Daily Archives: February 25, 2016

The mind of a heroin addict: the struggle to get clean and stay sober

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For a heroin addict, recovery is a life-long process. Philip Seymour Hoffman had been clean for 23 years before he relapsed in 2013, and died from an apparent overdose last week.

To many people who have never grappled with addiction, it can be difficult to comprehend the desperate desire to use, even after so many years sober. To gain deeper insight into drug addiction, we asked recovering heroin users to share their experiences with us. Nearly 300 people responded, describing their struggle to get clean, and the ongoing battle to stay sober. Here, we publish a selection of those responses.

For the past 26 years I’ve thought of heroin every day

When I first gave up heroin, I could never tell myself it was forever  

I see what happened to Philip Seymour Hoffman everyday in my hometown  

I live in real fear that I’ll relapse

No one sets out to be a heroin addict. It’s not a lifestyle choice

If you are an addict you are either using, clean
or dead. There is nothing in between  

After all these years, I still have some kind of sick fascination with heroin  

Hoffman’s death has not resulted in feelings of sorrow, but thoughts and feelings of nostalgia  

It’s easy to think that because you have been clean and sober for so long that using one time will be OK. It’s easy to become complacent in your recovery  

Every single time I relapse, my life spins out
of control  

The ‘War On Drugs’ has been a dismal failure  

I wish people would understand that addiction is a symptom  

The media’s ‘It’s so sad’, ‘How could this happen?’
style coverage of a celebrity overdose pisses me right off 

There are panicked rushes to inject in public toilets, a desperation to hide injection sites from employers and perpetual fear of a crackdown 

I spent 14 years begging on the streets, eating out of bins, almost dying from infections and having hell inside my skull  

Once addicted, your life then becomes a dedication to your addiction  

The feeling is almost impossible to explain to someone who has never done an opiate  

It’s important to maintain a strong support system

When I was living in Amsterdam at the height of my habit, junkies were being fished out of the canals two-at-a-time most weekends. None of us expected to live very long  

Heroin encases you in a little cotton-wool house and nothing hurts anymore  

I believe in giving up drugs on your own terms  

I have no words of wisdom to offer an addict as he destroys everything he loves for 30 minutes of nirvana 

We are all fighting life and pain  

I was essentially babysat for a couple of weeks by people in Narcotics Anonymous, who fed me, talked to me and took me to meetings until I could look after myself again  

Addiction is a great equal-opportunities malady. It takes one and all regardless of class, creed or distinction  

I have four sons. The two youngest were born addicts 

If something happens to trigger my need, the craving comes back as fresh as it was the very first week of sobriety  

It shames me to write this now, but I did continue using – mainlining – for the first few months of the pregnancy  

Once you’ve relapsed, the life you had in recovery seems like someone else’s  

Sometimes I think I would like to shoot up water just to experience the whole ceremony surrounding the event 

I started using when I was 12, by the age of 36 I was shooting up methadone between my toes  

I came so close to total disaster. It was like I was walking blindfolded towards the edge of the cliff

As an addict in my early 20s, I nearly succumbed to several heroin overdoses  

When I heard about Seymour ‘going out’ (as we say in recovery) after 23 years, it scared the crap out of me

We get deaths like this every few months, either in the media or in our recovery community  

Whenever I hear of a celebrity drug death, especially when it relates to smack (heroin), often the first thing that comes to mind is the hypocrisy which surrounds drugs and junkies  

I find it hard to remain vigilant when there is a high-profile overdose. 


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1. They don’t hide their anxiety, they hide their symptoms. To have concealed anxiety isn’t to deny having it – only to do everything in your power to ensure other people don’t see you struggle.

2. They have the most anxiety about having anxiety. Because they are not comfortable letting people see them in the throes of an irrational panic, the most anxiety-inducing idea is… whether or not they’ll have anxiety at any given moment in time.

3. They come across as a paradoxical mix of outgoing but introverted, very social but rarely out. It is not that they are anti-social, just that they can only take being around others incrementally (which is mostly normal). Yet, on the surface, this may come across as confusing.

4. They make situations worse by trying to suppress their feelings about them. They are extremely uncomfortable with other people seeing them in pain, and they don’t want to feel pitied or as though they are compromising anyone’s time. Yet, they make things worse for themselves by suppressing, as it actually funnels a ton of energy into making the problem larger and more present than it already was.

5. They are often hyper-aware and highly intuitive. Anxiousness is an evolutionary function that essentially keeps us alive by making us aware of our surroundings and other people’s motives. It’s only uncomfortable when we don’t know how to manage it effectively – the positive side is that it makes you hyper-conscious of what’s going on around you.

6. Their deepest triggers are usually social situations. It’s not that they feel anxious in an airplane, it’s that they feel anxious in an airplane and are stuck around 50 other people. It’s not that they will fail a test, but that they will fail a test and everyone in school will find out and think they are incompetent and their parents will be disappointed. It’s not that they will lose love, but that they will lose love and nobody will ever love them again.

7. It is not always just a “panicked feeling” they have to hide. It can also be a tendency to worry, catastrophizing, etc. The battle is often (always?) between competing thoughts in their minds.

8. They are deep thinkers, and great problem-solvers. One of the benefits of anxiety is that it leads you to considering every worst case scenario, and then subsequently, how to handle or respond to each.

9. They are almost always “self-regulating” their thoughts. They’re talking themselves in, out, around, up or down from something or another very often, and increasingly so in public places.

10. They don’t trust easily, but they will convince you that they do. They want to make the people around them feel loved and accepted as it eases their anxiety in a way.

11. They tend to desire control in other areas of their lives. They’re over-workers or are manically particular about how they dress or can’t really seem to let go of relationships if it wasn’t their idea to end them.

