Showing posts with label depression. Show all posts
Showing posts with label depression. Show all posts

Saturday, March 7, 2009

Why weight loss experts fail their clients--Part 2


I am a little behind on this post, it's been a busy week!

I wanted to continue with part 2 of a series on why weight loss experts fail their clients. In my first post, just below this one, I described a study looking at brain changes that happen in the presence of depression.

One finding was that the prefrontal cortex, important for memory retention and coordination of complex behaviors, was compromised.

And what are dietitians notorious for doing? Handing over, in a one hour session, a volume of handouts as thick as Tolstoy's War and Peace, full of do's and dont's and calorie counts and exchanges and label reading information. And then they wonder why the client didn't return for a follow up visit.

I will never forget the client who shared with me that he sometimes made two lunches, not because he was hungry for lunch #2, but because he forgot he'd even eaten lunch #1 until he went to put lunch #2's dishes in the sink and encountered remnants from lunch #1.

Yes, it's sometimes that simple. Yet, the dietitian who even takes the time to ask about memory is a rare one.

Reasons for memory issues with depression, in addition to decreased blood flow, include loss of neurons in the hippocampus, another memory center, and low levels of DHA, an omega-3 fatty acid that is an essential component of brain matter.

If those issues are not accounted for and accommodated in a treatment plan, guaranteed your clients are at great risk for dropping out of treatment. Maybe even not remembering appointments they had made, if they actually did want to return.

Another brain center with compromised function with depression is the anterior cingulate, responsible for executive, evaluative, cognitive, and emotional functions, as well as learning and problem solving, error detection, motivation, and emotional modulation.

So if you're a dietitian trying to use the intuitive eating approach and you have a client who can't evaluate how they feel, decide what to do with how they feel, set boundaries in situations that trigger feelings that trigger eating....just how far are you going to get with your approach?

And you know what we do when clients don't do what we think they should? We diagnose them with mental health issues, refer them out, and potentially set them up to be prescribed medication that only exacerbates their metabolic and weight issues.

Just think about it over the weekend. I'll be back next week with a way around this dilemma that may actually help the client to get better and leave the dietitian less frustrated.

Elizabeth Sublette M, Milak MS, Hibbeln JR, Freed PJ, Oquendo MA, Malone KM, Parsey RV, John Mann J. Plasma polyunsaturated fatty acids and regional cerebral glucose metabolism in major depression. Prostaglandins Leukot Essent Fatty Acids. 2009 Jan;80(1):57-64. Epub 2009 Jan 6.

Monday, March 2, 2009

Why weight loss experts fail their clients--Part 1


As a dietitian with somewhat of a reputation as having expertise in disordered eating/eating disorders, I have often found myself in the middle of debates about whether or not a structured "meal plan" approach or an "intuitive eating" approach is best. I don't really agree with either, alone, though I do think that restoring someone's ability to eat intuitively should be the ultimate goal.

A recent research project helps me to define why I say that.

Mood disorders are associated with changes of fatty acid content in the brain. A group of neuroscientists finally decided to use their technology to look at how blood flow in different brain regions differed in depression, and to look at how those differences correlated with essential fatty acid levels.

In neuro-ese, here are the results:

DHA% and AA% correlated positively with rCMRglu in temporoparietal cortex. In addition, DHA% correlated negatively with rCMRglu in prefrontal cortex and anterior cingulate. No correlations were seen with EPA%. Thus, under conditions of low plasma DHA, rCMRglu was higher in temporoparietal cortex and lower in anterior cingulate/prefrontal cortex.

Translated into English, what that means:

1. In depressed subjects, the lower the level of DHA and ARA in the tempoparietal cortex, the less blood circulation there appeared to be. This is the part of the brain that integrates and coordinates sensory information.

2. Blood circulation to the prefrontal cortex and the anterior cingulate were compromised when DHA levels were low.

The prefrontal cortex is thought to be important for memory retention and coordination of complex behaviors.

The anterior cingulate is important for carrying out executive, evaluative, cognitive, and emotional functions. It is also important for learning and problem solving, error detection, motivation, and emotional modulation.

