Understanding Anxiety and Panic Attacks - Empowering Yourself with Knowledge (and a Little Humour!) added November 2024
If you suffer from anxiety or panic attacks, you’re not alone—and you’re certainly not “broken.” Anxiety and panic are natural reactions, deeply ingrained in the human experience, even if they sometimes kick in at the wrong times. Understanding why your body reacts this way and viewing these sensations as protective, rather than harmful, can empower you to handle these moments with strength and even a bit of humour. Let’s dive into the purpose of anxiety and panic, why it shows up the way it does, and some tips for regaining control.
Why Anxiety and Panic Happen
Anxiety and panic aren’t “disorders” in themselves. They’re natural reactions that our ancestors relied on for survival. Picture our early ancestors suddenly confronted with a wild animal. Their bodies would respond by preparing to fight, flee, or freeze, giving them the best chance to survive. These reactions are so ingrained that they still activate today—even when the “danger” might be a stressful meeting or an uncomfortable conversation.
What Happens During a Panic Attack?
A panic attack is like your body’s emergency system firing up, even if you’re safe. Here’s how it works:
• Rapid heartbeat and breathing: Your body is preparing for quick movement, as if you needed to run or fight.
• Sweaty palms: A little extra grip to climb or escape if needed.
• Feeling “stuck” or frozen: If the “danger” feels overwhelming, your body might freeze first, a bit like hitting pause to decide your next move.
• Digestive upset (and here’s the messy part): Just like other animals, when humans experience intense fear, the body loosens its sphincter muscles, lightening the load by encouraging an exit from… well, let’s just say, both ends. And while the original purpose of this was to help you get away quickly—nothing slows you down like a full stomach! —it also has the bonus effect of making you a bit less appealing to predators. After all, what wild animal wants to dine on something that’s “marked its territory” so dramatically?
Seeing these symptoms for what they are—your body’s overly enthusiastic attempt to protect you—can help you view them with a little less fear and maybe even a smirk. Your body is only trying to help, even if it feels like it’s overdoing it!
You Are Not Alone: Anxiety is Common
Many people experience anxiety and panic, but because it can look different from person to person, it may feel isolating. Knowing that others feel the same, even if it shows up differently for them, can make these feelings less lonely.
Reframing Your Symptoms
Let’s take a fresh look at some common symptoms:
• Fast breathing and heart rate: Preparing for action, even if the action is imaginary.
• Sweaty palms: Great for grip if you’re about to climb (though perhaps less useful at a meeting).
• Racing thoughts: Your mind is in “quick decision/ reflex mode,” simplifying your choices to either “fight” or “flee.”
These reactions are like your body’s automatic alarm system—just a bit oversensitive. The goal isn’t to turn it off but to reset it so it only sounds when truly necessary.
Breaking the Fear Cycle
Anxiety and panic often come with a “fear of the fear” itself. When you understand your body’s quirky survival tactics, you can meet these sensations with a little humour. The next time you feel panic rising, try thinking, “Ah, my body’s just prepping me for the next big escape!” Or “My ancient survival system is ready to help me dodge that tiger in the break room!” Humour doesn’t erase anxiety, but it can lessen its intensity, helping you move from dread to amusement.
Moving Forward: Empowerment and Practice
Learning to work with panic takes time, but practice helps. Each time you acknowledge these survival tactics with less fear, your body learns that it can stand down. It’s not about “curing” anxiety but rather realigning it with reality. With understanding, these reactions stop feeling so overwhelming, making room for more peace and control.
Final Thoughts
Remember, anxiety and panic aren’t enemies—they’re parts of you, just a little overzealous in their protective efforts. By reframing these responses as quirky body quirks rather than flaws, you can regain a sense of control and maybe even a laugh along the way. With each step, you’re moving toward a life where anxiety is just one small part of a bigger, healthier picture.
How We See Ourselves Affects Anxiety and Depression updated October 2024
The way we see ourselves, called self-concept, has a big effect on our feelings. If you struggle with anxiety or depression, understanding your self-concept can help you feel better.
Here are the three main parts of self-concept:
- Self-Esteem: This is how much you value yourself. If you have high self-esteem, you feel more confident and positive. If you have low self-esteem, you might feel sad, guilty, or not good enough, which can make anxiety and depression worse.
- Self-Efficacy: This is your belief in your ability to handle problems. If you believe you can deal with challenges, you’re likely to feel more in control and less anxious. If you doubt yourself, you may feel helpless, which can increase anxiety and depression.
- Self-Identity: This is how you see yourself in your roles, like being a parent, partner, or worker. When you feel good about your roles, you feel positive emotions. But when something challenges these roles, like losing a job or a relationship, it can lead to confusion, frustration, or sadness.
