Daily Archives: November 21, 2015

My friend and I were talking

Recently, my friend “A” and I met for coffee. She is a part of a book club that decided to go to a movie without taking her schedule into account. Consequently, she couldn’t go. So she was feeling bad about being left out. I had gone through something like this many months ago, some people I know had decided to make a group video. Although I was part of this group, they did not ask me to be in the video. I was feeling left out because of this. I had spoken to my brother about my situation months earlier, and he had said not to wallow in self pity. He recommended that I simply get in touch with these people about including me for the videos and tell them the reasons why I really belonged in it. I was going to do that but the video project fell through. So I decided if there was ever a situation like this again, instead of feeling sorry for myself and feeling justifiably outraged and pitiful at the same time, I would contact people and let them know my feelings.

So when my friend “A” told me about her situation, I was sort of ready. I listened to her and told her exactly what my brother had told me, i.e. to not wallow in self pity because someone didn’t include her, but to contact people and let them know that you would like to be a part of this little soiree. Basically, speak up instead of feeling sorry for yourself.

It is so much better to take control and advocate for your self than to sit and do the “Poor me” thing! It is empowering and strengthening rather than feeling bad and weak and unwanted.

And one more thing, I love this! My sister sent me this video of Oprah, so, so, so empowering. I must share it with my blogger friends and readers!




How Mental Illness Changed the Way I Feel About Birthdays


In my mind, celebrating the day I was born didn’t seem like a huge priority. In a way, you could say I’m making up for lost time.

Today I turned 24 years old (this is the point where half of my readers are like, WHAT, since I don’t think I’ve posted my age publicly until now – you’re welcome).

I know a lot of people who don’t make a huge deal out of their birthdays. They see it as just another day of the year. They don’t go out of their way to tell anyone. They stay in, enjoy a glass of wine, watch a movie, and fall asleep with the television on.

More power to them – really, whatever floats your boat – but I am definitely not one of those people.

I savor all the well wishes, the cards, the hugs, the birthday cake emojis. I buy myself a cake and a present; one year, I even sent myself a couple of e-cards (at the bottom it read “Love, You” – yes, I realize how weird this sounds) so I would have something fun to wake up to.

I stalk my Facebook wall, starting right at midnight, and revel in the outpouring of love and affirmation. I loudly tell waitstaff at restaurants that it’s my birthday with the hopes that they’ll sing a song.

But contrary to what it seems, I’m not actually a brat.

In fact, I didn’t always behave this way on my birthday. My birthdays used to be quiet. When I was no longer a kid and I was expected to organize my own party, they largely slid by, mostly unnoticed.

In my mind, celebrating the day I was born didn’t seem like a huge priority. In a way, you could say that I’m making up for lost time.

The thing about being a teenager in the throes of mental illness is that it was difficult, if not impossible, to motivate me to care about the fact that I was a year older.

To me, it was just a reminder that I had spent yet another year struggling without making any progress. You could say it was a new year, and you could even put it on a card and wrap it in a “happy occasion” bow, but to me, it felt insignificant.

The years all blended together underneath this dark cloud of bipolar and anxiety and they were rendered meaningless in the fog.

My birthdays as a teen went something like this:

  1. Resenting how damn cold Michigan is in late November. Resenting not having an earlier birthday so I could at least enjoy some sunshine on what was supposed to be “my day.” Sometimes this also meant staring angrily out the window at the snow on the ground.
  2. Wondering if any of my friends would remember (mind you, this was before Facebook was so popular). Being amazed when a few actually did.
  3. Eating carrot cake with my family (my mother makes a carrot cake that is out of this world, so I requested it every year).
  4. Going to bed and imagining a parallel universe where I actually did something important on my birthday.

Truthfully, I think that when you’re in survival mode, the idea of celebrating the fact that you exist seems so asinine when you spend more days than not wishing you didn’t exist.

When my mental health started to rebound, though – therapy, meds, rinse, repeat – I started to feel differently about birthdays.

The first birthday I can remember feeling distinctly different about was my 20th birthday. I remember thinking about how, when I was younger and deeply depressed, I had never imagined myself getting any older than 18. Turning that corner and getting into my twenties felt like a huge accomplishment.