12. They have all-or-nothing personalities, which is what creates the anxiety. Despite being so extreme, they are highly indecisive. They try to “figure out” whether or not something is right before they actually try to do it.

13. They assume they are disliked. While this is often stressful, it often keeps them humble and grounded at the same time.

14. They are very driven (they care about the outcome of things). They are in equal proportions as in control of their lives as they feel out of control of their lives – this is because they so frequently try to compensate for fear of the unknown.

15. They are very smart, but doubt it. A high intelligence is linked to increased anxiety (and being doubtful of one’s mental capacity are linked to both).


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From my personal experience, I can tell you that recovering from an eating disorder is a full-time job.

Day in and day out, it takes a tremendous amount of mental, emotional and physical effort to fight the familiar ways of living and make the positive choices recovery requires.

Recovery is absolutely vital.

It not only improves every aspect of your life, but it also prevents you from becoming a part of the alarming statistic.

Eating disorders have the highest mortality rate of all mental illnesses.

Unfortunately, as hard as recovery typically is, people in our everyday lives — including our loved ones — often don’t help the healing process.

It isn’t that our friends and family members have bad intentions.

On the contrary, I’ve found these individuals genuinely think they are saying something helpful.

But, they don’t realize how their words may have the opposite effect.

There are many eating disorder myths, and there are tremendous stereotypes regarding them as well.

Many people think of the phrase “eating disorder” and associate it with weight and food.

Although weight and food are related to eating disorders, one must remember an eating disorder is fundamentally a disease of the mind.

I have personally struggled with severe eating disorders in many forms, including anorexia, bulimia and binge eating disorder.

Although my body took on wildly different shapes, I can assure you my mind remained stubbornly the same.

From personal experience, you need to know the mind will often misinterpret what you say, no matter how the eating disorder is physically manifested.

Therefore, it is important to recognize the kinds of statements you should avoid making to anyone recovering from an eating disorder, in order to best support his or her continued progress:

1. “Wow, you’ve gained so much weight. You look great!”

While you may intend this to be a compliment, it is often twisted into the exact opposite.

For instance, when I put on weight while battling anorexia, those around me were so relieved because, to them, things “looked” to be getting better.

What they didn’t know is, I heard their words and turned them into insults.

Endless thoughts ran through my mind.

Am I fat?

Do I look healthy now?

Have I gained too much weight?

If people think I look great, why does my treatment team say I haven’t yet reached an appropriate weight?

Should I stop gaining weight now?

Maybe I should lose weight to make sure this doesn’t get out of hand. In fact, I should probably lose a lot of weight so people stop complimenting me because my mind sure doesn’t match my appearance.

As you can see, I created a host of dangerous thoughts, thanks to one simple compliment.

Remember that the body can physically recover in a matter of months, but the mind can take years.

Just because one appears better on the outside does not mean the person is mentally ready in the recovery process to handle such feedback.

2. “Wow! You’ve lost so much weight.”

This is, again, a very dangerous statement.

When I was struggling with anorexia, I would take this as a compliment.

In fact, I loved it when people told me I had lost weight, even when they didn’t mean it as a compliment.

The statement only served to fuel my disease and make me feel more in control and successful.

This, in turn, often caused me to relapse.

It is important to note that not everyone struggling with anorexia is underweight.

When you praise people for their changing appearance, you may not realize the dangerous behaviors that lie behind the transformation.

This type of statement can also harm the recovery process for those with bulimia and binge eating disorder.

When I was overweight, praise for my weight loss almost always caused my recovery efforts to backfire.

Often, I would take such statements as insults, thinking, “I must have been so much fatter before.”

This would often cause me to want to take drastic, unsustainable measures to lose weight even faster, which would inevitably lead to disappointment when I couldn’t meet my unrealistic goals.

The sense of failure — along with starvation — would then lead me to binge and put back all the weight I had lost, if not more.

The result was a vicious cycle and desperate trap.

Remember that recovery is about making healthy and sustainable choices, which can be tough when others give you positive validation for your weight loss.

3. “I wish I had your control and discipline.”

No, you don’t.

Having an eating disorder is a disease. It is a mental illness I wouldn’t wish upon my worst enemy.

You might see a glimpse of our lives and think they look controlled and orderly, but you don’t see the insane rituals and behaviors that constantly consume us.

You don’t hear a monster in your head, screaming at you to live a life that is bound by rules and discipline.

We want nothing more than to be free and to trust that we don’t need our eating disorder to keep us safe.

Part of our recovery process is learning to let go of the obsessive rigidity.

Please don’t reinforce the ridiculous rules we desperately need to break before they completely destroy us.

4. “Do you have any weight loss advice?”

No, no and no again.

I can’t tell you how many people who know about my long history of struggling with eating disorders have come to me for weight loss advice.

In fact, I’ve had people ask me for such advice when I was clearly anorexic.

This is incredibly disturbing to me, and it should be for you as well.

Obviously, I could give anyone weight loss advice, but it would be at the expense of my own mental well-being.

It’s not up for bargain.

Most people with eating disorders could have degrees in nutrition.

Most of us know the calorie count of almost every single food in the world, without even having to look it up.

When it comes to diets and dangerous ways to lose weight, we know it all.

But those of us trying to leave this awful lifestyle behind never — under any circumstances — want to talk about it.

5. “You’re eating so healthily. Are you on a diet?”

There might only be good intentions behind this question, but for those in recovery, it isn’t going to sit well.

For example, if I were trying my hardest to recover from anorexia and someone made this statement while I was eating an apple, my mind might start spinning.

Am I not in recovery?

Should I be eating ice cream or something more challenging?