I believe, and have written profusely about it on this blog, that imbalance in fatty acids not only causes depression, but it causes changes in brain chemistry that change eating behaviors. And those eating changes only make the brain chemistry worse. It becomes a vicious cycle that can become incredibly difficult to break out of.

Both diet approaches operate on the assumption that the brain is intact and functioning completely normally. If that were the case, I argue, the client wouldn't be asking for help with an activity that should be primarily intuitive and without thinking too much about it. My clients often demonstrate signs and symptoms that the above described imbalance exist, which sets them up to fail with commonly endorsed nutrition counseling approaches.

Wednesday I'll continue with how changes in these brain regions interfere with nutrition counseling. For now, suffice it to say that a fatal error nutrition and exercise counselors make is to assume that their clients have the brain power and function that allows them to make the changes we advise them to make. And in doing so, we work against their ability to change. If we understand what's going on in the brain, we can develop therapies that harness their potential to succeed!


Elizabeth Sublette M, Milak MS, Hibbeln JR, Freed PJ, Oquendo MA, Malone KM, Parsey RV, John Mann J. Plasma polyunsaturated fatty acids and regional cerebral glucose metabolism in major depression. Prostaglandins Leukot Essent Fatty Acids. 2009 Jan;80(1):57-64. Epub 2009 Jan 6.

Friday, February 20, 2009

Are "vegetarians" at risk for depression?


One of my biggest jobs in this specialty is clarifying what vegetarian eating IS...and what it is NOT. Unfortunately, the vast majority of people I know who are vegetarian define that by describing what they DON'T eat, rather than what they DO eat. That is why the word "vegetarians" is in quotes in my title, because it refers to what many vegetarians consider the definition, and that is absolutely not what I define it as.

My definition of vegetarian is a person who replaces the essential nutrients found in animal based foods with non-animal sources.

People who don't eat fish have an incredibly difficult time getting omega-3 fatty acids, because they are primarily found in seafood. In addition, if they're eating more salads, thinking they are "healthy", they may be getting excessive amounts of the proinflammatory omega-6 fatty acids, which are often the base for commercial salad dressings.

"Vegetarians" with a more disordered bent to their habits, who are filling up on baked goods and processed foods, are also prone to excessive omega-6 fatty acids.

Which may explain the findings of this most recent study. Women experiencing psychological distress and symptoms of depression were divided into two groups. (It is my experience that of the two genders, women are the guiltiest when it comes to not eating meat and subsisting on salads and carbs.) The first group received 1.05 grams of EPA (a pretty hefty dose, given that most fish oil capsules have only 20-30% of that amount) plus .15 grams DHA. The second group received a placebo. They received this dose for 8 weeks.

The women on the fish oil supplement showed a degree of decrease in symptoms that the women on placebo did not.

Of the two omega-3 fatty acids found in fish oil, EPA is the one that is primarily found in fish. So if you're not eating fish, and you are having trouble with depression, chances are your food choices have something to do with that!

If you can't, off the top of your head, list five significant sources of DHA, your only other source of EPA (it can be converted when DHA stores are sufficient and there is excess in your diet), you're not getting enough. For a list of food products containing marine-algae based DHA...click here.

And, if your diet is heavy on processed foods and salads, and you are using salad dressings based on soybean or corn oil...you're likely breaking down whatever omega-3's are in your system before you can even benefit from them.

Maybe now you can see why I'm so fussy about where the line should officially be drawn between vegetarian and omnivore. It's not at all about what you don't eat...it's about what you DO eat.

Lucas M, Asselin G, Mérette C, Poulin MJ, Dodin S. Ethyl-eicosapentaenoic acid for the treatment of psychological distress and depressive symptoms in middle-aged women: a double-blind, placebo-controlled, randomized clinical trial. Am J Clin Nutr. 2009 Feb;89(2):641-51. Epub 2008 Dec 30.

Monday, February 9, 2009

More on zinc and depression



In my last post, I described a study in which zinc was shown to enhance antidepressant activity. In this study, rats whose depression and anxiety-related behaviors had been successfully treated with antidepressants were then placed on a zinc-deficient diet.

What happened?

