Yes, the solution can be worse than the problem

Stress exposure, and post-traumatic stress disorder, are horrible problems. I've seen them wreak havoc on peace of mind, careers, and relationships. I think sometimes, being on the outside looking at a friend, loved one, or patient going through something we'll never completely understand because we simply did not live through it, creates anxiety because we have no productive outlet for the compassion and healing we want to provide.

As much as the object of our concern may be struggling, and as hard as we may want to be the source of relief for their pain, we need to always be careful that the help we provide is not being administered on behalf of our own pain, and not the person who is truly suffering.

For example, consider this recent study, that looked at the consequences of administering alprazolam (Xanax), a benzodiazepene anxiolytic, to a stress-exposed individual.

Animals exposed to stress were then given alprazolam on two different schedules; one group was medicated for 3 days starting 1 hour after the stress, while the other group received the medication for 3 days starting a week later. Each group was tested for symptoms of PTSD 30 days after the initial trauma.

Those animals who were immediately medicated experienced immediate relief, with now observable problems at day 30. Sounds good, except that when the rats were exposed to the same trauma a second time, they had a greater "freezing response" (something that traumatized animals and people do in stressful situations).

Early exposure also disrupted normal stress hormone function both during and outside of the second stress exposure.

So while we might feel better giving someone medicine to help them feel better, we may actually be the only ones who feel better. In the long run, the person may suffer more and longer than if we'd let them process the trauma in the way the body is programmed to naturally do, providing a safe, supportive place to heal and only introducing chemical intervention if it is deemed absolutely necessary.

Matar MA, Zohar J, Kaplan Z, Cohen H. Alprazolam treatment immediately after stress exposure interferes with the normal HPA-stress response and increases vulnerability to subsequent stress in an animal model of PTSD. Eur Neuropsychopharmacol. 2009 Jan 22. [Epub ahead of print]

If you fix the real problem...you just might fix the problem

I just love the conclusions scientists come to when they're encouraged to promote the concept that for every problem...there's a medication.

Here we have a research group who took a group of rats and exposed them to chronic, unpredictable stress. The rats started developing neuron profiles consistent with cell death. So did the researchers recommend that in situations where it appears that chronic, unpredictable stress may be causing functional issues and medical risk, to implement support that reduces that stress? Of course not, silly reader, why would they do that? Support doesn't fund research or salaries. Drug companies do.

And that is why desipramine (Norpramin) was researched as the answer to this problematic observation. Never mind that this medication has been associated with increased insulin and prolactin levels in some people, a new use for this medication which increases the bottom line has been reported...let's give a big whoo hoo for stockholders!

Way back when I worked for someone else who had no boundaries when it came to employees' expectations, I was expected to bring my own laptop computer to work and use it most of my workday to enter data. After awhile, since laptops really aren't ergonomically superior, I developed carpal tunnel in both wrists. I had been pitching the pretty reasonable concept that since every other manager at my level in this company had both a desktop computer and an administrative assistant that I was not afforded, that I should have them too. So when I developed a medical issue that appeared to be directly related to my not being heard with regard to this issue, I viewed the doctor visit as an opportunity to finally get the note I needed mandating a repetetive motion activity restriction.

Unfortunately, the physician I visited was employed by the same man. And he decided what I really needed was a medication to dampen the pain. Isn't pain supposed to be telling you something? That you need to stop doing what's making you hurt?

Aren't dying neurons telling you something? That maybe something is killing them?

This mentality, that we can ignore the source of the problem and put a chemical bandaid on it so we don't have to change unhealthy situations, sure makes a lot of money for some people.

Did you ever consider that such money can only be made if you agree to hand it over? Medications can't hurt you if you decide not to take them. I am not advocating throwing all of your prescriptions away, at all. I'm just encouraging you to know exactly WHY you're being given a prescription and to consider proven non-pharmaceutical options whenever possible.

I ended up walking out on this company. From what I hear, it took several rounds of burning out successors for them to realize the problem was not the work ethic of the employee in the position. It was the expectations of the position created by the person who didn't understand the cost savings involved when you spend a little more on healthy work environments that help to retain hard working people. Me and my now-healthy wrists have never looked back.