Am I not doing as well as other people recovering from eating disorders? I see them posting pictures of all their food challenges on social media sites.

Am I still playing it too safe?

On the other hand, while eating that apple, I might be on the verge of relapse.

Then, the statement may cause my mind to spin differently.

I like that comment. It sounds familiar.

I bet I can do better. I bet I can eat healthier.

I can get thinner. I can take this further.

Forget recovery.

For those recovering from bulimia or binge eating disorder, it could be a challenge to just eat smaller portions or new foods.

They might be following instructions from a professional dietician, and they could be learning to eat all types of food groups in moderation.

By making comments on their food choices, you could be taking away from their progress toward balance.

Diet and recovery do not ever go together.

6. “That’s really unhealthy and has a lot of calories.”

This is such an unhelpful statement for anyone in recovery.

It doesn’t matter if you are recovering from anorexia, bulimia or binge eating disorder. The ultimate goal is to be able to eat all foods in moderation.

That means if you see us eating a donut or getting an ice cream, we actually may be experiencing a huge victory against our eating disorder by challenging ourselves to a fear food or a food we once abused.

Once again, calories and recovery do not go together.

7. “You look so healthy.”

This is an interesting statement, but one I feel needs to be brought up.

Often times, people with eating disorders fear the word “healthy” more than any other word.

I used to believe that if I were healthy, I would lose my identity.

I would have no reason to struggle, and so I would lose my excuse for not attaining success or happiness.

There are many different reasons people with eating disorders fear getting healthy, but it is a commonly shared expression.

Many of us aren’t sure who we are without an eating disorder, so we think healthy equals recovered.

It does not.

This is where society can, unfortunately, unintentionally interfere with the recovery process.

Remember eating disorders are about the mind, not the body.

Our appearance tells you very little about the state of our health.

8. “All you have to do is eat and exercise normally.”

This isn’t helpful at all.

As someone without an eating disorder, you may think the answer is to simply eat and exercise normally.

You have to understand this is like telling a recovering alcoholic to just have one drink while partying with friends every night.

Then, everything will magically be fine.

Of course, it’s not so easy.

9. “You look really different. Are you relapsing?”

Recovery is anything but linear.

Recovery is full of ups and downs, and it is often composed of two steps forward and one step back.

During the recovery process, our weight might swing to what the public perceives as the “wrong” direction.

But, that doesn’t always equate to relapse.

This is a very sensitive subject, and it’s not one to bring up unless you are significantly worried.

If  you are worried, it is best to involve an experienced treatment professional.

I also find it important to note we are human. We are not robots.

It’s natural for our weight to fluctuate from time to time.

No one is more sensitive to weight changes than we are, so you don’t need to point it out to us.

We are working overtime to overcome our fears and insecurities, and we don’t need to feel like others believe we are failing.

10. “You have such a great life. How can you be struggling?”

This is a tough one.

I personally grew up in a beautiful town with a loving, supportive family and athletic and academic gifts.

So how could such a picture-perfect girl end up with such a terrible eating disorder?

People develop eating disorders for several reasons, including genetics, personality, peers, environment, family and traumatic events.

What could be the right combination to trigger an eating disorder in one person might have a far different effect on another.

There are so many factors that combine to create “the perfect storm,” and it has little to do with “having a great life.”

If anything, hearing such a comment only makes those struggling feel even more guilty.

In reality, they have enough guilt to overcome.

Eating disorders do not discriminate, and they are not a choice.

11. “I had an eating disorder too for a few months. I understand.”

No, you probably don’t understand.

I have struggled immensely with eating disorders for over a decade, and I have enough personal experience to probably be considered an expert.

Still, I will never be able to fully put myself in another sufferer’s shoes.

I can relate and I can offer support, but I can never fully know the pain or complete life story of another person.

There isn’t anything wrong with supporting someone or looking to inspire him or her to get better.

But at the very least, make sure you don’t take the position of a know-it-all.

Please save yourself from appearing silly, and educate yourself on what struggling with an eating disorder really entails before you make a casual statement.

The word “eating disorder” should never be thrown around lightly, period.

End of story.

12. “You don’t look like you have an eating disorder.”

This is a huge red flag.

I have touched on this previously, but I will give you one alarming example.

When I was struggling with bulimia, I was at a normal weight.

To the public eye, I looked healthy.

I put on a smile, and no one would think, “Oh, she’s struggling with an eating disorder.”

But what they didn’t see was the rest of my life. They didn’t see the other 23 hours of my day.

They couldn’t possibly know from my appearance that I could have lost my life at any time due to the dangerous behaviors I exhibited.

Remember this is a mental illness.

This is about the mind.

You can’t see that, can you?

These are some major statements I feel are important to avoid saying while interacting with someone recovering from an eating disorder.

But that doesn’t mean you shouldn’t talk to us.

If anything, we want to be included. We want to have conversations, and we want to hear praise.

It’s just about picking the right types of things to discuss and the right types of praise to provide.

Ask us how our day went.

Talk about the weather, the news or anything else unrelated to body, weight and food.

Sometimes, what we need most is just your quiet, compassionate presence while you listen to us speak, no matter whether you understand what we’re going through or not.

Those of us in recovery have had more than our fair share obsessing about food and weight, so as we are looking to break free from our negative thoughts and dangerous behaviors, we want to learn we have a place in this world without our eating disorder.

Show us we are incredible people, just as we are.

In fact, show us that life without an eating disorder is only going to offer us more love, safety and acceptance.

Show us we have something wonderful to look forward to.

No one should struggle in silence, and no one should recover alone.

Please take the time to view many of the helpful eating disorder resourcesavailable to better support yourself or those you care about.

