Cancer pill fights disease and gives lifelong protection.

British scientists have discovered a drug which fights all cancers by boosting the body’s defences and prevents the disease returning by increasing natural immunity

A pill which boosts the immune system so thebody can naturally fight off cancer has been developed by scientists

A pill which boosts the immune system so thebody can naturally fight off cancer has been developed by scientists

A pill which boosts the body’s natural defences could help fight off all cancers and stop them ever returning, scientists believe.

‘Delta-inhibitors’ were already known to help leukaemia patients, but researchers were amazed to find they also work on a whole range of other cancers.

The drugs, which are taken orally as a pill, were so successful in leukaemia trials that the control group, who were taking placebos, were immediately switched to the medication on ethical grounds.

Now, scientists at UCL and the Babraham Institute in Cambridge, have discovered that the same ‘delta inhibitors’ are also effective against lung, pancreatic, skin and breast cancers, and probably many more.

Cancer suppresses the immune system by producing an enzyme called ‘p100delta’ which tells it to power down, making it difficult for the body to fight the disease. The drugs ‘inhibit’ that enzyme, allowing the immune system to attack tumour cells.

The added benefit is that once the body has learned to fight off the cancer, it has in-built immunity, so that the disease can never return, unlike if it had been killed by chemotherapy.

Although the study was conducted in mice, researchers are confident it would work in humans and are hopeful that human trials will begin soon.

“This helps your own immune system fight off the cancer better. The good guys win. And it seems to work on all cancers,” said study co-leader Professor Bart Vanhaesebroeck of the UCL Cancer Institute, who first discovered the p110 delta enzyme in 1997.

“It will work to a certain extent on its own, if the tumour is not too big, but it would be very effective after surgery, to prevent spreading.

“So it is very exciting. We have shown that blocking ‘p110delta’ also has the remarkable effect of boosting the body’s immune response against leukaemias as well as other cancers.”

The team showed that inhibiting the enzyme in mice significantly increased cancer survival rates across a broad range of tumour types, both solid and blood cancers.

Mice given the drug survived breast cancer for almost twice as long.

Their cancers also spread significantly less, with far fewer and smaller tumours developing. Survival after surgical removal of primary breast cancer tumours was also vastly improved, which has important clinical implications for stopping breast cancer from returning following surgery.

And they discovered that the immune system ‘remembers’ the cancer and can fight it off completely again. Mice who were given cancer a second time all survived.

“Our work shows that delta inhibitors can shift the balance from the cancer becoming immune to our body’s defences towards the body becoming immune to the cancer,” said study co-leader Dr Klaus Okkenhaug of the Babraham Institute at Cambridge University.

“This provides a rationale for using these drugs against both solid and blood cancers, possibly alongside cancer vaccines, cell therapies and other treatments that further promote tumour-specific immune responses.”

The drugs are already being used in clinical trials and have been granted Breakthrough Therapy status by the Federal Drugs Agency in the US, which means their development has been speeded up.

They could be available within just a few years if approved by European regulators and the National Institute of Clinical Excellence.

Professor Nic Jones, Cancer Research UK’s chief scientist and director of the Manchester Cancer Research Centre, said: “Treatments that train the immune system to recognise and kill cancer cells are showing huge promise in several types of cancer.

“This new finding, although only at an early stage, offers the potential to develop more treatments that can do this in many more cancers, including ones that have real need for more effective treatments such as pancreatic cancer.”

‘Elixir of Youth’ Found? New Experimental drug.

As seen on Learning Mind| Scientists from Harvard Medical School claimed that they have finally found the ‘elixir of youth’ which can not only slow down the aging process, but also reverse it. This rejuvenating substance created by American scientists currently works only on mice.

“We worked on understanding the mechanisms of aging and conducted experiments on mice. For this purpose we selected mature enough animals that were older than two years, and began to introduce the experimental drug. To our surprise, just in a week the mice got younger. They became vigorous and energetic as if they were six-month old,” said Prof David Sinclair of Harvard Medical School.

The muscles of the rejuvenated mice were in tone, and their cardiac muscles were as new. It’s as if a 60-year-old man turned into a 17-year-old. The coenzyme nicotinamide adenine dinucleotide (NAD) has played a major role in this incredible transformation. In a living organism, NAD serves as a conduit between the nucleus and mitochondria. The latter generates energy, and NAD delivers it to the cell nucleus. At low concentration of NAD, communication between mitochondria and the nucleus of cells weakens.

