an answer to the non-believer…

Earlier today I noticed the following comment from IDHC2 on my “careful she’s bipolar” post:

What a bunch of self-indulgent crap. My brother blames everything in being bipolar. You guys are all alike. It s a copout to avoid being responsible. You are really no different than the rest of us. What proof do you have that bipolar is a real disease? None.

To which I responded:

IDH2-

Well, it is good to see that you actually have something to say, other than just the idiotic insults featured on my other page. And; although I imagine you will never read it (since you have obviously made up your mind about bipolar disease), I am going to answer your question in a new post later today.

I am saddened that your brother is related to someone with so much anger and ignorance about his disease. On the off chance that you decide to read my answer to your question, try to do so with an open mind.

I want to berate you, IDHC2. I want to humiliate and shame you on behalf of everyone who lives with bipolar disease. But, more than being pointless, that would be a waste. Because you are not unique in your thoughts. An unfortunate amount of people question the validity of mental disease as a disease. And, since you somehow found your way in here, I can only assume that others like you will also. If I focused my energy and resources on belittling you, I would alienate them as well. And I hope, more than anything, that people who stumble upon my little piece of the world wide web leave a little more educated.

“What proof do you have that bipolar is a real disease?”

To make sure that we are playing on the same field, let’s define disease. I am comfortable going with Merriam-Webster

disease: a condition of the living animal or plant body or of one of its parts that impairs normal functioning and is typically manifested by distinguishing signs and symptoms

It’s a little vague, but I am going to tighten it up by showing examples of physiological differences between the bi-polar and non-bipolar brain. It’s easy to assume that everyone knows this already, but I am learning that many people do not. There are two main ‘neuro-circuits’ involved in mood regulation.

  • the limbic-thalamic-cortical circuit
  • the limbic-striatal-pallidal-cortical circuit
  • Bipolar patients have physical abnormalities in the areas of the brain associated with these circuits.

    From left: view of a nomal brain; patient with bipolar disorder has enlarged ventricles; bright white spots of hyperintensity associated with bipolar illness.

    Over 100 MRI studies have found that the ventricles are significantly enlarged in patients with bipolar disease. Additionally, the ventricles become larger as patients have more manic episodes. It is important to understand that the size of the brain (total cerebral volume) is the same for bipolar and non-bipolar patients, regardless of the number of episodes. Why is this important? Well if the total brain size is the same, but one part of the brain is bigger, than somethings gotta give. There has to be less brain tissue in some areas to make up for the enlarged ventricles.

    There is a basic agreement among the scientists who study this sort of thing that there is a significant loss in grey matter within the ventral striatum, an area of the brain that is responsible for controlling impulsive and gratification oriented behaviors. The pre-frontal cortex also suffers a loss. This part of the brain regulates emotion. It also controls the way that we understand motivation and process rewards. The brain stem is also affected, specifically an area called the raphe nucleus which is responsible for managing neurotransmitters (I am going to assume that you know what those are). Bipolar patients have a large loss of seratonin receptors in this area, which is a contributing factor in the deterioration of neurons (more about this later). An important symptom in bipolar disorder is the inability of patients to correctly identify the intensity of emotions. We can, generally, tell what a person is feeling. However, we do not consistently recognize the intensity of the emotion. This is caused by physical abnormalities in the amygdala. The amygdala is an emotional center, it helps you to understand all of the little ways that others show emotion. When you see someone frown, it is the amygdala (mostly) which tells you that this person is sad. As the stimulus becomes more emotional, neurons fire more frequently. Thus you feel stronger about watching someone being brutally attacked than you do about someone crying over a bad hair day. The attack is more emotional, it illicits more ‘neuron-firings’, if you will. Habituation is what happens when you see the same emotional situation over and over again. You become desensitized to it, your neurons do not fire as much as they did the first time. Physical differences in the amygdala cause a slower habituation to stimuli in bipolar patients. We respond to emotional situations more strongly and for longer periods of time than the non-bipolar brain. Finally, there is a loss in density and number of ‘connections’ in the hippocampus, which is not only a memory center (this explains some of the memory loss that bipolar patients experience); but also the main area for recognizing dangerous situations and processing rewards.