New York Becomes First State to Legalize Heroin

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The state of New York made history this week, following on the heels of the wave of marijuana legalizations across the country. Recreational use of heroin will become fully legal in the state by the end of this year.

The decision was met with controversy, but “no more or less than the original decision to legalize marijuana,” Governor Andrew Cuomo stated. The state is still figuring out some guidelines and ground rules for suppliers, such as purity levels, permits, and health code requirements.

One of the major points in making this decision came from the number of dealers and users of the drug who repeatedly end up in New York’s correctional facilities.

By legalizing, monitoring, and taxing heroin, we will not only cut down on inmates and care costs, but also open up a whole new job market,” Cuomo explained. “It’s a good situation all around, especially for taxpayers.”

By legalizing, monitoring, and taxing heroin, we will not only cut down on inmates and care costs, but also open up a whole new job market,” Cuomo explained. “It’s a good situation all around, especially for taxpayers.”

11 of the Most Realistic Portrayals of Mental Illness in Novels

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There is a great tradition of mental illness in fiction. The Victorians loved stashing mad women up in towers or attics, where they could slow-w-wly peel the wallpaper from the walls or moan and groan with such abandon that it would frighten the young governesses trying to catch some sleep down below. Later, books would introduce readers to evil nurses, forced lobotomies, and botched attempts at electro-shock therapy. Needless to say, mental illness was even less understood in the past than it is today.

The last few decades have brought improvement in the way mental illness is treated and the way it is portrayed in literature. Characters are allowed to come down from the attic and tell their own stories. In memoirs, authors share their experiences in raw, first person accounts. Girl, Interrupted, Prozac Nation, and Running with Scissors are just a few examples — check out this list of the 20 Greatest Memoirs of Mental Illness for more suggestions.

The 11 novels listed below talk candidly of mental illness, too. Sometimes the veil of fiction permits authors to tell even truer stories — they can write without worrying about their own reputations or the reactions from their family members. Their books give us a deeper understanding of mental illness and the way we deal with mental illness in our culture. They also do what all great literature should do — let us get to know and care about the characters as people.

Mrs. Dalloway by Virginia Woolf (1925)

A day in the life of Clarissa Dalloway, a high society English woman. Through the character of Septimus, a shell-shocked veteran of World War I, the book criticizes the treatment of the mentally ill. Woolf used her own struggles with bipolar disorder to inform Septimus’s character.

Tender is the Night by F. Scott Fitzgerald (1934)

F. Scott Fitzgerald wrote this novel while his wife, Zelda, was in the hospital being treated for schizophrenia. Set on the French Riviera in the 1920s, Tender is the Night is the story of psychoanalyst Dick Diver and his wife Nicole… who also happens to be his patient.

Catcher in the Rye by J.D. Salinger (1951)

The quintessential tale of disaffected youth, The Catcher in the Rye still sells around a quarter million copies a year. Holden Caulfield, our young hero, first appeared in a 1945 short story in Collier’s called “I’m Crazy.”

The Bell Jar by Sylvia Plath (1963)

Originally published under a pseudonym, The Bell Jar is the semi-autobiographical account of Plath’s own clinical depression, a sensation she describes thusly: “Wherever I sat — on the deck of a ship or at a street cafe in Paris or Bangkok — I would be sitting under the same glass bell jar, stewing in my own sour air.”

I Never Promised You a Rose Garden by Joanne Greenberg (pen name: Hannah Green) (1964)

Deborah Blau, diagnosed with paranoid schizophrenia, spends three years in a psychiatric hospital. Her story echoes the author’s experiences, and the doctor in the story was based on her real-life doctor, the German psychiatrist Frieda Fromm-Reichmann.

Disturbing the Peace by Richard Yates (1975)

This semi-autobiographical novel tells the story of John C. Wilder, an adman-turned-screenwriter who spends some time in a mental hospital and suffers (as Yates did) from alcohol-induced delusions.

Ordinary People by Judith Guest (1976)

Conrad tries to commit suicide after the tragic death of his older brother, so his parents send him to a psychiatric hospital. After his release, with help from his psychiatrist, Conrad examines his depression and attempts to understand his frosty relationship with his mother. The movie adaptation of Ordinary People, starring Mary Tyler Moore, won the Academy Award for Best Picture in 1980.

She’s Come Undone by Wally Lamb (1992)

Delores Price slowly unravels after dealing with a traumatic event as a young teenager. As a twentysomething woman, she spends years in an institution after a suicide attempt. She eventually quits therapy and attempts to rebuild her life on her own terms. Lamb continues to write about mental illness in his next book, I Know This Much is True.

The Hours by Michael Cunningham (1998)

Inspired by the first book on our list, Mrs. Dalloway, the story reveals a single day in the lives of three women from three different time periods, including Virginia Woolf herself. The Hours won the Pulitzer Prize for fiction in 1999.

The Passion of Alice by Stephanie Grant (1998)

One of the lesser-known novels on this list, The Passion of Alice is a moving, unflinching portrait of a 25-year-old woman who is admitted into an eating disorders clinic after she almost dies of heart failure.

The Marriage Plot by Jeffrey Eugenides (2011)

Leonard, one of the main characters in this novel, lives with manic depression, which affects his work, his friendships, and his romantic relationships. In an interview with Slate, Eugenides squelches the rumor that Leonard is based on David Foster Wallace.

Some Things About Breast Tumors

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A tumor is a mass of abnormal tissue. There are two types of breast cancer tumors: those that are non-cancerous, or ‘benign’, and those that are cancerous, which are ‘malignant’.

cancer stages are not the same as tumor grades

Benign Tumors

When a tumor is diagnosed as benign, doctors will usually leave it alone rather than remove it. Even though these tumors are not generally aggressive toward surrounding tissue, occasionally they may continue to grow, pressing on organs and causing pain or other problems. In these situations, the tumor is removed, allowing pain or complications to subside.