It was a revelation. It was like unlocking a bonus level or discovering a sequel when you thought the book series had ended. I felt like I had cheated death – like I was living when I wasn’t really supposed to be.

Looking at that number as it shifted from 19 to 20, I had this sense that my being alive was a tremendous accomplishment; my birthday stood as a reminder of the resilience it took to keep living, to keep fighting, to stay.

That year, I actually did celebrate for the first time in a long time. Mx. Justin Vivian Bond, radical faerie extraordinaire, had a show in Ann Arbor. I went with a new friend of mine – a new friend I would eventually start dating a couple months later. It was a magical evening.

I realized that night something that had never really occurred to me before: I had a future.

And if that future involved radical transgender performance artists and some cute queer who buys me coffee on my birthday, I suspected that my future might not be so bad (spoiler alert: the cute queer who bought me coffee that night was also the cute queer who I married three years later).

Life didn’t stop at 18. And if I could live to be 20, maybe I could live to be 25, or 30, or… wow, is there really life after 30? They tell you life is short and that you should never assume you have more time, but the thought that I could live another decade, another two decades, even more – that thought shook me to my core.

Finally reaching my twenties made me feel like I had a whole new lease on life – and that’s when my obsession with birthdays really began.

I’m a big believer in making a huge fuss out of your birthday, but it’s not because I’m self-absorbed (okay, I may be a little self-absorbed – I am a blogger, after all).

It’s because I love any and every excuse to celebrate the fact that we’re still here. When somebody says “Happy Birthday” to me, what this translates to in my mind is, “Hey, kid, you made it. You’re alive.”

Still being here – which, when I was younger, was never something I imagined – is a big fucking deal. There were times when I thought I wouldn’t make it another day, let alone another five, ten years.

This year is the most important year yet. I am 24, and my first major depressive episode happened when I was 14. I look back at where I was ten years ago – ten years, can you believe that? – and I’m amazed.

Ten years ago, I didn’t think I would make it through geometry class, let alone grow up to be an actual adult (another spoiler alert: taxes are terrible, paying rent is painful, but being an adult is, all in all, the best thing ever and totally worth the wait).

Ten years later, I did make it through geometry. And not only that, but I survived many depressive episodes (and manic ones, too). I graduated from high school – hell, I graduated from college. I came out as transgender. I moved across the country to California, I got married, I started my career as a writer-

Hold up, y’all, as a writer. Which is its own bucket of “what the actual fuck” because when I was 14, I refused to show my writing to anyone because I was embarrassed and afraid that I wasn’t good enough.

Can you imagine what teenage Sam would have to say about all this?

Birthdays, for me, are the one day of the year where I have an undeniable excuse to celebrate everything that I’ve overcome to reach this stage in my life.

And, yes, while I believe that we should dabble in self-love and affirmation every day of the year, there’s something magical about getting older that makes those affirmations feel so much more meaningful.

Ten years ago I never imagined that this was my future. Hell, what future, I never imagined a future! I didn’t know that, on the other side of all of that pain, there were was something worth waiting for.

I realize that birthday cake emojis or balloons are not remarkable in themselves. I know that to most people, cards and parties and waiters singing songs are all superficial things to care about.

But they all remind me of perhaps the most tremendous thing I’ve learned in my 24 years on this planet: You just never know.

Every single time I claimed to know what the future had in store, I was wrong. 

And never in my life have I been so happy, so glad to be wrong. It’s a kind of “wrong” that’s worth celebrating.


After a week of crisis intervention, starting with calling 911 upon realizing my mom had had a stroke last Saturday, I’m coming undone. Time for a break. 

Luckily, my sister and I got reserves (husbands and sons) helping us out with our parents today. I plan to go home and take Sunday as a day of rest. Wish me well. Wish us well. Keep up the prayers. Thank you. 

