I’ve been sober for 11 years this year after nearly drinking myself to death for nearly a decade. If i hadn’t stopped and got the help i needed, i wouldn’t have seen my 24th birthday.
When you’re first in recovery, the first couple of years are the hardest. You’ll want to use or drink or go back to your old ways, whatever your addiction - they don’t call it a habit for nothing.
When you feel like you want to use, call someone. If you can’t call someone, then distraction is the key. Go for a walk, hit the gym, clean your room, dance around the kitchen like a twat, anything. Distracting yourself from those antsy, restless feelings will help and the moment will pass.
But you can do this, i know you can. I’m so proud of you for making the choice to admit you have a problem and deciding that you’re going to kick your addiction’s backside into submission. You can totally do this.
You are strong, you are brave and you are amazing. Keep doing what you’re doing and it will get easier, i promise you. Take it from a former alcoholic who used to self harm, IT GETS EASIER.
finished treatment, things will get better.
Once you get your
addiction under control, things will get better.
When entering recovery, these are things that everyone will
tell you; fellow addicts/alcoholics, counselors, family, friends… They all
say the same thing: once you do it,
things will get better. It is the promise of better things to come that
brings so many of us to the starting point of our journey in recovery. For me,
it was no different.
While I was drinking, my life was a mess. I was going
nowhere fast and I couldn’t seem to “get my shit together.” The promise that
“things will get better,” is what kept me motivated; I had felt like a “loser,”
for too long. I was ready to go out and do the things that many people my age
were doing – I was ready to take control of the direction that my life was
moving in, and start working towards a future. What everyone failed to mention,
however, was how long it would take before things started getting better.
I had thought that “things will get better,” meant that I
could get back to living my life – get back on the track that most my age are
on, and work on building a future for myself. A year in to sobriety, I felt
trapped; I had a part-time job that I hated, but couldn’t find work elsewhere
and was far too in debt from my drinking days. Trapped in a part-time job that
made me miserable was so familiar that it had felt hardly anything had changed
at all. It was discouraging to look to my peers, building their list of
accomplishments, and think “Well, this is as good as things are going to get
for you. You’ve made too many mistakes; buried yourself far too deeply. You’ll
spend the rest of your life going nowhere while you pay for the choices you’ve
It took me quite a while to realize that “things getting
better,” is a process. It started with happiness, self-value, and inner peace –
that was the first part to get better. Next was my health - both physical and
mental well-being. Then, my relationships started improving; my life was
filling up with good people, the type of people that wouldn’t have been around
if I wasn’t a good person myself. Sadly, though, it was difficult to see these
things. I couldn’t appreciate them because I had expected everything to get
better at once – I didn’t understand the process, I didn’t understand patience.
I am writing this entry so that I may have the opportunity
to say what I wished had been said to me; “Once
you’re in recovery, things will start to get better. Trust the process and
enjoy the small victories, because they are steps in the staircase to ‘better.’
Take time to give yourself a pat on the back. Nothing magically ‘gets better’
overnight, but you will get there if you keep moving forward.”
I am at a point now where I can look back on these days and
laugh at my impatience. I have finally come to a place where I am achieving my
goals, and I have accomplishments that I can be truly proud of. I am doing the
things that I need to do for my future – things that I never, ever could have
done if I hadn’t gotten sober. Now, I understand what they mean when they say “Once you’re sober, things will get better.”
Wake Forest Baptist Medical Center researchers are gaining a better understanding of the neurochemical basis of addiction with a new technology called optogenetics.
In neuroscience research, optogenetics is a newly developed technology that allows researchers to control the activity of specific populations of brain cells, or neurons, using light. And it’s all thanks to understanding how tiny green algae, that give pond scum its distinctive color, detect and use light to grow.
The technology enables researchers like Evgeny A. Budygin, Ph.D., assistant professor of neurobiology and anatomy at Wake Forest Baptist, to address critical questions regarding the role of dopamine in alcohol drinking-related behaviors, using a rodent model.
“With this technique, we’ve basically taken control of specific populations of dopamine cells, using light to make them respond - almost like flipping a light switch,” said Budygin. “These data provide us with concrete direction about what kind of patterns of dopamine cell activation might be most effective to target alcohol drinking.”
The latest study from Budygin and his team published online in last month’s journal Frontiers in Behavioral Neuroscience. Co-author Jeffrey L. Weiner, Ph.D., professor of physiology and pharmacology at Wake Forest Baptist, said one of the biggest challenges in neuroscience has been to control the activity of brain cells in the same way that the brain actually controls them. With optogenetics, neuroscientists can turn specific neurons on or off at will, proving that those neurons actually govern specific behaviors.
“We have known for many years what areas of the brain are involved in the development of addiction and which neurotransmitters are essential for this process,” Weiner said. “We need to know the causal relationship between neurochemical changes in the brain and addictive behaviors, and optogenetics is making that possible now.”
The researchers used cutting-edge molecular techniques to express the light-responsive channelrhodopsin protein in a specific population of dopamine cells in the brain-reward system of rodents. They then implanted tiny optical fibers into this brain region and were able to control the activity of these dopamine cells by flashing a blue laser on them.
“You can place an electrode in the brain and apply an electrical current to mimic the way brain cells get excited, but when you do that you’re activating all the cells in that area,” Weiner said. “With optogenetics, we were able to selectively control a specific population of dopamine cells in a part of the brain-reward system. Using this technique, we discovered distinct patterns of dopamine cell activation that seemed to be able to disrupt the alcohol-drinking behavior of the rats.”