Malignant tumors

Malignant tumors are cancerous and aggressive because they invade and damage surrounding tissue. When a tumor is suspected to be malignant, the doctor will perform a biopsy to determine the severity or aggressiveness of the tumor.

Metastatic cancer

Metastatic cancer is when cancer cells of a malignant tumor spread to other parts of the body, usually through the lymph system, and form a secondary tumor.

Tumor grading is a system used to classify a malignant breast cancer tumor based upon the severity of the mutation and the likelihood that it will spread. The breast cancer cells are examined under a microscope to determine, among other factors, how closely the breast cancer cells resemble the healthy cells (called the histologic grade) and the shape and size of the tumor cells’ nuclei (called the nuclear grade) as well as how rapidly those cells divide and multiply.

When dealing with breast cancer, tumors are often graded based on a scale of one to three indicating how aggressive the cancerous cells are:

  • Low grade (1) – Well-diffentiated
  • Intermediate grade (2) – Moderately differentiated
  • High grade (3) – Poorly differentiated

Low grade tumors look more like normal tissue under the microscope. High-grade tumors look abnormal and less like normal tissue and tend to be more aggressive.

Breast cancer tumor grades are not to be confused with cancer stages. Tumor grades help to determine the best treatment plan, and in general, a lower grade tumor means a better chance for a full recovery. However, there are individuals who make full recoveries at every stage and with even the highest grades of aggressive tumors.

Mushroom poisoning

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Mushroom poisoning (also known as mycetism or mycetismus) refers to harmful effects from ingestion of toxic substances present in a mushroom. These symptoms can vary from slight gastrointestinal discomfort to death. The toxinspresent are secondary metabolites produced in specific biochemical pathways in the fungal cells. Mushroom poisoning is usually the result of ingestion of wild mushrooms after misidentification of a toxic mushroom as an edible species. The most common reason for this misidentification is close resemblance in terms of colour and general morphology of the toxic mushrooms species with edible species.

To prevent mushroom poisoning, mushroom gatherers need to be very familiar with the mushrooms they intend to collect as well as with any similar-looking toxic species. In addition, edibility of mushrooms may depend on methods of preparation for cooking. Collectors also need to be well aware that edibility or toxicity of some species varies with geographic location.

There are many folk traditions concerning the defining features of poisonous mushrooms.[1][2] However, there are no general identifiers for poisonous mushrooms (only guidelines to identify mushrooms themselves exist, if one knows what mushroom is toxic), and so such traditions are unreliable guides. Use of folk traditions to try to identify edible mushrooms is a frequent cause of mushroom poisoning.

Examples of erroneous folklore “rules” include:

  • “Poisonous mushrooms are brightly colored.” – While the fly agaric, usually bright-red to orange or yellow, is narcotic and hallucinogenic, there have been no reported human deaths; the deadly destroying angel, in contrast, is an unremarkable white, and the deadly Galerinas are brown. Some choice edible species (chanterelles, Amanita caesarea, Laetiporus sulphureus, etc.) are brightly colored, while most poisonous species are brown or white.
  • “Insects/animals will avoid toxic mushrooms.” – Fungi that are harmless to invertebrates can still be toxic to humans; thedeath cap, for instance, is often infested by insect larvae.
  • “Poisonous mushrooms blacken silver.” – None of the known mushroom toxins have a reaction with silver.
  • “Poisonous mushrooms taste bad.” – People having eaten the deadly Amanitas reported that the mushrooms tasted quite good.
  • “All mushrooms are safe if cooked/parboiled/dried/pickled/etc.” – While it is true that some otherwise-inedible species can be rendered safe by special preparation, many toxic species cannot be made toxin-free. Many fungal toxins are not particularly sensitive to heat and so are not broken down during cooking; in particular, α-amanitin, the poison produced by the death cap (Amanita phalloides) and others of the genus, is not denatured by heat.
  • “Poisonous mushrooms will turn rice red when boiled”.[3] – A number of Laotian refugees were hospitalized after eating mushrooms (probably toxic Russula species) deemed safe by this folklore rule and this misconception cost at least one person her life.[4][5]
  • “Poisonous mushrooms have a pointed cap. Edible ones have a flat, rounded cap.” – The shape of the mushroom cap does not correlate with presence or absence of mushroom toxins, so this is not a reliable method to distinguish between edible and poisonous species. Death cap, for instance, has a rounded cap when mature.
  • “Boletes are, in general, safe to eat” – It is true that, unlike a number of Amanita species in particular, in most parts of the world, there are no known deadly varieties of the Boletus genus, which reduces the risks associated with misidentification. However, mushrooms like the Devil’s Bolete are poisonous both raw and cooked and can lead to strong gastrointestinal symptoms, and other species like the lurid bolete require thorough cooking to break down toxins. As with other mushroomgenera, proper caution is, therefore, advised in determining the correct species.

Clinical Interaction between Brain and Kidney in Small Vessel Disease

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Patients with chronic kidney disease (CKD) are well known to have a higher prevalence of cardiovascular disease from epidemiological studies. Recently, CKD has also been shown to be related to neurological disorders, not only ischemic brain injury but also cognitive impairment. This cerebrorenal connection is considered to involve small vessel disease in both the kidney and brain, based on their hemodynamic similarities. Clinical studies suggest that markers for CKD such as estimated glomerular filtration rate (eGFR), proteinuria, and albuminuria may be helpful to predict brain small vessel disease, white matter lesions (WMLs), silent brain ischemia (SBI), and microhemorrhages. Recently, changes in the vascular system of the brain have been shown to contribute to the onset and progression of cognitive impairment, not only vascular dementia but also Alzheimer’s disease. Patients with CKD are also reported to have higher risk of impaired cognitive function in the future compared with non-CKD subjects. These results indicate that CKD markers may be helpful to predict the future risk of neuronal disease.