Filed under: Bipolar Disorder, Family, Health, Mood Cycling, Triggers to Mood Cycling Tagged: self care, stroke, stroke rehabilitation

Bacterial protein can help convert stem cells into neurons

Korean scientists have found a way to make stem cells differentiate into neurons by using a two step method. Stem cells are cells that are capable of becoming or differentiating into any cell type in the body. They are the progenitor cells. This Korean group serendipitously discovered that a protein from the bacterium E. coli, called Skp, upon bonding to a stem cell protein called Sox2, suppresses their “sremness” as they call it. Then when these suppressed stem cells are exposed to two small molecules called Neurodazine and Neurodazole, they differentiate into neurons! This is a good way to get neurons in large quantities. Then these neurons can be used for various therapies. For example, stem cells (without prior differentiation) have been used as a treatment for Parkinson’s disease with good results.

This is a great discovery as one can have the cells one needs beforehand and can lead to treatments for many diseases. 

http://www.neuroscientistnews.com/research-news/bacterial-protein-can-help-convert-stem-cells-neuronsAs the recipe book for turning stem cells into other types of cells keeps growing larger, the search for the perfect, therapeutically relevant blend of differentiation factors is revealing some interesting biology. A study published in Chemistry & Biology, for example, found that a protein in E. coli bacteria combined with small molecules can act synergistically to push pluripotent cells into functional neurons.

The research began when Sungkyunkwan University scientists in Korea made a serendipitous discovery that Sox2–one of the four Yamanaka factors that affect a stem cell’s ability to remain a stem cell or differentiate–can bind to a bacterial chaperone protein, Skp. They then tested what would happen if Skp was introduced into stem cells and found that it could initiate differentiation. This led to the hypothesis that Skp could be combined with other techniques to make differentiation more efficient.

“Although there has been considerable research in this field, there is still a bottleneck in being able to produce a high number of stem cells efficiently,” says study co-author Kyeong Kyu Kim, of the Sungkyunkwan University School of Medicine. “This problem can be solved, but we need to look for new ways to guide stem cell differentiation and then understand the molecular mechanisms underlying improved protocols.”
Injae Shin of Yonsei University and Kim say that the differentiation of pluripotent stem cells can be conceived as two simple steps: first, a stem cell decides to no longer be a stem cell and begins to differentiate; second, the cell decides what kind of cell it wants to be. In their protocol to induce neuron differentiation, the bacterial protein Skp acts in the first step by binding to Sox2 and inhibiting its function. The small chemicals neurodazine (Nz) and neurodazole (Nzl) then act in the second step by telling the stem cell to become a neuron.
By influencing both steps, more functional neurons can be produced per batch of stem cells and at a faster rate if using either protein or small molecules alone. “The synergy thus mainly arises from combining suppression of stemness by protein and directing lineage-specific commitment by chemical inducers,” Shin says. “Hence this process stands as an example of rationally designed cell differentiation to achieve a high level of lineage commitment efficiency.”

One weakness of the protocol is that there are safety concerns around using bacterial proteins such as Skp in a therapeutic setting. However, using this protein is advantageous compared to introducing genetic elements because protein cannot cause any genetic alteration or instability, which are the major concerns of using virus-mediated gene delivery to the stem cells. The authors hope that this study can encourage others to develop similar approaches based on small molecule mimics of the first stage of stemness suppression.
They are now working on using similar combinatorial approaches to explore how to make differentiation more efficient in other cell types, particularly those in the heart.

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“… girls need clothes and food and tender happiness and frills, a pan, a comb, perhaps a cat.” L Ron Hubbard Getting through things doesn’t necessarily get you to a shiny happy place, sometimes it’s a hard, flat, desolate place, with an ill wind blowing. You blink and you’re numb and you’re as lonely as […]


Hope: to want something to happen or be true and think that it could happen or be true; archaic: trust

Did I really produce this picture? Did this actually come out of my brain? Because I cannot remember the last time I actually felt hopeful. Does that make me hopeless?

My therapist recently asked me “What do you hope for?” My answer was “Nothing.” She looked at me oddly, “Do you mean you have no hope?” “Exactly.”

For many years during my lifetime I hoped for something from myself, employers, family, friends, lovers, life. The majority of the time, what I hoped for didn’t happen…so I stopped hoping. It’s interesting that the archaic definition is “trust.” Trust in whom? Trust in what? Nope, don’t have much of that either.

