Stress and inflammation
Inflammation: The Key to the Link between Stress and Disease
Human beings are wired to respond to physical threat in some predetermined ways. This is our body’s way of preserving our lives. The problem is that our normal stress response is meant to be acute, not chronic. But the types of stressors modern humans encounter are often chronic, and so our stress response is out of sync with the realities of our world. When stressors are chronic, our stress response malfunctions and actually increases our risk of disease.
There are three main components of the stress response. When you understand these, you will understand the basic concepts underlying mind-body medicine.
The first is the catecholamine, or fight-or-flight response, and it kicks in as soon as we are threatened.
This is also what is more commonly know as your adrenaline response.
The second is the response of the HPA axis. HPA stands for hypothalamic-pituitary adrenal axis. When faced with a threat, the HPA axis responds with a cascade of chemicals, the final one being the stress hormone cortisol.
The third component is the immune system’s response. When faced with danger, the immune system increases inflammation by releasing molecules known as proinflammatory cytokines. Cytokines are basically messenger molecules of the immune system. Inflammation has a very important role in protecting your health. These molecules protect you against infection and heal wounds. But when levels of these cytokines continue to be high, they can actually damage your body.
A key finding in mind-body research is that psychological stress can trigger the inflammatory response.
You’ll notice that I’ve drawn this three-component response with arrows connecting each component. In a normally functioning system, these three components serve as checks and balances to each other. When one part gets too high, the others activate to lower it. The problem is that when this system is overloaded, as it is in stress and depression, the components no longer serve as checks and balances. Instead, they start actually enhancing the negative effects.
Depression and Inflammation: The Surprising Link
Depression is risk factor for depression. Researchers have known that for many years but couldn't really explain why—until now.
In the past 10 years, researchers have firmly established that a lot of common diseases--such as diabetes, cancer, Alzheimer’s, and yes, even heart disease--are due to inflammation. For example, physicians have noted that elevated levels of an inflammatory marked called C-reactive protein is an early harbinger of heart disease.
But here’s where the plot really thickens. Depression is also caused by inflammation, and specifically by elevated levels of molecules called proinflammatory cytokines. In fact, by specifically treating people with cytokines, as they do for conditions such as MS, doctors have actually caused depression. The more cytokines patients received, the more depressed they got. When the patients started to taper off of the cytokines, the depression got better too.
Depressed people have significantly higher levels of the cytokines in their plasma than non-depressed people. And this is where the disease-depression link comes from. High levels of proinflammatory cytokines damage blood vessels, and elevate other factors in the blood that increases the risk of clots.
And in another interesting twist, we now know that most of the effective treatments for depression have one thing in common: they are also anti-inflammatory. In fact, that knowledge has fueled some very interesting discoveries. For example, antidepressants lower inflammation levels in cardiac patients. And they’ve been added to steroids for treating asthma, leading to the use of fewer steroids in these patients.
This discovery has also led to some novel ways of treating depression. For example, anti-inflammatory medications, such as ibuprofen, which is not an antidepressant, have been added to antidepressants to make them more effective. Adding Omega-3 fatty acids to a treatment regimen helps with depression for the same reason.
Human beings are wired to respond to physical threat in some predetermined ways. This is our body’s way of preserving our lives. The problem is that our normal stress response is meant to be acute, not chronic. But the types of stressors modern humans encounter are often chronic, and so our stress response is out of sync with the realities of our world. When stressors are chronic, our stress response malfunctions and actually increases our risk of disease.
There are three main components of the stress response. When you understand these, you will understand the basic concepts underlying mind-body medicine.
The first is the catecholamine, or fight-or-flight response, and it kicks in as soon as we are threatened.
This is also what is more commonly know as your adrenaline response.
The second is the response of the HPA axis. HPA stands for hypothalamic-pituitary adrenal axis. When faced with a threat, the HPA axis responds with a cascade of chemicals, the final one being the stress hormone cortisol.
The third component is the immune system’s response. When faced with danger, the immune system increases inflammation by releasing molecules known as proinflammatory cytokines. Cytokines are basically messenger molecules of the immune system. Inflammation has a very important role in protecting your health. These molecules protect you against infection and heal wounds. But when levels of these cytokines continue to be high, they can actually damage your body.
A key finding in mind-body research is that psychological stress can trigger the inflammatory response.
You’ll notice that I’ve drawn this three-component response with arrows connecting each component. In a normally functioning system, these three components serve as checks and balances to each other. When one part gets too high, the others activate to lower it. The problem is that when this system is overloaded, as it is in stress and depression, the components no longer serve as checks and balances. Instead, they start actually enhancing the negative effects.
Depression and Inflammation: The Surprising Link
Depression is risk factor for depression. Researchers have known that for many years but couldn't really explain why—until now.
In the past 10 years, researchers have firmly established that a lot of common diseases--such as diabetes, cancer, Alzheimer’s, and yes, even heart disease--are due to inflammation. For example, physicians have noted that elevated levels of an inflammatory marked called C-reactive protein is an early harbinger of heart disease.
But here’s where the plot really thickens. Depression is also caused by inflammation, and specifically by elevated levels of molecules called proinflammatory cytokines. In fact, by specifically treating people with cytokines, as they do for conditions such as MS, doctors have actually caused depression. The more cytokines patients received, the more depressed they got. When the patients started to taper off of the cytokines, the depression got better too.
Depressed people have significantly higher levels of the cytokines in their plasma than non-depressed people. And this is where the disease-depression link comes from. High levels of proinflammatory cytokines damage blood vessels, and elevate other factors in the blood that increases the risk of clots.
And in another interesting twist, we now know that most of the effective treatments for depression have one thing in common: they are also anti-inflammatory. In fact, that knowledge has fueled some very interesting discoveries. For example, antidepressants lower inflammation levels in cardiac patients. And they’ve been added to steroids for treating asthma, leading to the use of fewer steroids in these patients.
This discovery has also led to some novel ways of treating depression. For example, anti-inflammatory medications, such as ibuprofen, which is not an antidepressant, have been added to antidepressants to make them more effective. Adding Omega-3 fatty acids to a treatment regimen helps with depression for the same reason.