1. Introduction

Recently, the relation between chronic kidney disease (CKD) and neurological disorders, not only cerebrovascular disease such as ischemic brain injury but also cognitive impairment such as Alzheimer’s disease, has been highlighted. This cerebrorenal interaction is considered to be based on small vessel disease. Cerebral and glomerular small vessel disease might have a common soil of pathogenesis, as these organs are closely connected with each other through anatomic and vasoregulatory similarities. Because small vessel disease is a systemic disorder, information about small vessel disease in one organ may provide information on damage in another organ. For the kidney, damage markers are albuminuria/proteinuria and a reduction in estimated glomerular filtration rate (eGFR), which is also a marker of CKD. On the other hand, damage markers in the brain could be magnetic resonance imaging- (MRI-) documented small vessel alterations. Recently, clinical investigations have suggested a relation between these damage markers in the kidney and the brain. Here, we review the cerebrorenal interactions mainly from a clinical view.

2. Clinical Relation between CKD and Cerebrovascular Disease

2.1. Stroke

Recently, the relation between CKD and the onset of stroke has been highlighted. The Northern Manhattan Study (NOMAS), which followed 3298 stroke-free subjects for vascular outcomes with a mean follow-up time of 6.5 years, showed that CKD, which was estimated using serum creatinine and the Cockcroft-Gault formula, between 15 and 59 mL/min is a strong risk factor for stroke (hazard ratio (HR) = 2.65) [1]. In contrast, Bos et al. demonstrated that decreased eGFR (<60 mL/min/1.73 m2) is a strong risk factor for hemorrhagic but not ischemic stroke (HR = 4.10 for hemorrhagic stroke versus 0.87 for ischemic stroke) in the Rotterdam Study [2]. The authors considered two hypotheses for this relation. The first, decreased GFR indicates small vessel disease not only in the kidney but also in the brain. Small vessel disease seems to be the main pathophysiological mechanism in hemorrhage rather than brain infarction; therefore, the authors suggested that GFR may be a marker of cerebral small vessel disease, especially hemorrhage. The second, the authors considered platelet dysfunction to be an inducible factor by CKD. Severe CKD patients show prolonged bleeding time and mucosal oozing [3], indicating that platelet dysfunction may be involved in the relation between eGFR and hemorrhagic stroke. In the relation between microalbuminuria and incident stroke, prospective cohort studies using meta-analysis with 12 prospective cohort studies including 48,596 individuals with more than 1200 stroke events have been very recently published [4]. The presence of microalbuminuria was greatly associated with stroke onset even after adjustment for cardiovascular risk factors (overall HR 1.92), indicating that albuminuria contribute to be a strong predictor for the incidence of stroke. Recently, asymptomatic cerebral small vessel disease has been investigated as a predictor of the risk of future stroke. Oksala et al. demonstrated that cerebral small vessel disease is closely associated with kidney function in patients with acute stroke. Patients with cerebral small vessel disease and impaired kidney function (eGFR < 60 mL/min/1.73 m2) exhibit poor poststroke survival [5]. These results indicate that Representative cerebral small vessel diseases include white matter lesions (WMLs), silent brain infarction (SBI), and microhemorrhages as well as lacunar infarcts and subcortical atrophy.

2.2. White Matter Lesions

WMLs are detected as hyperintense areas on T2-weighted MRI in areas that are bilaterally and symmetrically sited in the hemispheric white matter. The prevalence of WMLs is significantly related to the risk of stroke, cognitive decline, and dementia [6–8]. The NOMAS demonstrated that white matter hyperintensity volume is associated with moderate-to-severe CKD, which was estimated using serum creatinine and the Cockcroft-Gault formula, between 15 and 59 mL/min [9]. Wada et al. demonstrated that subjects with lower eGFR (less than 60 mL/min/1.73 m2) tended to have more lacunar infarcts and higher grade of WMLs; moreover, mean grade of WMLs and the mean number of lacunar infarcts in subjects with albuminuria were greater than those in subjects without albuminuria [10]. Furthermore, they also reported that urinary albumin level was associated with cerebral small vessel disease, independently of traditional cerebrovascular risk factors, in community-based elderly [11]. Similarly, Ikram et al. investigated the relation between kidney function evaluated by eGFR and cerebral small vessel disease via MRI analysis. They clearly showed that decreased eGFR was related to subclinical markers of cerebral small vessel disease such as deep white matter volume and WNLs independent of cardiovascular risk factors such as age, sex, blood pressure, and diabetes [12]. Interestingly, they also demonstrated that persons with lower eGFR had a smaller brain volume, indicating that CKD may relate to brain atrophy.

2.3. Silent Brain Infarction

On the other hand, SBI is defined as a cerebral infarction detected by brain imaging without clinical symptoms. Kobayashi et al. also reported that there is an independent association between SBI and eGFR [13]. The prevalence of SBI and the number of SBIs increased markedly as eGFR decreased. The presence of SBI is reported to predict clinical overt stroke [14, 15] or cognitive impairment. Therefore, patients with CKD should be assessed for SBI by MRI during the follow-up period. In contrast, Uzu et al. followed 608 patients with type 2 diabetes for 7.5 years and very recently reported that SBI may predict the progression of kidney disease in these patients [16]. The risk of end-stage renal disease (ESRD) or death was significantly higher in patients with SBI than in those without (HR 2.44). The estimated eGFR declined more in patients with SBI than in those without; however, the presence of SBI did not increase the risk of progression of albuminuria.