“This substance is present in our body. However, with age, its concentration becomes lower and lower. We hypothesized that this might be the cause of aging, and introduced a drug to increase the level of this substance in mice,” said Prof Sinclair. Moreover, young mice, which also were given a dose of NAD, became more alert and energetic. At the moment, the scientists have the following tasks to be accomplished: to determine how long the rejuvenating effect will hold, to identify side effects of the drug, as well as to find out whether it may be used in humans.

The study’s authors hope to test the drug on humans this year. However, it is worth noting that the cost of a single drop of NAD – which is a daily dose for a mouse – is about $ 1,000. Therefore, in case of successful outcome of further testing, it is necessary to find a way to reduce its cost to launch the mass production of the drug.


– See more at:

20 useless inventions

Have you hear for those inventions that sounded good on paper, but when they were actually designed, they weren’t so cool anymore?

Shoes umbrella

Walking sleeping bag

Airco shoes

Private TV

baby mop

Cats wigs

Finger protection

Rock pet


 watch  the video:

Dangers of Garcinia Cambogia Extract .

Don’t get tricked by this popular diet scam


Tons of people are buzzing about garcinia cambogia extract diet pills—thanks in part to an Internet scam that illegally used the Women’s Healthbrand likeness and copyrighted materials (and the likeness and materials of other respected health brands) to promote the pills. We wrote about the scam at length here, in addition to how to identify if you’ve been scammed.

But here’s something else super troubling about all this: All backstory about scammers aside, this particular diet pill can be dangerous to your health.

Garcinia cambogia, which on its own is pretty darn delicious and healthy, is a tropical fruit grown in Indonesia. (It also goes by the name tamarind fruit.) According to Purdue University, it’s rich in calcium, phosphorus, iron, thiamine, riboflavin, and niacin. All good things, right?

Well, here’s where things get tricky: Its rind contains a compound called hydroxycitric acid (HCA), which proponents claim decreases appetite and prevents your body from storing food as fat. However, since garcinia cambogia extract diet pills are supplements, not drugs, the Food and Drug Administration doesn’t regulate their use or review their effectiveness or safety unless, as was the case with OxyElite Pro, their use becomes linked to multiple hospitalizations, says medical weight-loss expert Sue Decotiis, M.D. That means that it’s up to manufacturers to decide how much garcinia cambogia their pills pack, as well as what other health-impacting ingredients are added to the mix.

“Most brands of garcinia cambogia extract diet pills, including big names, have failed independent laboratory quality and quantity testing,” says Decottis. “Also, there have been no large-scale trials comparing garcinia to placeboes or other supplements. There probably will never be any objective data on garcinia.”

What’s more, a 2005 study in Food and Chemical Toxicology found that high doses of garcinia cambogia extract caused testicular atrophy and toxicity in mice. Even if you don’t have testicles, that’s sure to make you cringe.

Our advice? Ditch the fads and check out these five easy ways to lose weight fast—no pills required.

Scientists condemn ‘crazy, dangerous’ creation of deadly airborne flu virus .

Researchers say recreation of Spanish flu strain highlights risk of pandemic, but critics say work puts global population at risk
The avian flu strain H5N1, seen in gold, grown in Madin-Darby canine kidney cells. It has killed at least 386 people since 2003. Photograph: AP/CDC/C Goldsmith

Scientists have created a life-threatening virus that closely resembles the 1918 Spanish flu strain that killed an estimated 50m people in an experiment labelled as “crazy” by opponents.

US researchers said the experiments were crucial for understanding the public health risk posed by viruses currently circulating in wild birds, but critics condemned the studies as dangerous and called on funders to stop the work.

Scientists at the University of Wisconsin-Madison used a technique called reverse genetics to build the virus from fragments of wild bird flu strains. They then mutated the virus to make it airborne to spread more easily from one animal to another.

“The work they are doing is absolutely crazy. The whole thing is exceedingly dangerous,” said Lord May, the former president of the Royal Society and one time chief science adviser to the UK government. “Yes, there is a danger, but it’s not arising form the viruses out there in the animals, it’s arising from the labs of grossly ambitious people.”