There are a multitude of positive and uplifting quotes to be found all over the interwebs (I typed “hope” into my search engine: “About 1,790,000,000 results.” My timeline is inundated daily with hopeful memes. Sometimes I just want to scream at the computer “Lies!” Sometimes I cry and sometimes hope tries to wheedle it’s way in to my brain.

There are times when I catch myself feeling hopeful, then I think “Oh yeah, that again. Sorry but no, not today.”

Tagged: depression, hopeless, mental illness



Hah, snagged you. Bet you thought “Oh yay, Sheri slipped; we get to read that she believes she was a badass armadillo in another life.”

Nope, sorry. I’m talking about my blog, which has been through many incarnations in the past few years. It started out quite eclectic, then there was The Wedding, then everybody got to watch Sheri crash and burn.

The most recent saw your intrepid writer wanting to give just the facts, ma’am.

An interesting phenomenon has made itself be known throughout…the majority of comments in all their forms (social media, comments, contact form, private messages) said in many ways, had to do with being grateful for having someone be honest about what it’s like in the trenches.

So I will stop my quest to be the foremost blog on mental health and domestic violence (like that would really happen), and just go back to being me, but still always willing to honestly answer questions, and research facts/fallacies.

Tagged: blogging, gratitude, writing

Dear Diary


I thought it may be helpful to some but boring to others, so my detox journey (sounds so new-agey) now has a separate page.

Tagged: new page

Yin and yang of serotonin neurons in mood regulation



More nuanced view of brainstem neurons could lead to better drugs for depression, anxiety

Low levels of serotonin in the brain are known to play a role in depression and anxiety, and it is customary to treat these disorders with medications that increase the amount of this neurotransmitter. However, a new study carried out by researchers at Columbia University Medical Center (CUMC) suggests that this approach may be too simple. It appears that neighboring serotonin-producing brainstem regions exert different and sometimes opposing effects on behavior.

The findings, published in the online edition of Cell Reports, provide new insights into the development of mood disorders and may aid in designing improved therapies.

“Our study breaks with the simplistic view that ‘more is good and less is bad,’ when it comes to serotonin for mood regulation,” said study leader Mark S. Ansorge, Ph.D., assistant professor of psychiatry at CUMC and research scientist at New York State Psychiatric Institute. “Rather, it tells us that a more nuanced view is necessary.”

From anatomical studies, researchers knew that the brainstem contains two distinct clusters of serotonergic neurons: one in dorsal raphe nucleus (DRN) and another in the median raphe nucleus (MRN). Together both regions harbor the vast majority of neurons that supply serotonin to the rest of the brain, but it was unclear how neuronal activity within these clusters controls behavior.

To learn more, the CUMC team used a technique called pharmacogenetics to control the activity of serotonergic neurons in the DRN and MRN in both normal mice and in a mouse model of depression- and anxiety-like behavior. (The model was created by giving mice the drug fluoxetine shortly after birth, which produces long-lasting behavioral changes.)

The experiments revealed that alterations in serotonergic neuronal activity in the DRN and MRN produce markedly different behavioral consequences.

“Going into the study, our hypothesis was that reduced activity of serotonergic neurons is what drives these mood behaviors,” said Dr. Ansorge. “But what we found was more complicated. First, it appears that hyperactivity of the MRN drives anxiety-like behavior. We also observed that decreased DRN activity increases depression-like behavior, while decreased MRN activity reduces it. This led us to conclude that an imbalance between DRN and MRN activity is what leads to depression-like behavior.”

“This new understanding of the raphe nuclei should help us better understand why certain medications are effective in treating depression and anxiety, and aid in designing new drugs,” Dr. Ansorge added. “In the future, it may be possible to find treatments that selectively target the DRN or the MRN, or that correct any imbalance between the two.”

Jeffrey Lieberman, M.D., chair of the department of psychiatry at CUMC, observed that “Neurobiological studies such as this are essential to elucidate the molecular mechanisms of antidepressant treatments and to develop more effective therapies.”

