Genes and Intelligence plus other stuff

[Black Rose]

I have a 23andMe account for both me and my mother.
I took my info and put it into genomelink.com
you can get 312 traits analyzed (not in great detail but some)
I was most interested in the intelligence analysis but only got a sample (you must pay to unlock all of the traits)

summary

Bigger input, output, and middle of hippocampus

more fat to the brain

channels proteins faster into mitochondria

disposes of malfunctioning cells

-here is a summary of the information about your intelligence and brain from your genetics test:

Your hippocampus is larger than average. The hippocampus is a brain region that is important for memory and learning. A larger hippocampus may mean that you have better memory and learning abilities.

You have a genetic variant that may help to transport more fat to your brain. Fat is an important energy source for the brain, and having more fat available may help your brain to function better.

You have a genetic variant that may help to transport proteins into your mitochondria faster. Mitochondria are the powerhouses of the cell, and they need proteins to function properly. Having a faster rate of protein transport may help your mitochondria to produce more energy.

You have a genetic variant that may help to dispose of malfunctioning cells. Malfunctioning cells can damage the brain and lead to cognitive decline. Having a more efficient way to dispose of these cells may help to protect your brain health.

Overall, these genetic variants suggest that you have a brain that is well-suited for learning and memory. They may also help to protect your brain from damage and cognitive decline.

Here is the full list of intelligence traits:

 

[Black Rose]

How is "Resurgence of Fear" encoded by the genome?​

Reference research​

ADRB2 gene polymorphism modulates the retention of fear extinction memory.​

CHECK REFERENCE RESEARCH​

Fear is something most people have experienced throughout their lives, and it’s evolutionarily essential for survival. But too much fear can indicate mental health illness: one example is post-traumatic stress disorder (PTSD), which affects up to 10% of the population. One common method for treatment has been exposure therapy, which is when patients are exposed to their trigger in a controlled setting to create memories that compete with the original fearful event. PTSD is very complex in its development and treatment, as not everybody who experiences trauma will have PTSD and exposure therapy is unfortunately not the silver bullet for this condition. In a study of 91 healthy Han Chinese men, investigators used a fear conditioning test involving visual stimuli (some accompanied by electric shocks) to see how participants with different genes respond. Interestingly, it was found that those who had the GG variant at a locus in the beta-2 adrenergic receptor (ADRB2) gene were more susceptible to becoming fearful, even after undergoing memory extinction (a process by which the visual stimulus is uncoupled from the electric shock). On the other hand, those who had the A allele were less prone to having their fear of the electric shock return after memory extinction. The ADRB2 gene is important because it has previously been linked to PTSD. Specifically, among those who have experienced childhood trauma, whether or not the child had a single mutation of the ADRB2 gene at the same locus in this study was highly predictive of whether the child would experience PTSD or not. Although the sample size of this study is limited for this kind of analysis, the results are very promising in that they can help inform how to identify susceptible populations and, ultimately, develop treatment methods for PTSD and other related psychiatric disorders.

 

[scorpiomover]

Interestingly, it was found that those who had the GG variant at a locus in the beta-2 adrenergic receptor (ADRB2) gene were more susceptible to becoming fearful, even after undergoing memory extinction (a process by which the visual stimulus is uncoupled from the electric shock).

I was curious about what the ADRB2 gene did, as if being overly fearful was a disadvantage, then the ADRB2 gene should have become rarer and rarer over time.

So I googled it and found this:

Genetics of β2-Adrenergic Receptors and the Cardiopulmonary Response to Exercise

Of the response to circulating catecholamines, the ADRB2 are primarily responsible for increases in bronchodilation, ventricular function, and vasodilation.

ADRB2 causes the lungs to widen and absorb more oxygen (bronchodilation), and causes the blood vessels to widen and absorb more oxygen (vasodilation). So the ADRB2 gene is what makes some people able to absorb much more oxygen via breathing through the lungs and get it to the blood and the rest of the body much quicker, including the brain.