Influenza viruses circulate freely in wild bird populations. Most remain in chickens, ducks and other birds, but occasionally strains mutate into a form that can infect humans. The H5N1 bird flu strain has killed at least 386 people since 2003, according to WHO figures. The Spanish 1918 flu is thought to have come from birds too.

Writing in the journal Cell Host and Microbe Yoshihiro Kawaoka describes how his team analysed various bird flu viruses and found genes from several strains that were very similar to those that made up the 1918 human flu virus. They combined the bird flu genes into a single new virus, making a new pathogen that was only about 3% different from the 1918 human virus.

The freshly made virus – the first of several the team created – was more harmful to mice and ferrets than normal bird flu viruses, but not as dangerous as the 1918 strain. It did not spread between ferrets and none of the animals died. But the scientists went on to mutate the virus, to see what changes could make it spread. Seven mutations later, they had a more dangerous version that spread easily from animal to animal in tiny water droplets, the same way flu spreads in humans.

Kawaoka, who led the research in a high-security lab at the University of Wisconsin-Madison, said the work highlighted how flu viruses found in wild bird populations had the potential to adapt to humans and cause a pandemic.

Follow-up experiments showed that the 2009 swine flu vaccine and the anti-viral drug tamiflu should be effective against the virus. “This is important information for those making decisions about surveillance and pandemic preparedness,” Kawaoka told the Guardian.

The work is the latest in a series of controversial studies that have split the scientific community. On the one side are researchers who create dangerous viruses in secure labs in the hope of learning how existing strains could mutate to make them a potential threat to humans. On the other are scientists who argue the work does little or nothing to help protect people, but instead puts the global population in more danger.

Marc Lipsitch, professor of epidemiology at Harvard School of Public Health, said: “I am worried that this signals a growing trend to make transmissible novel viruses willy-nilly, without strong public health rationale. This is a risky activity, even in the safest labs. Scientists should not take such risks without strong evidence that the work could save lives, which this paper does not provide,” he added.

In an article published last month, Lipsitch argued that experiments like Kawaoka’s could unleash a catastrophic pandemic if a virus escaped or was intentionally released from a high-security laboratory.

But Kawaoka defended the work, saying that critics failed to appreciate the impact of his and others’ work on dangerous viruses. “There were discussions on the usefulness of stockpiling H5N1 [bird flu] vaccines until our H5N1 papers were published. Similarly, this paper strongly supports stockpiling anti-influenza drugs. If this is not a ‘lifesaving benefit’, what is?” he said.

Many of the groups that create dangerous viruses to understand their workings are funded by the US National Institutes of Health (NIH). Lord May said he suspected the NIH supported the work because officials there were “incompetent” and believed the justifications that scientists told them. “This is work that shouldn’t be done. It’s as simple as that,” he said.

The experiments show that a 1918-like flu virus could emerge in the wild as bird viruses swap genes and mutate. “Influenza viruses readily swap genes to generate new viruses, so something like this could happen, especially since many of these viruses have circulated in recent years,” Kawaoka said. The viruses “have the potential to become adapted to mammals and possibly cause a human pandemic,” he added.

The study identifies particular mutations that made the virus spread so easily. But that is not much use for surveillance, said Lipsitch, because there are scores of other mutations that could have the same effect. “The chance that a virus very similar to the one they study will appear in nature is extremely remote,” he said. Kawaoka argues that his team is fully aware of this, and that the underlying mechanisms that make the virus so dangerous are more important for preventing future pandemics.

Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, said he feared that governments and funding bodies would only take the risks seriously once an accident had happened. “It’s madness, folly. It shows profound lack of respect for the collective decision-making process we’ve always shown in fighting infections. If society, the intelligent layperson, understood what was going on, they would say ‘What the F are you doing?'”

Carole Heilman, director of microbiology and infectious diseases at the National Institute of Allergy and Infectious Diseases (Niaid) in the US, said: “This study was conducted as part of a research project on understanding the molecular mechanisms of virulence of the 1918 influenza virus. NIH peer review determined that the research was scientifically meritorious. It was also determined that the information gained had the potential to help public health agencies in their assessment of circulating and newly emerging strains. In addition, NIH determined that all the research was being done under appropriate biosafety conditions and with appropriate risk mitigation measures.”