Weiner said there is translational value from the study because “it gives us better insight into how we might want to use something like deep-brain stimulation to treat alcoholism. Doctors are starting to use deep-brain stimulation to treat everything from anxiety to depression, and while it works, there is little scientific understanding behind it, he said.
Budygin agreed and said this kind of project wouldn’t be possible without cross campus collaboration between neurobiology and anatomy, physiology and pharmacology and physics. "Now we are taking the first steps in this direction,” he said. “It was impossible before the optogenetic era.”
As recovering spring breakers are regretting binge drinking escapades, it may be hard for them to appreciate that there is a positive side to the nausea, sleepiness, and stumbling. University of Utah neuroscientists report that when a region of the brain called the lateral habenula is chronically inactivated in rats, they repeatedly drink to excess and are less able to learn from the experience. The study, published online in PLOS ONE on April 2, has implications for understanding behaviors that drive alcohol addiction.
While complex societal pressures contribute to alcoholism, physiological factors are also to blame. Alcohol is a drug of abuse, earning its status because it tickles the reward system in the brain, triggering the release of feel-good neurotransmitters. The dreaded outcomes of overindulging serve the beneficial purpose of countering the pull of temptation, but little is understood about how those mechanisms are controlled.
U of U professor of neurobiology and anatomy Sharif Taha, Ph.D., and colleagues, tipped the balance that reigns in addictive behaviors by inactivating in rats a brain region called the lateral habenula. When the rats were given intermittent access to a solution of 20% alcohol over several weeks, they escalated their alcohol drinking more rapidly, and drank more heavily than control rats.
“In people, escalation of intake is what eventually separates a social drinker from someone who becomes an alcoholic,” said Taha. “These rats drink amounts that are quite substantial. Legally they would be drunk if they were driving.”
The lateral habenula is activated by bad experiences, suggesting that without this region the rats may drink more because they fail to learn from the negative outcomes of overindulging. The investigators tested the idea by giving the rats a desirable, sweet juice then injecting them with a dose of alcohol large enough to cause negative effects.
“It’s the same kind of learning that mediates your response in food poisoning. You taste something and then you get sick, and then of course you avoid that food in future meals,” explained Taha.
Yet rats with an inactivated lateral habenula sought out the juice more than control animals, even though it meant a repeat of the bad experience.
“The way I look at it is the rewarding effects of drinking alcohol compete with the aversive effects,” explained Andrew Haack, who is co-first author on the study with Chandni Sheth, both neuroscience graduate students. “When you take the aversive effects away, which is what we did when we inactivated the lateral habenula, the rewarding effects gain more purchase, and so it drives up drinking behavior.”
The group’s findings may help explain results from previous clinical investigations demonstrating that men who were less sensitive to the negative effects of alcohol drank more heavily, and were more likely to become problem drinkers later in life.
The researches think the lateral habenula likely works in one of two ways. The region may regulate how badly an individual feels after over-drinking. Alternatively, it may control how well an individual learns from their bad experience. Future work will resolve between the two.
“If we can understand the brain circuits that control sensitivity to alcohol’s aversive effects, then we can start to get a handle on who may become a problem drinker,” said Taha.
Neuroscientists at The University of Texas at Austin have generated mutant worms that do not get intoxicated by alcohol, a result that could lead to new drugs to treat the symptoms of people going through alcohol withdrawal.
The scientists accomplished this feat by inserting a modified human alcohol target into the worms, as reported this week in The Journal of Neuroscience.
“This is the first example of altering a human alcohol target to prevent intoxication in an animal,” says corresponding author, Jon Pierce-Shimomura, assistant professor in the university’s College of Natural Sciences and Waggoner Center for Alcohol and Addiction Research.
An alcohol target is any neuronal molecule that binds alcohol, of which there are many.
One important aspect of this modified alcohol target, a neuronal channel called the BK channel, is that the mutation only affects its response to alcohol. The BK channel typically regulates many important functions including activity of neurons, blood vessels, the respiratory tract and bladder. The alcohol-insensitive mutation does not disrupt these functions at all.
“We got pretty lucky and found a way to make the channel insensitive to alcohol without affecting its normal function,” says Pierce-Shimomura.
The scientists believe the research has potential application for treating people addicted to alcohol.
“Our findings provide exciting evidence that future pharmaceuticals might aim at this portion of the alcohol target to prevent problems in alcohol abuse disorders,” says Pierce-Shimomura. “However, it remains to be seen which aspects of these disorders would benefit.”
Unlike drugs such as cocaine, which have a specific target in the nervous system, the effects of alcohol on the body are complex and have many targets across the brain. The various other aspects of alcohol addiction, such as tolerance, craving and the symptoms of withdrawal, may be influenced by different alcohol targets.
The worms used in the study, Caenorhabditis elegans, model intoxication well. Alcohol causes the worms to slow their crawling with less wriggling from side to side. The intoxicated worms also stop laying eggs, which build up in their bodies and can be easily counted.
Unfortunately, C. elegans are not as ideal for studying the other areas of alcohol addiction, but mice make an excellent model. The modified human BK channel used in the study, which is based on a mutation discovered by lead author and graduate student Scott Davis, could be inserted into mice. These modified mice would allow scientists to investigate whether this particular alcohol target also affects tolerance, craving and other symptoms relevant to humans.
Pierce-Shimomura speculated that their research could even be used to develop a ‘James Bond’ drug someday, which would enable a spy to drink his opponent under the table, without getting drunk himself. Such a drug could potentially be used to treat alcoholics, since it would counteract the intoxicating and potentially addicting effects of the alcohol.