    Now, the last brain scan above shows increased white matter hyperintensities. White matter is involved in transmitting information from one part of the brain to the other. We will talk more about this later.


    This PET scan shows the ‘energy-usage’ of a bipolar patient’s brain when depressed (top), manic (middle), and back to depressed (bottom).

    A common belief is that an increase (manic) or decrease (depressed) in neurotransmitters is the main cause of bipolar episodes. But the situation is not nearly that simplistic. The cells themselves do not function properly under the influence of neurotransmitters. It is important to grasp this distinction when considering the effectiveness of medication.

    Noradrenaline, seratonin, and dopamine are part of a group of neurotransmitters caused monoamines. Manic patients show increased concentrations of noradrenaline and noradrenaline metabolites. The density and uniformity of alpha2-receptors have been shown to be increased in the hypothalamus, amygdala, hippocampus and cerebellum of depressed suicide victims. This effectively leads to a decrease in noradrenaline.

    Seratonin receptors also play a significant role in bipolar disease. Many studies have shown an increase in the density of seratonin 2 receptors in the platelets and brain tissue of depressed patients. Again, this is an increase in the receptors, not the chemical. New evidence supports the theory that the increase in seratonin 2 receptor sites is a response to decreased production of seratonin in the raphe nucleus (discussed above).

    I discussed a number of physical abnormalities in the regions of the brain responsible for reward and motivation earlier. Dopamine is a vital chemical component of these processes. Studies have consistently shown a reduction in HVA, a major dopamine metabolite, in bipolar patients. Researchers are currently investigating the hypothesis that dopamine plays a role in severe manic episodes. Which is interesting given that most researchers feel noradrenaline plays a vital role in hypomania (which are the ‘lesser-manic’ episodes).

    To date, studies have failed to identify a direct connection between anti-depressants at the level of monoamines and receptor sites. Which begs the question, if the anti-depressants do not directly effect the levels of the chemicals involved, what do they effect? And the answer to this question is crucial in understanding how the bipolar brain is structured.

    A theory that is finding support in new research is that anti-depressants effect the pathway that monoamines follow after they are released and accepted by receptor sites in various areas of the brain. Neurotransmitters are created and distributed in one part of the brain. They travel through pathways and ultimately end up at a receptor site in another area of the brain. Now, once the neurotransmitter ‘clicks-in’ to the receptor (picture putting a key in a lock), the cell releases ‘messengers’ that go to the areas of the body that are supposed to do something and tell them what to do. New research implicates these messengers in bipolar disease. Three agents that are under scrutiny in this system are cyclic AMP (cAMP), phosphoinositol, and protein kinases (PKA).

    Cytoplasm is a jelly-like fluid that “fills” most cells. Scientists have sucked that jelly out, studied it and found that concentrations of the PKA regulatory subunits in the cytoplasm are significantly lower in cells of the frontal, temporal, occipital and parietal cortex, cerebellum and thalamus of bipolar disorder patients. Concentrations of calcium, another important chemical in the ‘messenger’ process, are increased in bipolar patients.

    cAMP stimulates the release of a protein called Rap1, interestingly there is an increase of this protein in the platelets of bipolar 1 patients. Remember the discussion on decreased grey matter in some areas of the bipolar brain, keep that in mind. Anti-depressants have been shown to cause sustained activation of the cAMP system. So, the cAMP releases a protein which, in turn, causes an increased expression of factors in neurons of the hippocampus and cerebral cortex. These factors are vital to the survival and function of particular neurons. We have already discussed the imaging studies which show a decreased amount of grey matter in these areas. So, the theory is that anti-depressents help to save failing neurons in the bipolar brain through the ‘messenger system’.

    There are other signaling systems which seem to be affected. I will not go over them here; because the principles are the same. Just different chemicals.

    As you can see, there is ample evidence to support the conclusion that bipolar disease is, in fact, a disease. There is so much more I could write. And there is a considerable amount of data that I am not aware of. This information is widely disseminated and available to anyone online. Just google bipolar and read. Your question shows a profound ignorance of a very serious and potentially lethal disease that your brother suffers from. You should be ashamed of yourself.