What do you want to know about sleep? Neuroscientists answer your questions

Sleep is vital for our mental and physical health, yet an increasing number of people are getting less than they need. Do you have problems sleeping? Neuroscientists from the University of Oxford answered your questions

Using Technology At Night in Bed
Do you get enough sleep? Ask your question in the comment thread 

Do you have difficulty getting enough sleep? Sleep problems affect one in three of us at any one time, and about 10% of the population on a chronic basis. Of Guardian readers who responded to a recent poll, 23% reported that they sleep between four and six hours a night.

With continued lack of sufficient sleep, the part of the brain that controls language and memory is severely impaired, and 17 hours of sustained wakefulness is equivalent to performing on a blood alcohol level of 0.05% – the UK’s legal drink driving limit.

In 2002, American researchers analysed data from more than one million people, and found that getting less than six hours’ sleep a night was associated with an early demise – as was getting over eight hours.

Studies have found that blood pressure is more than three times greater among those who sleep for less than six hours a night, and women who have less than four hours of sleep are twice as likely to die from heart disease. Other research suggests that a lack of sleep is also related to the onset of diabetes, obesity, and cancer.

Are you worried about how much sleep you get?

Study IDs ‘master’ protein in pulmonary fibrosis

The protein CHI3L1 works to protect injured cells and to repair damage. In lung tissue, damage repair means a buildup of scar tissue, which compromises the lung. Levels of CHI3L1 are higher in patients with idiopathic pulmonary fibrosis (right) than in healthy controls. Credit: Brown University/Yale University

This spring has brought rare but tangible moments of progress against the devastating lung disease idiopathic pulmonary fibrosis (IPF), which afflicts millions of people worldwide. Two drugs recently showed promise in clinical trials, and now a study in Science Translational Medicine offers both an unprecedentedly deep explanation of how the disease progresses and introduces another potential therapeutic avenue.

The new study features a central figure: an evolutionarily ancient protein called “chitinase 3-like-1” (CHI3L1). The authors implicate it as the “master regulator” of what appears to be a tragically errant repair response to the mysterious lung injuries that give rise to the disease. In describing how CHI3L1 works in IPF, the research also points to a strategy for treatment.

The report demonstrates that CHI3L1 is produced to help in response to the . It feeds back to protect injured cells from dying and simultaneously stimulates  to patch the damage that has occurred. But the study also shows how this dual role contributes to the ultimate problem. If IPF resulted from a single injury, like a paper cut, CHI3L1 would decrease the injury and cause local scarring while it restored tissue integrity. In that case, the amount of scarring would not be excessive and tissue function would not be significantly altered. But in IPF lungs, cells undergo ongoing injury, so CHI3L1 is chronically elevated and scar tissue accumulates. As CHI3L1 rescues cell after cell, the scarring builds up, eventually compromising the lung’s ability to breathe. In IPF, 70 percent of patients die within five years.

“The CHI3L1 is doing exactly what it is supposed to do—it is designed to shut off cell death and decrease injury,” said Dr. Jack A. Elias, a co-senior author of the study and dean of medicine and biological sciences at Brown University. He is joined on the paper by a host of his former colleagues and students at Yale University where the research occurred. “But at the same time it is decreasing cell death it is driving the fibrosis. You’ve got this ongoing injury so you’ve got these ongoing attempts to shut off injury which stimulate scarring.”

In patients and the lab

The research team, including co-senior author Erica Herzog of Yale and co-lead authors Yang Zhou (who is transitioning to Brown from Yale), Huanxing Sun of Yale, and Hong Peng of Central South University in China used various means to uncover CHI3L1’s central role in IPF.

They compared tissues and serum from normal patients, outpatients with IPF, and patients with an acute exacerbation (AE) of IPF. In AE, widespread lung injury is superimposed on the, which frequently occurs before patients die. In lung biopsies and serum, they found that CHI3L1 levels are elevated in both tissue compartments in the outpatients with IPF and that the levels of CHI3L1 correlated with their disease progression. In the patients with AE, elevated levels of CHI3L1 were not noted, showing that the levels of CHI3L1 decrease right before the patients die.

“This demonstrates that the CHI3L1 plays a key role in controlling  in this setting,” Elias said.

After documenting that elevated levels of CHI3L1 correlate with ongoing fibrosis and scarring and that a lack of the protein associates with widespread , the team engaged in several manipulations of CHI3L1 in mice to see how levels and the clinical outcomes might be related. (In mice, CHI3L1 is also called BRP-39.)