2.4. Microhemorrhages

Microhemorrhages are discrete or isolated punctate hypointense lesions smaller than 5 mm on T2*-weighted MRI. They are considered to be clinically silent but are strongly associated with advanced small vessel or microvascular ischemic disease [17, 18] and to be a marker for increased risk of future intracranial hemorrhage [19, 20]. Interestingly, Cho et al. showed that lower eGFR is associated with the presence of cerebral microhemorrhages [21]. Moreover, proteinuria is also strongly associated with both the frequency and number of cerebral microhemorrhages in patients with recent cerebral ischemia [22]. Therefore, CKD may increase the risk of hemorrhagic microangiopathy in the brain.

2.5. Hypertensive Nephroangiosclerosis

Hypertensive nephroangiosclerosis was observed in 25% of patients with ESRD in the United States [23]. Because nephroangiosclerosis is also mostly clinically silent, its prevalence in stroke patients is not well known. A recent autopsy data bank clearly demonstrated that nephroangiosclerosis is common in patients with fatal stroke. Indeed, nephroangiosclerosis is independently associated with the prevalence or history of hypertension in stroke patients (39.8% of patients with stroke versus 9.0% of patients with other neurologic diseases) [24]. These results suggest that senile kidney change is also commonly observed in patients with cerebrovascular disease and a true relation between kidney dysfunction and cerebral small vessel disease; however, the factors connecting kidney dysfunction and cerebrovascular disease remain under discussion.

3. Clinical Relation between CKD and Cognitive Impairment

Dementia and cognitive decline impair the quality of life and are associated with a profound disease burden, morbidity, and mortality, not only in patients but also in caregivers. Although an earlier approach to prevent cognitive dysfunction has been expected, there are few markers for evaluating the future risk of cognitive decline in subjects. Recently, impaired kidney function was reported to be associated with dementia and cognitive impairment. The REasons for Geographic and Racial Differences in Stroke (REGARDS) Study with 23,405 participants showed that reduced kidney function is associated with a higher prevalence of cognitive impairment [25]. In patients with CKD, each 10 mL/min/1.73 m2 decrease in eGFR below 60 mL/min/1.73 m2was associated with an 11% increased prevalence of cognitive impairment (HR = 1.11). Yaffe et al. conducted a chronic renal insufficiency cohort cognitive study in 825 adults aged 55 and older with CKD [26]. Participants with advanced CKD (eGFR < 30 mL/min/1.73 m2) were more likely to have clinically significant impairment of global cognition than those with mild-to-moderate CKD (eGFR 45–59 mL/min/1.73 m2) (HR = 2.0). Moreover, Buchman et al. reported a prospective, observational cohort study in 886 elderly without dementia [27]. Impaired kidney function (eGFR < 60 mL/min/1.73 m2) at baseline was associated with a more rapidly decline in cognitive, especially in semantic memory, episodic memory, and working memory. In contrast, Jassal et al. very recently demonstrated that baseline albuminuria, but not eGFR, was associated with reduced cognitive function only in men [28]. They indicated that albuminuria was a simple predictor of future cognitive decline. Although there is sex difference in the relation between albuminuria and cognitive impairment, kidney function may provide an important window on future cognitive impairment. Recently, changes in the vascular system in the brain have been shown to contribute to the onset and progression of dementia [29]. The so-called “central nervous system (CNS) neurovascular unit” is linked to many common human CNS pathological conditions including dementia. Although multiple mechanisms are involved in cognitive impairment and dementia associated with CKD, small vessel disease in the kidney and brain is also considered to have a key role in this connection.

4. Hemodynamic Similarities of Vascular Beds between Kidney and Brain

Unlike most organs, both the kidney and brain are low resistance end-organs that are exposed to high-volume blood flow throughout the cardiac cycle. These hemodynamic similarities are observed in the vascular beds in the kidney and the brain [30]; therefore, small vessel disease in the kidney may let us know of the presence of small vessel disease in the brain. Ito et al. proposed the very interesting “strain vessel hypothesis” as a possible mechanism for cerebro-cardio-renal connections [31]. Based on the similarity of the juxtamedullary afferent arterioles in the kidney to the perforating arteries in the brain, they are thought to be evolutionally developed to maintain the perfusion of vital tissues such as nephrons and the brainstem directly from large arteries to deliver blood to the tissue. These “strain vessels” are exposed to very high pressure and maintain a high vascular tone. Vascular damage induced by high arterial blood pressure and diabetes mellitus occurs in these similar strain vessels; therefore, microalbuminuria may be an indicator of vascular damage not only in the kidney but also in the brain. One of the common molecular components of small-vessel physiology that may also mediate microvascular dysfunction or injury is nitric oxide. Many papers have reported that nitric oxide deficiency could occur in renal disease, and this subject was been well reviewed by Baylis [32]. Nitric oxide regulates the microcirculation and the blood brain barrier [33], both of which are implicated in the development of WMLs and other manifestations of small vessel disease in the brain. Moreover, patients with impaired cognitive function show increased levels of endogenous inhibitors of nitric oxide synthesis and decreased nitric oxide metabolites [34]. Therefore, decreased nitric oxide may be one of the key factors in the cerebrorenal connection.