This has great significance for fear, as it is well known that increased oxygen reduces fear.

The GG variant also has a protective effect against myocardial infarction.

So the quick response to fear in the variant, is also associated with an increased ability to absorb oxygen and to be protected against heart attacks.

I would thus not be surprised if those with the GG variant are able to absorb more oxygen than most people, because the lungs and blood vessels are far more responsive to stress.

The increased fear is probably a similar effect, but would only occur when oxygen deprivation occurs, i.e. when the body is not engaged in deep breathing in general and particularly under stress.

But those with the GG variant, who exercise regularly to do regular deep breathing exercises, and who automatically breathe more deeply under stress, become far calmer, more capable, stronger and faster than most people under stress, because oxygen is the main way for our bodies to generate energy.

In most people, the increased stress and pressure from the heart can induce a heart attack due to a myocardial infarction (the blood vessels cannot get enough blood to the heart to match the strain). This sort of situation has caused strokes in people who were doing HIIT (High Intensity Interval Exercise).

But those with the GG variant are protected, which means their can push their bodies to do superhuman things that would give normal humans a heart attack, but would be no problem for them.

So what this could mean, is that if you have the GG variant, you're an ideal candidate for cardio and powerful deep breathing exercises, such as Pranayama.

See: Pranayama Benefits for Physical and Emotional Health

I expected there would be a counter-effect to the increased fear.

But I already know that due to the Krebs cycle, which is the way body processes oxygen, your body gets almost 20 times the energy output due to oxygen, on a minute by minute basis.

So this sort of effect could make anyone with the GG variant who engages in deep breathing, a powerhouse of energy, and also much, much calmer than a regular person.

The effects of increased oxygen on the brain also vastly increase the speed of thought and thus vastly increase intelligence.

So given your strong fear response, everything you are weak at, could actually be your greatest strength, as long as you get into deep breathing exercises.

I would seriously suggest you look into this, and start doing deep breathing exercises IMMEDIATELY and EVERY DAY, as this has the power to reverse your issues, into superhuman capabilities.

This isn't what I expected at all. But, I get a lot of surprises when I dig into things.

 

[Black Rose]

But I already know that due to the Krebs cycle, which is the way body processes oxygen, your body gets almost 20 times the energy output due to oxygen, on a minute by minute basis.

So this sort of effect could make anyone with the GG variant who engages in deep breathing, a powerhouse of energy, and also much, much calmer than a regular person.

The effects of increased oxygen on the brain also vastly increase the speed of thought and thus vastly increase intelligence.

So given your strong fear response, everything you are weak at, could actually be your greatest strength, as long as you get into deep breathing exercises.

I currently find it extremely hard to do physical activity because all the oxygen goes directly to the brain, not the body - I spend 12 hours a day doing mental activity not physical activity. But when I must do physical activity I have increased stamina as long as it is not running or jogging. normally I need to expand my lungs very little to keep up with the mental work. In school, I had to work long periods where I only did mental work. I take a deep breath about once every 5 minutes because I sometimes forget to sit up straight.

Fear also in me involves me avoiding everything painful. I have a low pain threshold so I avoid anything that causes it. Trauma is physical/neurological and so because of the emotions I have come to terms with certain limits. When I am alerted to danger I almost do have panic attacks but only if they have become unavoidable. Deep down inside I have extreme fear the oxygen keeps from arising which is what the article says is the result of not forgetting the trauma. My coping mechanism is to slow down and reflect. People see it as almost catatonia.

I saw a nurse practitioner today who told me I needed to see a neurologist. I believe that in me is some kind of basal ganglia function that causes OCD-like symptoms and nondetectable deep-level seizures. It feels painful to do nothing so that is why I do mental work all the time based on my interest. I avoid reading books or watching tv. - emotional burnout happens often when I don't sleep.