The study also demonstrated, in experiments using the fluoxetine-treated mice, that inhibition of serotonin reuptake early in life leads to long-lasting imbalances between the DRN and MRN. “This raises possible concerns about exposure to serotonin-specific reuptake inhibitors during gestation,” said Dr. Ansorge. “SSRIs cross the blood-brain barrier as well as the placenta, and bind maternal and fetal serotonin transporters alike. It’s too early to say whether this has any effect on behavior in humans, but it’s certainly something worth looking into.”

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The above post is reprinted from materials provided byColumbia University Medical Center. Note: Materials may be edited for content and length.

New Nerve Drugs May Finally Prevent Migraine Headaches



The 63-year-old chief executive couldn’t do his job. He had been crippled by migraine headaches throughout his adult life and was in the middle of a new string of attacks. “I have but a little moment in the morning in which I can either read, write or think,” he wrote to a friend. After that, he had to shut himself up in a dark room until night. So President Thomas Jefferson, in the early spring of 1807, during his second term in office, was incapacitated every afternoon by the most common neurological disability in the world.

The co-author of the Declaration of Independence never vanquished what he called his “periodical head-ach,” although his attacks appear to have lessened after 1808. Two centuries later 36 million American migraine sufferers grapple with the pain the president felt. Like Jefferson, who often treated himself with a concoction brewed from tree bark that contained quinine, they try different therapies, ranging from heart drugs to yoga to herbal remedies. Their quest goes on because modern medicine, repeatedly baffled in attempts to find the cause of migraine, has struggled to provide reliable relief.

Now a new chapter in the long and often curious history of migraine is being written. Neurologists believe they have identified a hypersensitive nerve system that triggers the pain and are in the final stages of testing medicines that soothe its overly active cells. These are the first ever drugs specifically designed to prevent the crippling headaches before they start, and they could be approved by the U.S. Food and Drug Administration next year. If they deliver on the promise they have shown in studies conducted so far, which have involved around 1,300 patients, millions of headaches may never happen.

“It completely changes the paradigm of how we treat migraine,” says David Dodick, a neurologist at the Mayo Clinic’s campus in Arizona and president of the International Headache Society. Whereas there are migraine-specific drugs that do a good job stopping attacks after they start, the holy grail for both patients and doctors has been prevention.

Migraine attacks, which affect almost 730 million people worldwide, typically last from four to 72 hours. Most sufferers have sporadic migraines and are laid low during 14 or fewer days a month. Those with a chronic form—almost 8 percent of the migraine population—suffer 15 or more monthly “headache days.” Attacks are often preceded by fatigue, mood changes, nausea and other symptoms. About 30 percent of migraine patients experience visual disturbances, called auras, before headaches hit. The total economic burden of migraine in the U.S., including direct medical costs and indirect costs such as lost workdays, is estimated at $17 billion annually.

In the 5,000 years since migraine symptoms were first described in Babylonian documents, treatments have reflected both our evolving grasp and our almost comical ignorance of the condition. Bloodletting, trepanation and cauterization of the shaved scalp with a red-hot iron bar were common treatments during the Greco-Roman period. The nadir of misguided remedies was probably reached in the 10th century a.d., when the otherwise discerning ophthalmologist Ali ibn Isa recommended binding a dead mole to the head. In the 19th century medical electricity had become all the rage, and migraine patients were routinely jolted with a variety of inventions, including the hydroelectric bath, which was basically an electrified tub of water.

By the early 20th century clinicians turned their attention to the role of the blood vessels, inspired in part by observations of strong pulsing of the temporal arteries in migraine patients, as well as patients’ descriptions of throbbing pain and the relief they got from compression of the carotid arteries. For decades to come, migraine pain would be blamed primarily on the dilation of blood vessels (vasodilation) in the brain.

That idea was reinforced in the late 1930s with the publication of a paper on the use of ergotamine tartrate, an alkaloid that was known to constrict blood vessels. Despite an array of side effects, among them vomiting and drug dependence, it did stop attacks in a number of patients.