Bachis A, Cruz MI, Nosheny RL, Mocchetti I. Chronic unpredictable stress promotes neuronal apoptosis in the cerebral cortex. Neurosci Lett. 2008 Sep 12;442(2):104-8.

McIntyre RS, Soczynska JK, Konarski JZ, Kennedy SH. The effect of antidepressants on glucose homeostasis and insulin sensitivity: synthesis and mechanisms. Expert Opin Drug Saf 2006 Jan;5(1)157-68.

Guzek JW, Olczak S, Lewandowska A. The hypothalamic and neurohypophyseal vasopressor and oxytocic content as influenced by alpha-adrenergic blockade in stressed rats. Acta Physiol Pol 1985 May-Jun;36(3):193-200.

I'll take a smoothie and a siesta over Ambien anytime

If you've ever dieted, and you have trouble sleeping...there may be a reason. Keep in mind, this study was done on rainbow trout, but there is still a message in it for humans. Three groups of trout were studied with regard to their melatonin (sleep hormone/antioxidant) levels and cortisol (stress hormone) levels. The three groups were defined as fed fish, fish that were fasted for 7 days, and fish that were fasted for 7 days then refed for 5 days.

Melatonin levels were disrupted in fasted fish. If you were human, this would likely mean if you were on a strict fasting/dieting protocol, you were probably having trouble sleeping as well.

Interestingly, nighttime serotonin levels were higher in these fasted fish. Melatonin is made from serotonin, so I would presume that what the body tries to do when you're not eating well is to keep you alert and thinking about getting some food. It does that by hanging on to serotonin and preventing its conversion into melatonin. That's a survival mechanism.

So if you're dieting and you're awake at night with cravings? That's a normal response. Don't obsess about what's wrong with you, don't surf the Internet looking for what to do about your cravings. In this kind of situation, you're thinking about food because you need it. Get some.

As far as cortisol, dieting reduced levels and they stayed low after refeeding. You could argue that this is a benefit of dieting...except for the fact that if you're cutting yourself short on melatonin, you're aging yourself more quickly than you should. There are plenyy of ways to reduce melatonin levels without dieting that don't cut your life short on the back end.

By the way, since I write so much about sleep I thought I should mention...I love naps. The long afternoon kind where my cats curl up with me, and I wake up with a little bit of drool on my pillow. I don't feel guilty at all. I completely buy into the idea of "beauty sleep"--sooooo much cheaper than all those anti-aging potions on the infomercials!

Ceinos RM, Polakof S, Illamola AR, Soengas JL, Míguez JM. Food deprivation and refeeding effects on pineal indoles metabolism and melatonin synthesis in the rainbow trout Oncorhynchus mykiss. Gen Comp Endocrinol. 2008 Apr;156(2):410-7. Epub 2008 Jan 8.

Now if I could just remember where I found this article...

If I were to be able to tally the time I've spent over a lifetime looking for lost things...especially my keys...there would probably be enough time there to pursue my Ph. D in neuroscience. And I'd likely find myself in a program conducting studies like this one, which looked at how stress affects the memory center (and why mine doesn't seem to ever register "last key location" in any functional part of my neurons).

Most researchers in the area of depression agree that a characteristic biological marker of depression is an elevated level of cortisol, a stress hormone. The researchers in this study decided to see just what cortisol does to the hippocampus, the brain's memory center, both short- and long-term.

Chronic exposure to cortisol decreased the ability of the hippocampus to regenerate neurons, and the volume of existing neurons decreased. These changes could be prevented with the administration of two different antidepressants, imipramine (Tofranil), and fluoxetine (Prozac).

Short-term exposure to stress brought out "depressed" behaviors in the rats. Long-term exposure seemed to create more of an anxious presentation.

The researchers concluded that the physically damaging effects of stress could be prevented with antidepressants.

I conclude that the next time I lose my keys, if I can remember to do so, I'm going to use that as an indicator that I may be trying to do too many things in too short a time. And that I need to do something to reduce my stress level. I really don't think I need to be taking an antidepressant to prevent memory loss!

Murray F, Smith DW, Hutson PH. Chronic low dose corticosterone exposure decreased hippocampal cell proliferation, volume and induced anxiety and depression like behaviours in mice. Eur J Pharmacol. 2008 Mar 31;583(1):115-27.