Scientists can induce an IPF-like response in mice using a drug called bleomycin. In mice given bleomycin, the researchers found that the levels of CHI3L1 declined at first and then surged. At the times when the protein levels were low, cell damage occurred, and when the protein surged, the excessive scarring set in.

In previous research the team had engineered several lines of genetically modified mice. Some were transgenic and can produce CHI3l1 on chemically delivered command. Other mice were engineered to never produce BRP-39—the mouse version of CHI3L1—at all.

Using these mice, the researchers found that if they triggered CHI3L1 production early after administering bleomycin, the mice fared well, experiencing less injury, less damage and less scarring than controls. If they waited several days after bleomycin to trigger CHI3L1, the mice fared very poorly and scarring and mortality went up.

Mice who couldn’t produce CHI3L1/BRP-39, had acute lung cell damage, somewhat like AE patients who have a relative deficiency of CHI3L1. However, without CHI3L1 they did not generate much scarring.

All of these findings were supplemented with several other experiments that were designed to learn how CHI3L1 interacts with other cells involved in the tissue repair response in both human and mouse lungs. The experiments, including studies conducted in a bioengineered 3-D model of lung tissue seeded with relevant cells, showed that CHI3L1 regulates a pathway that recruits cells such as macrophages and fibroblasts that produce the scarring, or fibrosis.

In all, the results show that CHI3L1 plays a fundamental role in the course, if not the origin, of IPF. An ongoing buildup of it results in excessive scarring. Too little and cells die much more frequently.

“To my knowledge this is the first comprehensive paper that’s been able to explain the many facets and presentations of IPF,” Elias said. “It explains and links the injury and the repair responses that are critical in the disease. It also provides an explanation for the slowly progressing patients and the patients that experience acute exacerbations.”

Toward treatment

Elias said he hopes the insights will lead to new therapies for IPF. The idea would be to preserve the cell-protecting function of CHI3L1, while tempering its ability to stimulate tissue scarring and repair.

There may indeed be a way to do that, Elias said. Some data suggest that the mechanisms for each CHI3L1 function – cell protection and tissue repair – involve different pathways and or receptors. In people, therefore, separate drugs could hypothetically enhance the injury prevention pathway and temper the repair pathway. Indeed, drugs that block a key repair pathway receptor exist and are undergoing testing in other diseases, Elias said.

“This research lays the foundation for potential therapies that would be designed to diminish injury and ameliorate fibroproliferative repair,” Elias said.

12 Common Diseases Caused by Vitamin D Deficiency.

Vit D Deficiency

Vitamin D deficiency is actually more common than you may think. Keep reading for common causes for lack of vitamin D and diseases and conditions that can result from vitamin D deficiency.

You maybe asking yourself where do I get Vitamin D and what does it do!! The good news is that our bodies can produce on its own when we expose our skin to sunlight, we can also get it from supplements and a very small amount comes from a few foods we eat, such as some fish, fish liver oils, egg yolks and in fortified dairy, cereals and grain products. Vitamin D is very important for good overall health. It helps to make sure our muscles, heart, lungs and brain function well. There is no set amount of time that you should be sat in the sun to make enough vitamin D as each and every person is different. It is said that if you are fair skinned you should have approximately 10-15 minutes where you are exposed without sunscreen. During the summer months this should be enough for most people to make enough vitamin D. You can speed it up, by exposing a large area of skin, the more chance there is of making enough vitamin D before you start to burn.

Common causes for lack of vitamin D
Limited exposure to sunlight – this can depend on where you live, if you have to wear long clothes everyday. You have a job where you mainly indoors.
Dark skin – People with dark skin have higher levels of melanin. It is this pigment that reduces the skin’s ability to make vitamin D when exposed to sunlight.
Kidney and liver function – The body uses these organs to convert vitamin D to its active form. Any sort of kidney or liver disease will dramatically reduce production of vitamin D.
Strict vegetarian diet – It is mainly animal based foods that contain vitamin D. These are fish and fish oils, egg yolks, cheese, fortified milk and beef liver.
Digestive problems – Some medical conditions can reduce the body’s ability to absorb vitamin D from food. Diseases such as Crohn’s disease, cystic fibrosis and celiac disease.
Obesity – Obesity may cause low vitamin D levels. Researchers have found that vitamin D may become ‘trapped’ inside fat tissue so less of it is available in our blood circulation.