Gaps Between Who You Are and Who You Want to Be
Psychologist E. Tory Higgins explains that we often have different versions of ourselves in our mind:
- Actual self: Who you think you are right now.
- Ideal self: Who you want to be.
- Ought self: Who you think you should be.
When there’s a gap between who you are and who you want to be, it can cause negative emotions. For example, if you don’t feel like you’re living up to your ideal self, you might feel sad or frustrated. If you think you’re not living up to who you should be, it can lead to guilt and anxiety. These gaps can make anxiety and depression worse.
Positive vs. Negative Self-Concept
If you have a positive self-concept, you’re more likely to feel good emotions, even during tough times. People who see themselves in a positive way usually handle stress better and feel more balanced.
A negative self-concept, however, makes anxiety and depression worse. If you see yourself negatively, you might feel more anxious or sad, and you may see normal situations as threatening. This can create a cycle where negative thoughts and feelings keep feeding each other.
How to Feel Better
Changing the way you think about yourself can help you feel less anxious and depressed. Start by being kind to yourself, setting realistic goals, and recognizing your strengths. Over time, this can improve how you see yourself and help you feel more positive emotions.
By making small changes in how you think, you can start to break the cycle of anxiety and depression, and feel more in control of your life.
Analysis-depression-is-probably-not-caused-by-a-chemical-imbalance-in-the-brain-new-study-july-22
Analysis: Depression is probably not caused by a chemical imbalance in the brain – new study July 22
This article originally appeared in The Conversation on 20 July 2022
Writing in The Conversation, Professor Joanna Moncrieff and Dr. Mark Horowitz (both UCL Psychiatry) report on their new research showing no clear evidence that serotonin levels or serotonin activity are responsible for depression.
For three decades, people have been deluged with information suggesting that depression is caused by a “chemical imbalance” in the brain – namely an imbalance of a brain chemical called serotonin. However, our latest research review shows that the evidence does not support it.
Although first proposed in the 1960s, the serotonin theory of depression started to be widely promoted by the pharmaceutical industry in the 1990s in association with its efforts to market a new range of antidepressants, known as selective serotonin-reuptake inhibitors or SSRIs.
The idea was also endorsed by official institutions such as the American Psychiatric Association, which still tells the public that “differences in certain chemicals in the brain may contribute to symptoms of depression”.
Countless doctors have repeated the message all over the world, in their private surgeries and in the media. People accepted what they were told. And many started taking antidepressants because they believed they had something wrong with their brain that required an antidepressant to put right.
In the period of this marketing push, antidepressant use climbed dramatically, and they are now prescribed to one in six of the adult population in England, for example.
For a long time, certain academics, including some leading psychiatrists, have suggested that there is no satisfactory evidence to support the idea that depression is a result of abnormally low or inactive serotonin. Others continue to endorse the theory. Until now, however, there has been no comprehensive review of the research on serotonin and depression that could enable firm conclusions either way.
At first sight, the fact that SSRI-type antidepressants act on the serotonin system appears to support the serotonin theory of depression. SSRIs temporarily increase the availability of serotonin in the brain, but this does not necessarily imply that depression is caused by the opposite of this effect.
There are other explanations for antidepressants’ effects. In fact, drug trials show that antidepressants are barely distinguishable from a placebo (dummy pill) when it comes to treating depression. Also, antidepressants appear to have a generalised emotion-numbing effect that may influence people’s moods, although we do not know how this effect is produced or much about it.
There has been extensive research on the serotonin system since the 1990s, but it has not been collected systematically before. We conducted an “umbrella” review that involved systematically identifying and collating existing overviews of the evidence from each of the main areas of research into serotonin and depression. Although there have been systematic reviews of individual areas in the past, none have combined the evidence from all the different areas taking this approach.
One area of research we included was research comparing levels of serotonin and its breakdown products in the blood or brain fluid. Overall, this research did not show a difference between people with depression and those without depression.
Another area of research has focused on serotonin receptors, which are proteins on the ends of the nerves that serotonin links up with and which can transmit or inhibit serotonin’s effects. Research on the most commonly investigated serotonin receptor suggested either no difference between people with depression and people without depression, or that serotonin activity was actually increased in people with depression – the opposite of the serotonin theory’s prediction.
Research on the serotonin “transporter”, which is the protein that helps to terminate the effect of serotonin (this is the protein that SSRIs act on), also suggested that, if anything, there was increased serotonin activity in people with depression. However, these findings may be explained by the fact that many participants in these studies had used or were currently using antidepressants.
We also looked at research that explored whether depression can be induced in volunteers by artificially lowering levels of serotonin. Two systematic reviews from 2006 and 2007 and a sample of the ten most recent studies (at the time the current research was conducted) found that lowering serotonin did not produce depression in hundreds of healthy volunteers. One of the reviews showed very weak evidence of an effect in a small subgroup of people with a family history of depression, but this only involved 75 participants.
