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I'll argue about depression being learned helplessness (it's so much more than that), but you have a good question about tipping points.
Not merely, but I believe it is a major component. There is criticism around the model Seligman developed, but it's mostly based around the inability to psychoanalyze other animals - that infamous blind spot of behavioral science.
Quote:
Originally Posted by rodentraiser
My dad had an awful temper and took it out on our family. I also had an terrible temper and took it out on my dog until I realized what I was doing. That was a watershed moment for me. It was obvious that one of us had to change. The dog wasn't going to change (he wasn't the problem anyway), so it was up to me and I did.
In all those years, though, my dad never had such a tipping point and since then I've always wondered why some people were able to reach through themselves and turn themselves around and why some weren't. Even having done it, I can't explain it.
We see this in people who are alcoholics, drug addicts, physical abusers, and others. Why do some people change and why don't others?
I think we also have to take into consideration how few people can actually get (affordable) mental help if they want it, let alone if they need it.
I can't explain what the "formula" is, either - what conditions, predispositions, medical situations, attitudes, experiences, etc. can precipitate a sudden turn-around (although even "sudden" change can unfold over long periods of time) or what can delay/prevent it. There is plenty of research on it, but it's a complex topic, and there is no one-size-fits-all solution.
Here's something interesting I just came across. It can explain a little of why people who are depressed today can't seem to help themselves all the time.
Here's something interesting I just came across. It can explain a little of why people who are depressed today can't seem to help themselves all the time.
This Viral Twitter Thread Explains What People With Mental Illness Really Mean When They Say "I'm Tired"
She's describing symptoms of burnout along with depression, funny enough (insomnia, sensory overload, exhaustion, tension). That is definitely an issue that seems to be on the rise recently, and loops with depression and anxiety disorders.
These conditions would validate the OP's observations, if burnout and work stress feed into depression and anxiety:
There was a thread somewhere here on CD...the OP said he ditched the internet for a while and was, as a result, MUCH HAPPIER. Could be something to that.
I don't recall. It was over a year ago. I did a free upload, the data is deleted after 45 days. On the report it said she had a tendency to be depressed. I didn't have it, neither did my son
The MAOA gene on chromosome "X" that regulates brain function? AKA: The Warrior Gene.
It involves an enzyme in the brain that breaks down neurotransmitters such as noradrenaline, adrenaline, serotonin, and dopamine. Being too high or too low will cause different negative effects but evolutionary-wise; high or low levels could have been advantageous in different environments.
If we have high levels of this enzyme, it means we’ll have fewer neurotransmitters. High producing MAO-A genes are more likely to have major depression, suicide, & sleep disturbances but abused children with high levels are less likely to develop antisocial behavior.
If we have low levels of this enzyme, we’ll have more neurotransmitters & we are overall more prone to violence, more likely to be risk takers, are more likely to take revenge & use greater force & abused children with low levels are more likely to develop antisocial behavior.
Three important SNP's on MAO A:
Rs90952: C = more aggressive. T = less aggressive & higher rates of suicide in males.
Rs206407: Male T = outward expression of anger. Female T = higher spontaneous aggression.
Rs6323: The G allele indicates higher levels of the enzyme & the T allele = lower levels of the enzyme. Female G = higher outward anger & male G = aggression. T=Anxiety. Female who attempted suicide with TT report higher self-aggression.
There was a thread somewhere here on CD...the OP said he ditched the internet for a while and was, as a result, MUCH HAPPIER. Could be something to that.
Oh, yes. Facebook hasn't improved MY life (for one).
Location: As of 2022….back to SoCal. OC this time!
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I think anxiety & depression were always around. I think in my parents day...or grandparents day, it just wasn't talked about as much & people couldn't constantly compare their lives to other people on the internet or social media. People made more of an effort to talk to neighbors or volunteer or work in some way...& now people are lonely because their main way to communicate to anyone is through the internet & we just have more time to "think" about it....so I think it's a little of both. You probably didn't notice it as much as before but some things like technology are probably making it worse too..............
& some people don't understand everyone feels a little down sometimes...
"Depression" (the mood) has always been around. Back in the day, however, a REAL major clinical depressive episode would've more vaguely been called "a nervous breakdown," as would a psychotic episode. Not much gradation there...
The MAOA gene on chromosome "X" that regulates brain function? AKA: The Warrior Gene.
It involves an enzyme in the brain that breaks down neurotransmitters such as noradrenaline, adrenaline, serotonin, and dopamine. Being too high or too low will cause different negative effects but evolutionary-wise; high or low levels could have been advantageous in different environments.
If we have high levels of this enzyme, it means we’ll have fewer neurotransmitters. High producing MAO-A genes are more likely to have major depression, suicide, & sleep disturbances but abused children with high levels are less likely to develop antisocial behavior.