Research is ongoing to see how vitamin D works within our body and how it affects our overall health. Though that said, there are a number of links between vitamin D deficiency and the following list of health problems:

1. Osteoporosis – We need an adequate amount of calcium and vitamin D to maintaining bone density and strength. Without it, it will cause bones to become weak and brittle and increases the risk of fractures.

3. Heart health – Vitamin D deficiency may be linked to a higher risk of high blood pressure (hypertension) as well as increased risk of death from cardiovascular disease.

4. Inflammation – Vitamin D deficiency has been linked with inflammation. Inflammatory diseases such as rheumatoid arthritis, lupus, inflammatory bowel disease (IBD) and type 1 diabetes.

5. Cholesterol – It has been shown that without adequate sun exposure vitamin D precursors will turn into cholesterol instead of vitamin D.

6. Allergies – Studies have shown that children with lower levels of vitamin D are more likely to have multiple food allergies.

7. Influenza – Some studies shown that people with the lowest vitamin D levels are found to have significantly more cases of cold and flu than those with higher levels.

8. Depression – Vitamin D deficiency has been linked to depression. The receptors for vitamin D are present in many areas of the brain and are involved in numerous brain processes, making it possible that lack of vitamin D could trigger depression.

9. Type-2 Diabetes – Studies have linked that low vitamin D levels could assist the development of type 2 diabetes. There are a few studies that provide evidence that vitamin D may contribute to glucose tolerance through its effects on insulin secretion and insulin sensitivity.

10. Oral health – It has been found that elderly patients with low vitamin D levels have a higher rate of tooth loss than those with high vitamin D levels.

11. Rheumatoid arthritis – Studies have found that women who get more vitamin D seem less likely to get rheumatoid arthritis. Also among people who already have rheumatoid arthritis, those with low vitamin D levels tend to have more active symptoms.

12. Cancer – a study has indicated that more than 75% of people with a variety of cancers have low levels of vitamin D, and the lowest levels are associated with more advanced cancers. Of course further research is required to link if higher vitamin D levels are related to lower cancer incidence or death rates.

Are you are worried that you may be lacking in vitamin D! All you need is a simple blood test to determine you vitamin D levels. Your doctor will then advise you if a supplement is necessary.

If you found this article useful, share with friends and family by clicking the links below.

Source: healthyandnaturalworld

Muller glial cell reprogramming and retina regeneration .

Müller glia are the major glial component of the retina. They are one of the last retinal cell types to be born during development, and they function to maintain retinal homeostasis and integrity. In mammals, Müller glia respond to retinal injury in various ways that can be either protective or detrimental to retinal function. Although these cells can be coaxed to proliferate and generate neurons under special circumstances, these responses are meagre and insufficient for repairing a damaged retina. By contrast, in teleost fish (such as zebrafish), the response of Müller glia to retinal injury involves a reprogramming event that imparts retinal stem cell characteristics and enables them to produce a proliferating population of progenitors that can regenerate all major retinal cell types and restore vision. Recent studies have revealed several important mechanisms underlying Müller glial cell reprogramming and retina regeneration in fish that may lead to new strategies for stimulating retina regeneration in mammals.

From the desk of Zedie.

Marijuana could be used to treat autoimmune diseases .

Researchers have found that cannabis can reduce inflammation and may be used to treat autoimmune diseases such as lupus.


A study conducted at the University of South Carolina, in the US, has shown that THC (tetrahydrocannabinol), one of the main ingredients in marijuana, may affect DNA expression and can reduce inflammation, meaning cannabis could be used as a treatment for arthritis, lupus, colitis, multiple sclerosis and other diseases in which inflammation plays a key role.

The study was conducted in mice, and although it shows promise, the scientists still need to understand how THC affects microRNA expression.

“MicroRNA therapeutics is an important, rapidly growing area with major pharmaceutical companies getting into this discovery and development,” Nagarkatti said in a press release. “While our study identifies the molecular mechanism of immune-altering effects of marijuana, select microRNA identified here could serve as important molecular targets to manipulate MDSC activity in cancer and inflammatory diseases.”

This is not the first time that cannabis has been shown to decrease inflammation. A study from 2003 reported that marijuana smokers had lowers levels of an inflammation-promoting protein known as interleukin-2.