 

[scorpiomover]

The 1st article I mentioned, says that ADRB2 regulates epinephrine, while the ADRB1 gene regulates norepinephrine.

This has interesting consequences, because of this article:

Plasma Catecholamines in Stress and Exercise

A technique was devised to monitor plasma catecholamines in a minimally obtrusive fashion in subjects going about their working activities. There was a disparity between plasma norepinephrine and epinephrine levels in different situations. During public speaking, epinephrine levels increase twofold, whereas during physical exercise, norepinephrine levels increase threefold. It seemed that while exercise induces a response of the sympathetic nervous system, psychological stress induces primarily an adrenal response.

So the ADRB2 gene is involved during public speaking, while the ADRB1 gene is involved during exercise.

This means that social anxiety is controlled via epinephrine which in turn is controlled by the ADRB2 gene, which in turn opens the blood vessels and the lungs, which in turn allows the body to pump much more oxygen into the cells and the brain, which in turn means that social anxiety is greatly reduced.

Physical exercise is controlled via norepinephrine, which in turn is controlled by the ADRB1 gene, which in turn expands the heart, which in turn allows the body to pump much more blood around the body, which in turn means more oxygen and glucose gets to the cells and allows for greater physical exercise.

The difference between increasing the heart rate, and expanding the blood vessels, is akin to how you increase speed in a car.

Increasing the heart rate, is like pressing down on the accelerator pedal, as that speeds up the revs. Great for a short burst of speed. This also puts more pressure on the engine, which makes the engine whine. That also explains the increased risk of myocardial infarction (heart attack), as pumping the revs for a long time will burn out the engine.

Expanding the blood vessels, means every blood vessel can carry more blood, which is equivalent to changing up a gear. This doesn't increase the speed of the car. It does, however, mean the car can travel at high speeds for long periods. Great for endurance. If the engine is already revving, then when you change up a gear, the engine whine goes away, as the engine is no longer under pressure.

However, if you're travelling at lower speeds, going up too high a gear can cause the engine to stall, which could also induce a heart attack in a human body. But in this case, since there is also mediation of the blood vessels, it means the gears are actually more responsive. So less chance of the engine stalling or burning out. So less chance of a heart attack in either case.

However, epinephrine has more of an effect on your heart, which is regulated by the ADRB2 gene, which has more of an effect on your blood vessels.

Norepinephrine has more of an effect on your blood vessels, which is regulated by the ADRB1 gene, which has more of an effect on your heart.

So both the heart and the blood vessels are involved in both processes.

I'm not sure how exactly the difference occur in reality.

But this article says that norephinephrine has a blunted effect on endurance training.

So I suspect that those with an increased reaction to fear, experience better effects when they keep breathing deeply during their social engagements, not just when they start to feel anxious, but all the way through the situation from beginning to end, as that would be equivalent to endurance training.

This is probably why social anxiety is so problematic. Most people who use deep breathing to calm down during social situations, tend to breathe deeply only while they feel very anxious. As soon as they calm down, they stop, which allows the social anxiety to return, first without the person being aware, until it builds to an extent the person feels the anxiety.

This article suggests that if the person keeps breathing deeply, even AFTER the anxiety subsides, the effects continue, and that's what continues to keep the anxiety at bay.

This difference isn't noticeable in physical exercise, as norepinephrine is increased during physical exercise at 1.5 times that of public speaking, but is blunted during endurance training. So after several breaths during physical exercise, it ceases to have as much effect. So prolonged breathing during physical exercise doesn't have a significantly increased effects.

But this isn't true during public speaking, where social anxiety is present. So the key may be PROLONGED breathing during social anxiety, which means it takes practice to get used to doing it consistently for a long time, and thus is normally dropped when it would be of most benefit.

 

[scorpiomover]

I currently find it extremely hard to do physical activity because all the oxygen goes directly to the brain, not the body

If you are better at regulating epinephrine than norepinephrine, then your body is less responsive to physical exercise.

