cell death, suggesting a possible biological mechanism for sensitization. The purpose of this study was to assess GNP radiosensitization at clinically relevant MV X-ray energies.

Methods and Materials

Cellular uptake, intracellular localization, and cytotoxicity of GNPs were assessed in normal L132, prostate cancer DU145, and breast cancer MDA-MB-231 cells. Radiosensitization was measured by clonogenic survival at kV and MV photon energies and MV electron energies. Intracellular DNA double-strand break (DSB) induction and DNA repair were determined and GNP chemosensitization was assessed using the radiomimetic agent bleomycin.


GNP uptake occurred in all cell lines and was greatest in MDA-MB-231 cells with nanoparticles accumulating in cytoplasmic lysosomes. In MDA-MB-231 cells, radiation sensitizer enhancement ratios (SERs) of 1.41, 1.29, and 1.16 were achieved using 160 kVp, 6 MV, and 15 MV X-ray energies, respectively. No significant effect was observed in L132 or DU145 cells at kV or MV energies (SER 0.97–1.08). GNP exposure did not increase radiation-induced DSB formation or inhibit DNA repair; however, GNP chemosensitization was observed in MDA-MB-231 cells treated with bleomycin (SER 1.38).


We have demonstrated radiosensitization in MDA-MB-231 cells at MV X-ray energies. The sensitization was cell-specific with comparable effects at kV and MV energies, no increase in DSB formation, and GNP chemopotentiation with bleomycin, suggesting a possible biological mechanism of radiosensitization.

source: IJROBP