If we have low levels of this enzyme, we’ll have more neurotransmitters & we are overall more prone to violence, more likely to be risk takers, are more likely to take revenge & use greater force & abused children with low levels are more likely to develop antisocial behavior.
Three important SNP's on MAO A:
Rs90952: C = more aggressive. T = less aggressive & higher rates of suicide in males.
Rs206407: Male T = outward expression of anger. Female T = higher spontaneous aggression.
Rs6323: The G allele indicates higher levels of the enzyme & the T allele = lower levels of the enzyme. Female G = higher outward anger & male G = aggression. T=Anxiety. Female who attempted suicide with TT report higher self-aggression.
Thank you! This is very interesting. I wouldn't have expected a gene involved in regulation of neurotransmitters would be sex-linked (or maybe I should have...). That means it is inherited from the mother, and males and females will show different phenotype ratios.
It should be said that "maladaptive behavior" is not monogenic (arising from one gene), as the phenotypes are not discrete. MAOA doesn't really have anything to do with depression directly, so I doubt that'd be the one that she was referring to.
This is a more informative article on MAOA, if anyone is interested:
Specifically, monoamine oxidase A is involved in the breakdown of the neurotransmitters serotonin, epinephrine, norepinephrine, and dopamine. Signals transmitted by serotonin regulate mood, emotion, sleep, and appetite. Epinephrine and norepinephrine control the body's response to stress. Dopamine transmits signals within the brain to produce smooth physical movements.
[…]
Monoamine oxidase A also helps break down monoamines found in the diet. It seems to be particularly important in the breakdown of excess tyramine, which is found in cheese and other foods.
Mutations in the MAOA gene cause monoamine oxidase A deficiency. This condition affects males almost exclusively and is characterized by mild intellectual disability and behavioral problems, including aggressive and violent outbursts. In some cases, particular foods seem to worsen symptoms of the condition. The MAOA gene mutations reduce monoamine oxidase A activity, which causes serotonin and other neurotransmitters to build up in the brain. It is unclear how this buildup leads to the signs and symptoms of monoamine oxidase A deficiency. Researchers speculate that an excess of certain neurotransmitters, particularly serotonin and norepinephrine, may impair an affected individual's ability to control his impulses, leading to aggressive outbursts.
[…]
Several common genetic variants (polymorphisms) in or near the MAOA gene have been found to affect the gene's activity. The most studied polymorphism, called MAOA-uVNTR, occurs in an area near the MAOA gene, called the promoter region, that controls gene activity. In this region, a string of 30 DNA building blocks (nucleotides) is repeated, end-to-end, two to five times. Studies show that when the string of nucleotides is repeated 3.5 or four times, more monoamine oxidase A protein is produced than when the nucleotides are repeated only two or three times. For this reason, versions of DNA (alleles) with 3.5 or four repeats are referred to as high-activity alleles. Versions with only two or three repeats, which result in lower than normal amounts of monoamine oxidase A, are considered low-activity alleles. It is unclear what effect five repeats has on MAOA gene activity.
Low-activity MAOA-uVNTR alleles are associated with aggressive behavior. Several reports found the effect only in males, but some other reports indicate that both males and females with low-activity alleles can be prone to aggression. Some studies indicate that low-activity alleles specifically increase the risk of violence and aggression in individuals who were abused as children. Researchers are studying how these MAOA gene polymorphisms are involved in modulating behavior and the role of environmental factors, such as childhood abuse or situations in which a person is provoked.
In contrast, high-activity MAOA-uVNTR alleles appear to increase the risk of panic disorder in females. Panic disorder is a severe anxiety disorder characterized by episodes of overwhelming fear (panic attacks) with no obvious trigger. It is unclear how high amounts of monoamine oxidase A contribute to panic disorder.
Other polymorphisms that can affect MAOA gene activity may also be associated with aggression. The roles of MAOA-uVNTR and other polymorphisms are also being studied in depression, bipolar disorder, alcoholism, drug addiction, and many other conditions.
1) The polymorphisms are not SNPs. The 2R, 3R, etc. refers to the repeated sequences in the promotor region that are 30 nucleotides long, not one. That means it is "easier" for whatever complex initiates the transcription of this gene to find it. Like turning up the volume saying "I'm here!"
The SelfHacked article admits this:
Quote:
There is no SNP that perfectly correlates with 2-5R version. There are only SNPs that correlate with these versions somewhat. It depends on groups of SNPs and also on your gender.
So diagnosing yourself based on DNA reports is pretty weak.
2) Note that MAOA deficiency is not the same as reduced MAOA transcription based on polymorphisms. That is key. Enzymes don't work in a vacuum - there is a pathway that triggers their activity (that complex I mentioned earlier would be part of it). It is one thing to have that process stalled by a defective enzyme, and another to modify the level of activity of the enzyme. What is 'normal' becomes highly subjective based on the population.
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