    I have added a page with more neuroimaging scans.

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    ~ by aikaterine on July 17, 2007.

    17 Responses to “an answer to the non-believer…”

    1. “Cytoplasm is a jelly-like fluid that “fills” most cells. Scientists have sucked that jelly out…”

      Snort ;~)

    2. I know one of my biologist friends read this yesterday and thought that was hilarious, but how do you explain testing cytoplasm to a broad audience?

    3. Your troll sounds a little like someone who hung around my site back in My Beginning. Trolls can be fun, but over time not so much… as long as you’re having fun and using your brain for good, have a good time playing with yours, but keep track of their IP address.

      I had no idea you were this deep into the science of MD, if you’re interested there’s a Brit worth reading called Experimental Chimp, I think you two would hit it off… http://experimentalchimp.wordpress.com/

    4. That’s funny, experimental chimp just posted on another of my topics. Is it fate?

    5. We’re like a big crazy club…

    6. It will be interesting to see just how long a group of blogging mental cases manages to keep it together.

    7. Oh you know…the casualty rate is pretty high, but we keep recruiting new voices to add some interest ;)
      FTS is our scouting party…

    8. Yes, it’s a big nutcase party…I’ve got all of you guys (chimp included) on my blogroll. I’m not bad at all of the neuro stuff but chimpy (as I affectionately call him) kicks my butt totally. We always have good talks and he always picks up on my posts and contributes when I write some bumbling pseudo-scientific jazz.

    9. I do not particularly enjoy writing the medical stuff. I just thought that it was the appropriate response to the comment. Hopefully feartheseeds and experimentalchimp will keep everyone up-to-date. I just like to read the research, file it away and move on.

    10. this post is amazing. thank you so much for writing it. im always having to explain myself and no one understands me…my friends and family also think its just an excuse. so thank u for this!

    11. you know i have bipolar and as much as i try to pretend i don’t have it and act like everyone else, there’s no denying that there is something characteristically different in a way that meds barely begin to resolve. for that, fack anyone who doesn’t think it is a disease. you’ll know what it’s like when you have it and get screwed over from it. i feel that will be punishment enough. it’s ashame when one looks just normal enough to not be believed yet is sick enough inside a sparkling face to watch herself slowly lose things one by one that she had no idea she was losing to begin with…take responsibility for it we must because the results come for us even when unwanted. i hope you have a child with its onset in her teen years, so you can experience the wild wonder of bipolar yourself.

    12. heyy heaps random, but does this site have a chat room?

    13. Hiya,
      I stumbled on this blog when trying to find biological proof of bipolar disorder for someone who doesn’t believe in mental illness. I was wondering if you have the brain scan pictures anywhere else or if you could email them to me? They aren’t showing up on my browser and I get a 404 error on another browser.
      This is a really good bit of writing here, I very much appreciate how you’ve put all the technicals in laymans terms. I’ve been living with this disease for over half my life and never had it explained to me so well. Thanks!!

    14. The flaw with the PET Scans is that they are pictures of a person already ‘diagnosed’ with bipolar disorder. Ergo, there is no proof that what is seen on the PET Scan is a cause of the behaviors doctors associate bipolar with, or if they are an effect of the behaviors doctors associate bipolar with. Also, the fact that a PET Scan looks different with a person who performs certain behaviors than it does in a person who doesn’t commit those behaviors proves nothing. This is because all behaviors/moods/thought have a PET Scan correlate, so it is no big deal that a person who is ‘diagnosed’ with bipolar disorder has a PET Scan that shows differences. As PET Scan changes are universal, no one PET Scan can prove anything about the existence of bipolar dx or any other ‘mental illness’ for that matter.

    15. […] some science for the skeptical or uninformed. […]

    16. […] Answer To The Non-Believer’; July 17, 2007 “A common belief is that an increase (manic) or decrease (depressed) […]

    17. […] Answer To The Non-Believer’; July 17, 2007 “A common belief is that an increase (manic) or decrease (depressed) […]

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