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Stress and Aggression P3

What happens is your feel good neurotransmitters, serotonin and dopamine, we shift more to a fight or flight response where we’re making adrenaline and norepinephrine, and the calcium in our bones to keep us strong and the magnesium in our muscles to make our muscles more flexible, what happens is we get a shift in this balance.  So, calcium can now be in your muscles.  That’s why your muscles feel more rigid because it’s helping to protect you from that wild animal, but it’s causing problems in your system.  We see a shift in T cell function from TH1 responses to TH2 responses.  So, we’re having more of an inflammatory cascade, and where we would normally use the DNA and RNA that we have for new cell synthesis and wound healing, this is going to be reduced under those situations.

We’re draining a lot of our resources from our methylation pathway over here instead of having them for DNA and RNA and building blocks. If you recall, if we need new DNA and RNA for building blocks, we also need this process to make GTP to make our DH4.  So, we sitting over here, all the types of things we talked about earlier today that are going to have an impact on the methylation cycle are going on in your body or your children’s body.

Just looking at this again, here is the cycle we’re used to looking at.  What we’re talking about is shifting the focus of the methyl groups from this pathway to make adrenaline, to deal with norepinephrine, and shifting over to this portion rather than keeping the methyl groups that we need in our methylation cycle for DNA and RNA to make their creatinine to methylate the phospholipids in the membrane for membrane fluidity.

We also use that COMT enzyme in order to break down epinephrine.  Again, we’re shifting the focus when we’re under stress to other intermediate than balancing our dopamine levels.  Just going backwards a little, we talked about vitamin C earlier in the role that it plays in terms of BH4 levels. It also plays a role in trying to help to balance this system.  So, certain drug companies are looking at covalently linking basically vitamin C to drugs to help for transport across certain barriers, and one of the reason I like to use powdered vitamin C is to take advantage of this without having to have covalent linkage.

Increased norepinephrine leads to increased cortisol and increased conversion of norepinephrine to epinephrine. Again, we’re using our methyl groups.  SAMe is our methyl donor.  If our SAMe is acting over here, we don’t have SAMe for all those other lovely things I talked about.  SAMe needs to do other parts of the pathway.  Earlier today, we spoke about the role of glucose, how it plays a role with CBS and insulin, and, other than in Cushing’s disease, what happens is that this is all tied together.

So, the BHMT enzyme we were talking about for the shortcut leads to an increase in norepinephrine.  Stress increases the shortcut, increases norepinephrine.  So, we get that imbalance in norepinephrine and dopamine levels.  Some of the glucocorticoids can play a role, and cortisol can play a balance in this.  That, again, is going to be affected by insulin and glucose levels which also play a role in CBS.  Again, all of these same players that we keep talking about keep coming up over and over again.  Looking at this globally, you want to be supporting to address CBS issues.  You want to be supporting the pancreas, looking at your VDR issues.  You want to have some activity through that shortcut, but we want to make sure we are also supporting the long route along the pathway.  We want to do things to address stress and make sure we keep these mediators in balance.

Again, methyls play a role. Environmental, genetic, and infectious issues all come together every step of the way.  So, if we have lead inhibiting this enzyme, we’re stuck at norepinephrine rather than epinephrine, and that can cause issues with attention or hyperactivity.

Earlier today we saw a version of this slide, talking about what happens with CBS and SUOX mutations or low molybdenum levels.  We’re going in depth with higher levels of sulfides which play a role here, high copper levels playing a role in this symptomatic pathway inhibited by lead.  The norepinephrine receptor itself is inhibited by this higher sulfur, and we need to have sufficient methylation pathway function to generate the SAMe that we need for this conversion assuming it’s not inhibited by the lead.

So, increase CBS activity can lead to a stress response due to the excess sulfur and its effect on cortisol levels.  Then, the norepinephrine receptor is inhibited by high sulfur.  So, between these two, we can end up with a situation where we have very high circulating levels of norepinephrine.  Looking at the fact that acute stress leads to norepinephrine increase, this in turn, leads to an increase in certain enzymes in the body but not increase in dopamine.  So, we end up with this imbalance that you see in neurotransmitter tests with high norepinephrine relative to dopamine.

Again, the pathway we’ve been looking at but thinking about it a little differently, looking at the role of BH4 in this pathway so that the A1298C and CBS mutations will play a role here.  This enzyme is also shared by the tryptophan pathway so if we have chronic bacterial infection, we’re diverting this enzyme elsewhere for breakdown of tryptophan.

The role of heavy metals in this portion of the pathway and excess sulfur groups that we just talked about and the fact that we need methylation and SAMe for this portion of the pathway so that when you’re triggering this response, as a protective response, your body will trigger the fight or flight cortisol response over anything for survival.  You’re playing a role in impacting everything else we’ve talked about here as we make this shift.

Also, sulfur-containing amino acids will increase norepinephrine release, and that runs through glutamate receptors and excitotoxin mechanism.  So, again, dealing with excess sulfur, dealing with CBS upregulations, and keeping the glutamate and GABA in balance.