- I spend 12 hours a day doing mental activity not physical activity.

Tht would be psychological stress, which would again suggest you are more responsive to epinephrine, and it's epinephrine which is more responsive to endurance training, such as doing or thinking for 12 hours.

But when I must do physical activity I have increased stamina as long as it is not running or jogging.

This also makes sense, as norephinephrine is less responsive to endurance training, and so it would be epinephrine that is more responsive to endurance and stamina.

Running would put increased pressure, which is the opposite of endurance.

So you can probably jog or run for a very long time, as long as you start slowly to get your body into endurance mode.

normally I need to expand my lungs very little to keep up with the mental work. In school, I had to work long periods where I only did mental work. I take a deep breath about once every 5 minutes because I sometimes forget to sit up straight.

This indicates that you are very responsive to oxygen, i.e. breathing. This in turn means that by getting used to deep breathing all the time, your fear levels would reduce drastically and consistently. Since this would require stamina, which is your forte, this would be something that you would find easy to do, once you get used to it.

Fear also in me involves me avoiding everything painful. I have a low pain threshold so I avoid anything that causes it. Trauma is physical/neurological and so because of the emotions I have come to terms with certain limits. When I am alerted to danger I almost do have panic attacks but only if they have become unavoidable. Deep down inside I have extreme fear the oxygen keeps from arising which is what the article says is the result of not forgetting the trauma. My coping mechanism is to slow down and reflect. People see it as almost catatonia.

I suspect that's because you have naturally high stamina. So your body doesn't respond that well to swift changes. So in order for deep breathing to have a strong effect on your metabolism, you'd have to keep breathing deeply for a long time.

Your mechanism to slow down and reflect, reduces your fight-or-flight effect, which allows your natural stamina to come to the fore. So you might be breathing deeply for longer as a consequence. But you don't notice, because you're trying to remain calm, and not really noticing that you've been breathing deeply for 20 minutes or longer.

But you would know if this was happening, because if it was, after 30 minutes of reflection, when you walk somewhere, you are seriously outpacing everyone else because of the increased oxygen.

I saw a nurse practitioner today who told me I needed to see a neurologist. I believe that in me is some kind of basal ganglia function that causes OCD-like symptoms and nondetectable deep-level seizures. It feels painful to do nothing so that is why I do mental work all the time based on my interest. I avoid reading books or watching tv. - emotional burnout happens often when I don't sleep.

Could be.

But I am also starting to think that while you are thinking, you would benefit from also consciously breathing deeply for as much as 2 hours a day.

But it's your choice what to do. Remember that.

 

[Black Rose]

However, epinephrine has more of an effect on your heart, which is regulated by the ADRB2 gene, which has more of an effect on your blood vessels.

Norepinephrine has more of an effect on your blood vessels, which is regulated by the ADRB1 gene, which has more of an effect on your heart.

I once had stage one hypertension, but I talked to the doctor and I calmed down.

I calm down when talking to people. And I do continuously breathe.

It was this specific doctor who said I had OCD - and autism and the third thing.

I cannot feel my heartbeat, but my vessels feel contricted.

I suspect that's because you have naturally high stamina. So your body doesn't respond that well to swift changes. So in order for deep breathing to have a strong effect on your metabolism, you'd have to keep breathing deeply for a long time.

Talking to people helps me breathe.

it is also why I spend so much time writing things down to organize my thoughts.

I take Abilify (Antipsychotic) and streteria (ADHD) atorvastatin (statin) and oxcarbazepine (siezers).

Recently I bought some magnesium.

 

[Black Rose]

Working Memory is low

Multitasking is low


(COMT) Val/met polymorphism:

dopamine, norepinephrine, and epinephrine.
Is broken down 4 times faster than average.