5. Prevention and Future Perspectives

These reports above strongly suggest that a brain and kidney connection exists and that systematic treatment targeting small vessel disease is therapeutically effective on not only the apparent damaged organ but also on the silently damaged organs (Figure 1). According to their unique shared susceptibility to vascular injury from central aortic pressure as a strain vessel, a logical preventive approach to cerebrorenal-related dysfunction is to achieve a reduction of central pulse pressure. A reduction of the central pulse pressure involves a reduction of the wave reflection by dilation of conduit arteries, since drugs do not directly affect the aorta and large arteries. Therefore, antihypertensive drugs should be selected to reduce the central pulse pressure, such as renin-angiotensin system (RAS) blockers and calcium-channel antagonists (CCB). For the kidney, there is good evidence from large clinical studies that blockade of RAS is highly effective to prevent renal damage compared with other antihypertensive drugs. In the brain, recent large clinical trials indicate that RAS blockade with angiotensin receptor blockers (ARBs) is effective to prevent a first or recurrent stroke beyond their blood pressure-lowering effect [35–37]. Moreover, a very recent paper clearly demonstrated that patients treated with ARBs have less severe deficit after stroke [38]. These results suggest that treatment with ARBs may be effective not only to reduce blood pressure but also to protect both the kidney and brain via preventing small vessel disease. However, the Blood Pressure Lowering Treatment Trialists’ Collaboration (BPLTTC) demonstrates that all of the blood pressure-lowering regimens have broadly similar protection against stroke [39]. Moreover, there are not any large clinical studies that demonstrate the effect of ARBs on dementia or cognitive impairment. Therefore, there is few evidence of the preventive effect of RAS blockade in the brain compared with that in the kidney. On the other hand, CCBs are proved to have preventive effect on dementia in the Systolic Hypertension in Europe (Syst-Eur) study [40]. CCB, nitrendipine was found to be effective to reduce the incidence of dementia. This is the only large clinical study that shows the effect of anti-hypertensive drug on dementia. Although several CCBs are reported to have renoprotective effects, generally CCBs do not have a remarkable effect on CKD prevention compared with RAS blockade due to the preferentially dilate afferent arteriole. Therefore, preventive effect of CCBs on cerebrorenal connection is also still under investigation. Furthermore, although hypertension may be involved in each pathological change in brain and kidney, it can be result of high blood pressure “in parallel,” indicating that direct evidence of common mechanistic factors in hypertension-induced cerebrorenal damage is still under investigation.

What effects does heroin have on the body?

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Heroin binds to and activates specific receptors in the brain called mu-opioid receptors (MORs). Our bodies contain naturally occurring chemicals called neurotransmitters that bind to these receptors throughout the brain and body to regulate pain, hormone release, and feelings of well-being.9 When MORs are activated in the reward center of the brain, they stimulate the release of the neurotransmitter dopamine, causing a sensation of pleasure.10 The consequences of activating opioid receptors with externally administered opioids such as heroin (versus naturally occurring chemicals within our bodies) depend on a variety of factors: how much is used, where in the brain or body it binds, how strongly it binds and for how long, how quickly it gets there, and what happens afterward.

Once heroin enters the brain, it is converted to morphine and binds rapidly to opioid receptors.11Abusers typically report feeling a surge of pleasurable sensation—a “rush.” The intensity of the rush is a function of how much drug is taken and how rapidly the drug enters the brain and binds to the opioid receptors. With heroin, the rush is usually accompanied by a warm flushing of the skin, dry mouth, and a heavy feeling in the extremities, which may be accompanied by nausea, vomiting, and severe itching. After the initial effects, users usually will be drowsy for several hours; mental function is clouded; heart function slows; and breathing is also severely slowed, sometimes enough to be life-threatening. Slowed breathing can also lead to coma and permanent brain damage.12

Brain image highlighting the limbic system, brain stem and spinal cord

Opioids Act on Many Places in the Brain and Nervous System

  • Opioids can depress breathing by changing neurochemical activity in the brain stem, where automatic body functions such as breathing and heart rate are controlled.
  • Opioids can increase feelings of pleasure by altering activity in the limbic system, which controls emotions.
  • Opioids can block pain messages transmitted through the spinal cord from the body.

World’s first kosher cannabis will let Jewish people enjoy medical marijuana

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The world’s first kosher cannabis strain is set to go on sale in the state of New York.

Smoking weed is set to become legal in New York in January 2016 under medical marijuana laws.

Cannabis plants

Now a local firm called Vireo Health has successfully won kosher certification for a cannabis product after applying to the Orthodox Union, which decides if products conform to ancient religious codes.

“Being certified kosher by the OU will not only help us serve the dietary needs of the largest Jewish community in the United States, but also combat unfortunate stigmas associated with medical cannabis,” said CEO Ari Hoffnung in a statement.

A group of people use a bong to smoke cannabis

“Today’s announcement sends an important message to New Yorkers of all faiths and backgrounds that using medical cannabis to alleviate pain and suffering does not in any way represent an embrace of ‘pot’ culture.

“Patients should never feel guilty or ashamed for using a product recommended by their physicians.”

Rabbi Menachem Genack, CEO of OU Kosher, added: “Judaism prioritises health and encourages the use of medicine designed to improve one’s health or reduce pain.”

“Using medical cannabis products recommended by a physician should not be regarded as a chet, a sinful act, but rather as a mitzvah, an imperative, a commandment.”

Cannabis has been smoked by humans for several thousand years and some academics believe its name may have been derived from the ancient Hebrew phraseqěnēh bośem.

Some pro-pot people even think cannabis is mentioned in the Old Testament of the Bible, where it was one of the ingredients in an anointing oil.

GettyMan smoking cannabis

Herodotus, an ancient Greek historian, was introduced to smoking cannabis by a civilisation called the Scythians.

“The Scythians, as I said, take some of this hemp-seed, and, creeping under the felt coverings, throw it upon the red-hot stones,” he wrote in his book The Histories .

“Immediately it smokes, and gives out such a vapour as no Grecian vapour-bath can exceed; the Scyths, delighted, shout for joy.”