Hydrogen sulfide we were talking about earlier today.  We talked about the effect that has on the brain, that it causes brain fog, and the role that stress proteins play related to hydrogen sulfide exposure.  Also, the impact of thyroid hormones, and we’ll talk a little bit about that tomorrow in terms of bacterial infection, the tie in between the stress response and the effect on the thyroid.  Again, we’ve mentioned over and over again today, nucleotide requirements, why we need RNA, why we need to add nucleotides.  When you have cortisol and the stress response, what happens is we end up with inhibition of RNA synthesis, and so, on top of any methylation cyclomutations, we have a difficulty of making our building blocks.  We have a decrease in the synthesis via the second pathway.

Chronic stress promotes tumor growth.  So, keeping your body in better balance, taking care of yourself, pulling down that stress response will help to protect you against some types of diseases that none of us would like to have.  Also if we think about I just finished saying that the stress response will pull from your methylation, and we started the day talking about the importance of the methylation cycle and how that plays a role in cancer, if you’re diverting your methylation cycle to deal with stress, it’s not surprising that you’re going to increase cancer or cancer aggressiveness because it’s as if you’ve depleted your methylation cycle with mutations, and that tie in to mutations in that pathway in cancer.

The level of invasion of ovarian cancer cells.  So, how aggressive that cancer is is directly related to the stress hormone in your body.  Again, chronic stress promotes tumor growth and angiogenesis in mouse models of ovarian cancer, and more on the same topic.  So, stress has an effect on the methylation cycle.  Methylation cycle mutations will predispose us to cancer.  Stress will create a situation where the cancer could be more aggressive, and the stress directly impacts the methylation cycle, drawing from it to create a greater likelihood of issues with cancer.  So, again, we need to break this cycle and look at what we can do to stop the constant stress and aggression on the pathways.

Stress also triggers high levels of VEGF, and VEGF is a key mediator in problems with tumor vascularization and aggressiveness of cancer.  So, look at the type of change one might see.  Two weeks after tumor inoculation, stressed mice had two to threefold more tumor nodules with similar increases in tumor weight gain compared with unstressed controls.

Getting back to what we were talking about earlier with the ACE deletion, the angiotensin I and angiotensin II and those higher levels of aldosterone, in order to create these higher levels of aldosterone that we’re seeing, we’re also using some of the same enzymes.  So, again, we need SAMe for this conversion.  So, we’re drawing methyl transferases, and we’re drawing from our methylation cycle when we’re dealing with stress.

So, the ACE deletion causes this increase in aldosterone which, of course, is competing with cholesterol for calming down the stress response, and ultimately, we end up with lower levels of dopamine.  So, we want to keep this in balance. Using the anxiety support formula helps.  Looking at a balance of topical progesterone cream can help to support another pathway, too, but again, moderation.  Remember that the ACE deletion is going to bring down our bradykinin faster.  Breaking bradykinin is going to help us with the stress aggression response.

Again, everything in moderation.  More isn’t always better. Small amounts of a variety of herbs, supplements, RNAs to try to keep the system in better balance so that we’re toning down this effect without having a negative impact on the breakdown of bradykinin.

Now, aldosterone can cause essential mineral loss during detoxification stress leads to increased aldosterone.  ACE deletions lead to increase aldosterone.  When you see elevated excretion of potassium, that’s a sign this is going on, and then, the higher aldosterone triggers epinephrine which is using an enzyme that’s drawing our methylation groups from our methylation cycle.

We’ve talked about this before.  Signs of aldosterone excess and aldosterone deficiency, and as I just mentioned, hormones will play a role also.  Progesterone will compete with aldosterone to pull it down.  Estrogen actually increases aldosterone levels. Aldosterone plays a role in terms of potassium excretion so if we’re seeing high levels of potassium dumping we want to think about if the aldosterone levels are too high.

Licorice, which I alluded to earlier, inhibits and enzyme in this pathway, and this can lead to inactive of cortisol and aldosterone excess. Even in the absence of ACE deletion, if you’re eating a boatload of licorice, it’s going to have a similar effect on the system.

So, overall consequences of the stress response:  Weight gain in the belly, muscle aches, reduced calcium in bones, reduced responses because of the TH1 to TH2 shift, infection, memory issues, reduced wound healing. We’re depleting or hijacking the methyl groups from our methyl pathway, and that, of course, has an impact on cancer.  Increased levels of aldosterone and also cortisol levels.  That’s not a happy picture.

Stress, calcium, and muscle. Just a reference for the fact that stress depletes your calcium from your muscles, and it is replaced with calcium.  Looking at how the bones are compromised and the calcium depletion of calcium from the bone.  Stress also stimulates breakdown of serotonin, and we’ve talked about the swinging and fluxes of serotonin levels that we don’t want to see.  We want nice, even serotonin.  So, stress is going to work against us when it comes to serotonin levels as well as allergic reactions.

Stress and magnesium levels again, and that MAP38 kinase pathway that’s involved with protein kinase C.  Stress is able to trigger that same pathway related to aggression and the protein kinase C pathway.  Inflammation in the brain as a result of this. I’ll go through some of these fairly quickly because I talked at this at length in February, and I’d like to leave some time for questions today.


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