TaqIA polymorphism:

Reduced D2 receptor availability in the striatum
Lower mean relative glucose metabolic rate in dopaminergic regions
less receptive to reward signals

The DRD3 Ser9Gly polymorphism:

increases dopamine affinity by 4–5 times.
increased calcium levels
increased GABA levels
nucleus accumbens less inhibited

 

[Black Rose]

Summary:

more norepinephrine leads to better calcium regulation.

calcium balance is maintained better

meaning calcium stays where it is supposed to be

The precise mechanism by which atomoxetine produces its therapeutic effects in Attention-Deficit/Hyperactivity Disorder (ADHD) is unknown, but is thought to be related to selective inhibition of the pre-synaptic norepinephrine transporter

Regardless of how and where it is released, norepinephrine acts on target cells by binding to and activating adrenergic receptors located on the cell surface.

Adrenergic receptors, also known as adrenoceptors, are a class of G protein-coupled receptors that bind to catecholamines like norepinephrine and epinephrine.

G protein-coupled receptors (GPCRs) primarily regulate hormonal regulation of adrenal function. GPCRs are present on almost all peripheral tissues and many neuronal populations within the central and sympathetic nervous system. They activate intracellular signaling cascades in response to the binding of the endogenous catecholamines adrenaline and noradrenaline

G proteins, also known as guanine nucleotide-binding proteins, are a family of proteins that act as molecular switches inside cells. They play a crucial role in calcium signaling by integrating extracellular signals and initiating downstream calcium responses. G proteins modulate intracellular Ca2+ mobilization, arachidonic acid release, and membrane potential. They can also inhibit voltage-gated calcium channels, regulating calcium entry into presynaptic endings.

GABA can induce norepinephrine exocytosis from hippocampal noradrenergic axon terminals through a dual mechanism that involves different voltage-sensitive calcium channels. Norepinephrine (NE) is a neuromodulator that regulates the activity of neuronal and non-neuronal cells. It can bind to three main receptors: alpha1 (alpha-1), alpha-2, and beta receptors. These receptors classify as G-protein coupled receptors with either inhibitory or excitatory effects and different binding affinities to norepinephrine. Norepinephrine evokes a biphasic calcium response in olfactory bulb astrocytes, consisting of an initial and transient calcium peak. The initial peak reflects internal calcium release, followed by a sustained plateau phase established by calcium influx via SOCE channels. NE enhances both Ca2+ and K+ fluxes, probably by a β-receptor-mediated mechanism, in the dentate gyrus.

 

[Black Rose]

Impulsivity Gene

rs1049353

The endocannabinoid system (ECS)

Positively to inwardly rectifying and A-type outward potassium channels.
Negatively to D-type outward potassium channels
Negatively to N-type and P/Q-type calcium channels.

Receptors for cannabinoid binding are less activated.
Less likely to seek pleasure because pain is not inhibited by the release of dopaminergic opioids.

 

[Black Rose]

TT Wider, larger head chr12 rs2066827 European

The largest effects are reported for low-frequency variants within TP53, with 0.5 cm wider heads in increaser-allele carriers versus non-carriers during mid-childhood, suggesting a previously unrecognized role of TP53 transcripts in human cranial development.

CDKN1B/GPR19 gene

GPR19 upregulates E-cadherin

E-cadherin is a transmembrane glycoprotein that helps calcium-dependent cell-cell adhesion in epithelial tissues. It also plays a role in maintaining cell differentiation and the normal architecture of epithelial cells.

Cadherins are a family of transmembrane proteins that mediate calcium-dependent cell-cell adhesion.

Calcium-dependent cell-cell adhesion is the attachment of one cell to another via adhesion molecules that require calcium for the interaction

Calcium is important for cell adhesion, as it helps cells attach to each other and to substrates. Calcium also regulates the interplay between the tight junction and epithelial adherens junction at the plasma membrane.

-

summary: more efficient cell-to-cell connections because of calcium bonds on the cell surface