Diokine
Member
- Joined
- Mar 2, 2016
- Messages
- 624
Until very recently, the only kinin I'd ever even heard of was bradykinin. Forget about trying to define what it even did in the body, something with blood pressure? I found some information referencing kinins and how they interact with histamine, serotonin and estrogen and my interest was immediate. I was very surprised to find almost no information from a Peat perspective, although it is a very new area of research and the system is very poorly understood.
To sum it up, the kinin-kallikrein system is intimately involved in the production and influence of nitric oxide and histamine, and is potently modified by serotonin and estrogen. Looking at the cell, or a system of cells in an organism, we can qualify a measure of coherence in the production of energy. This shouldn't be news to any of us here, Dr. Peat talks about the ideas of Gilbert Ling, Gerard Pollack, Mae Won Ho, etc., when discussing the implications of this energy production. It was always very apparent that there is some sort of signaling system in place to allow the organism to deal with reduced energy production and subsequent "decoherence."
If we look at the form of a cell being comprised of structural proteins and lipids modified by steroids and held together with water, then we can ask what happens when this form is disturbed, by low blood sugar for instance. Lack of proper glucose oxidation will change the reductive potential of the cell and will introduce a measure of decoherence. This can lead to the release of histamine and nitric oxide, which can activate platelets that release serotonin. This is a classic example of a local stress response, leading to increased vascular permeability and further decreased glucose oxidation. These actions are all mediated in part by the kinin system.
Kinins are directly involved in the production and maintenance of prostaglandins and eicosanoids. They are modified by serotonin and estrogen. I remember reading a quote by Dr. Peat talking about how aspirin works on a very fundamental level, since it opposes both estrogen and serotonin. A large part of that mechanism is due to interaction with the kinin system. Anaphylaxis is mediated largely by kinins.
There is a lot more I'd like to discuss, but for now I found it convenient to just introduce the concepts. I was curious if anyone else had done any research on kinins?
For some more meat to chew on, plug these search terms into google;
kinin serotonin
kinin estrogen
kinin histamine
kinin nitric oxide
kinin sepsis
kinin steroid
To sum it up, the kinin-kallikrein system is intimately involved in the production and influence of nitric oxide and histamine, and is potently modified by serotonin and estrogen. Looking at the cell, or a system of cells in an organism, we can qualify a measure of coherence in the production of energy. This shouldn't be news to any of us here, Dr. Peat talks about the ideas of Gilbert Ling, Gerard Pollack, Mae Won Ho, etc., when discussing the implications of this energy production. It was always very apparent that there is some sort of signaling system in place to allow the organism to deal with reduced energy production and subsequent "decoherence."
If we look at the form of a cell being comprised of structural proteins and lipids modified by steroids and held together with water, then we can ask what happens when this form is disturbed, by low blood sugar for instance. Lack of proper glucose oxidation will change the reductive potential of the cell and will introduce a measure of decoherence. This can lead to the release of histamine and nitric oxide, which can activate platelets that release serotonin. This is a classic example of a local stress response, leading to increased vascular permeability and further decreased glucose oxidation. These actions are all mediated in part by the kinin system.
Kinins are directly involved in the production and maintenance of prostaglandins and eicosanoids. They are modified by serotonin and estrogen. I remember reading a quote by Dr. Peat talking about how aspirin works on a very fundamental level, since it opposes both estrogen and serotonin. A large part of that mechanism is due to interaction with the kinin system. Anaphylaxis is mediated largely by kinins.
There is a lot more I'd like to discuss, but for now I found it convenient to just introduce the concepts. I was curious if anyone else had done any research on kinins?
For some more meat to chew on, plug these search terms into google;
kinin serotonin
kinin estrogen
kinin histamine
kinin nitric oxide
kinin sepsis
kinin steroid