But if vasodilation was part of the puzzle, it was not the only thing going on in the brains of migraine sufferers, as the next wave of treatments suggested. In the 1970s cardiac patients who also had migraines started telling their doctors that the beta blockers they were taking to slow rapid heartbeats also reduced the frequency of their attacks. Migraine sufferers taking medicines for epilepsy and depression, and others receiving cosmetic Botox injections, also reported relief. So headache specialists began prescribing these “borrowed” drugs for migraines. Five of the medications eventually were approved by the FDA for the condition. Unfortunately, it is still not known exactly how the adopted drugs (which are effective in only about 45 percent of cases and come with an array of side effects) help migraines. Dodick says they may act at various levels of the brain and brain stem to reduce excitability of the cortex and pain-transmission pathways.

The first migraine-specific drugs, the triptans, were introduced in the 1990s. Richard Lipton, director of the Montefiore Headache Center in New York City, says triptans were developed in response to the older idea that the dilation of blood vessels is the primary cause of migraine; triptans were supposed to inhibit it. Ironically, subsequent drug studies show that they actually disrupt the transmission of pain signals in the brain and that constricting blood vessels is not essential. “But they work anyway,” Lipton says. A survey of 133 detailed triptan studies found that they relieved headache within two hours in 42 to 76 percent of patients. People take them to stop attacks after they start, and they have become a reliable frontline treatment for millions.

What triptans cannot do—and what Peter Goadsby, director of the Headache Center at the University of California, San Francisco, has dreamed about doing for more than 30 years—is prevent migraine attacks from happening in the first place. In the 1980s, in pursuit of this goal, Goadsby focused on the trigeminal nerve system, long known to be the brain’s primary pain pathway. It was there, he suspected, that migraine did its dirty work. Studies in animals indicated that in branches of the nerve that exit from the back of the brain and wrap around various parts of the face and head, overactive cells would respond to typically benign lights, sounds and smells by releasing chemicals that transmit pain signals and cause migraine. The heightened sensitivity of these cells may be inherited; 80 percent of migraine sufferers have a family history of the disorder.

Goadsby co-authored his first paper on the subject in 1988, and other researchers, including Dodick, joined the effort. Their goal was to find a way to block the pain signals. One of the chemicals found in high levels in the blood of people experiencing migraine is calcitonin gene-related peptide (CGRP), a neurotransmitter that is released from one nerve cell and activates the next one in a nerve tract during an attack. Zeroing in on CGRP and interfering with it was hard. It was difficult to find a molecule that worked on that neurotransmitter and left other essential chemicals alone.

As biotech engineers’ ability to control and design proteins improved, several pharmaceutical companies developed migraine-fighting monoclonal antibodies. These designer proteins bind tightly to CGRP molecules or their receptors on trigeminal nerve cells, preventing cell activation. The new drugs are “like precision-guided missiles,” Dodick says. “They go straight to their targets.”

It is that specificity, and the fact that scientists actually know how the drugs work, that has Dodick, Goadsby and others excited. In two placebo-controlled trials with a total of 380 people who had severe migraines up to 14 days per month, a single dose of a CGRP drug decreased headache days by more than 60 percent (63 percent in one study and 66 percent in the other). In addition, in the first study, 16 percent of the patients remained totally migraine-free 12 weeks into the 24-week trial. Larger clinical trials to confirm those findings are currently under way. So far the CGRP drugs work better at prevention than any of the borrowed heart or epilepsy drugs and have far fewer side effects. They are given to patients in a single monthly injection.

Migraine specialists are also exploring other treatments, including forehead and eyelid surgery to decompress branches of the trigeminal nerve, as well as transcranial magnetic stimulation (TMS), a noninvasive way of altering nerve cell activity.

Lipton says he has had some good results with TMS. He has also referred patients for surgical interventions but says the experience “has been disappointing,” and he is not recommending it. For his part, Goadsby views surgeries and high-tech efforts as a kind of desperation: “They strike me as a cry for help. If we better understood migraine, we’d know better what to do.”

Even though the cause now appears rooted in the trigeminal nerve system, the origin of its overactive cells is still a mystery, Goadsby says. “What’s the nature of what you inherit when you inherit migraine?” he asks. “Why you, and why not me?” If researchers untangle the genetics of migraine, Jefferson’s “periodical head-ach” may loosen its painful modern grip.