Very large studies involving tens of thousands of patients looked at gene variation, including the gene that has the instructions for making the serotonin transporter. They found no difference in the frequency of varieties of this gene between people with depression and healthy controls.
Although a famous early study found a relationship between the serotonin transporter gene and stressful life events, larger, more comprehensive studies suggest no such relationship exists. Stressful life events in themselves, however, exerted a strong effect on people’s subsequent risk of developing depression.
Some of the studies in our overview that included people who were taking or had previously taken antidepressants showed evidence that antidepressants may actually lower the concentration or activity of serotonin.
The serotonin theory of depression has been one of the most influential and extensively researched biological theories of the origins of depression. Our study shows that this view is not supported by scientific evidence. It also calls into question the basis for the use of antidepressants.
Most antidepressants now in use are presumed to act via their effects on serotonin. Some also affect the brain’s chemical noradrenaline. But experts agree that the evidence for the involvement of noradrenaline in depression is weaker than that for serotonin.
There is no other accepted pharmacological mechanism for how antidepressants might affect depression. If antidepressants exert their effects as placebos, or by numbing emotions, then it is not clear that they do more good than harm.
Although viewing depression as a biological disorder may seem like it would reduce stigma, in fact, research has shown the opposite, and also that people who believe their own depression is due to a chemical imbalance are more pessimistic about their chances of recovery.
It is important that people know that the idea that depression results from a “chemical imbalance” is hypothetical. And we do not understand what temporarily elevating serotonin or other biochemical changes produced by antidepressants do to the brain. We conclude that it is impossible to say that taking SSRI antidepressants is worthwhile, or even completely safe. People need all this information to make informed decisions about whether or not to take antidepressants.
His wife begged him to try hypnosis. It turned Cameron Davis’ career around in two weeks
By Adam Pengilly
At face value, there shouldn’t be much wrong with Cameron Davis’ life. Happily married, a multimillionaire travelling the world playing his chosen sport, a top 12 finish in The Masters, the world’s biggest golf tournament (maybe The Open excluding), well under par in the bigger picture of things.
But two weeks ago, he was so down on his sport and how hard it was to get a little white ball in the hole, he started speaking to a hypnotherapist. His wife, Jonika, had been spouting the benefits.
Australian golfer Cam Davis almost sunk a long-range birdie putt as he fought to hold a lead at the Rocket Mortgage Classic.
Finally, Davis caved.
“She felt like it helped her a lot,” Davis said. “I resisted for quite a long time. But I decided my game was going in the wrong direction, and I was feeling more and more stressed day-to-day with my golf. I was kind of falling out of love with the game a little bit. My career trajectory was not where I wanted it.”
It’s not hypnosis as most people would assume.
Davis wasn’t being paraded on a stage in front of hundreds of people, spontaneously break dancing to Jean-Martin Charcot’s command, mocked to a gallery in fits of laughter.
As he explains it, he walks through a deep meditation where you think about situations you want to deal with better, like when he launched his fairway wood to the green with his second shot of the par-five 14th hole in the final round of the Rocket Mortgage Classic, only to see it clamber back into the water. Australian Ian Baker-Finch was incensed in commentary, claiming no ball should land on a green like that and roll back into a watery grave without thick grass to stop it.
Davis dealt with it, maybe because he’d already seen it.
“My golf has come from a pretty rough place to where it’s at,” Davis said.
“It had been a long time since I’d won, and I wasn’t playing anywhere near good enough golf to keep up with the best players in the game. We’ve only been working together [with his hypnotherapist] a couple of weeks, and I’ve almost gone from almost disliking the game to feeling like I’ve got a bit of the magic back.
“It’s been a huge difference.”
On Monday morning (AEST), Davis won his second PGA Tour event in Detroit, the same event he won three years ago for his maiden win in the United States. This one felt like it meant more.
American Akshay Bhatia (-17) three-putted for the first time all tournament on the 72nd hole, blowing the chance to head to a play-off with Davis (-18), who finished with two-under 70.
“Just a little bit of nerves, honestly,” Bhatia said. “I’m human.”
Maybe hypnotherapy will help?
Davis’ treatment came after missing the cut at the PGA Championship and US Open the past two months. He sprayed it everywhere for a seven-over start at Pinehust No.2 in the US Open and thought there must be a better way.
It was enough to beat Bhatia, fellow Australian Min Woo Lee, American Davis Thompson and England’s Aaron Rai, who all shared a tie for second. It was the first time an Australian had won on the PGA Tour since May last year (Jason Day in the Byron Nelson Classic).
“It’s been a long few years of really not recapturing that magic,” Davis said. “To be back here, it feels extra special.”