They started to act anxious and depressed again.

We live in a culture that has created the mentality that if you're not feeling well, you go to the doctor, she prescribes you a pill, you take the pill, and you feel all better.

Unfortunately, pills can only work some of the time. And they tend to work best when you're using them in conjunction with healthy self-care behaviors. As far as I know, and I am a voracious consumer of psychiatric and neurological research, there is no pill developed that will overcome what you choose not to do.

Medication, in most cases, should be considered an ADJUNCT to treatment, not the ONLY solution to a medical problem.

The whammy here is that when you're depressed, it can be challenging to feel like doing anything for yourself at all. If you're not up to "healthy living" but you ARE motivated to take your prescription medication...at least consider taking a zinc supplement alongside the prescription. They are easy to find and inexpensive.

And they just might be what determines whether you crawl out of that whole.....

...or feel hopelessly stuck there.

Whittle N, Lubec G, Singewald N. Zinc deficiency induces enhanced depression-like behaviour and altered limbic activation reversed by antidepressant treatment in mice. Amino Acids. 2009 Jan;36(1):147-58. Epub 2008 Oct 31.

Friday, February 6, 2009

A little red meat may help your depression


If you have depression, you are not depressed because there is a deficiency of antidepressants in your body...

...however...

...you may be depressed because you have some basic nutritional deficiencies. One mineral that is involved in numerous brain and nervous system functions, and that has been extensively studied with regards to its role in the development of depression, is zinc.

Various doses of zinc were recently shown to improve immobility time in rats. Immobility in a stressful situation is a common behavior in depression. (When you are not depressed, you have better decision making and response times when it comes to managing stressful situations.)

That's exactly what fluoxetine (Prozac), paroxetine (Paxil), imipramine (Tofranil), desipramine (Norpramin), and bupropion (Wellbutrin) do!

When zinc and antidepressants were administered together, immobility time was reduced by more than either therapy produced on its own.

Practically what that says is that:
(1) if you are at risk for, or have had a history of depression, emphasizing high-zinc dietary choices and/or zinc supplementation would be a smart strategy, and
(2) if you are on an antidepressant, supplementing with zinc would be important to be sure that you get enough medication to do the job without getting so much that you set yourself up for detrimental side effects.

In fact, it seems to me that it should be an automatic recommendation of any physician, when prescribing an antidepressant, to write "zinc supplement" in the script as well...

FYI, your best sources of zinc include: red meats, liver, and oyster. And, when the originating soil is in good condtion...wheat, sweet corn, lettuce, beans, nuts, almonds, whole grains, pumpkin seeds, sunflower seeds and blackcurrant. That's a lot of different options, something for practically everyone, meat eater or not!

Cunha MP, Machado DG, Bettio LE, Capra JC, Rodrigues AL. Interaction of zinc with antidepressants in the tail suspension test. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Dec 12;32(8):1913-20. Epub 2008 Sep 11.

Friday, December 5, 2008

Which came first, the high glucose or the depression?



There are reams of references in the National Library of Medicine database reporting on what happens to blood glucose in the presence of numerous psychotropic medications. It seems that group wisdom points to the repeated finding that glucose can elevate as a result of some medication options.

Now, a group of researchers has shown that glucose changes can actually change how serotonin receptors work.

In the short term (several hours), elevated glucose decreased serotonin uptake.

In the long term (4 to 6 months), elevated glucose increased serotonin uptake.

It wasn't the attraction of the receptor to the molecule that was the problem. It was the activity of the receptor itself.

Which has me wondering a few things.

1. What is the point of giving a medication that increases the number of serotonin molecules when the limiting issue is about a completely different issue--whether or not the serotonin receptors are actively engaging with those molecules? You can put a million molecules out there, but if they can't get the attention of the receptors, seems like a moot strategy.

2. Seems like a setup for a vicious cycle--meds, higher glucose, more depression, more meds...yadayadayada. That is, when doctors don't let a medication sit and "brew" in the system long enough to see how it's really going to work. That's not what I see. Physicians often have very short attention spans and tend to stop one medication and start another one, frantically looking for the "fix". Looks like you truly have to let a med settle in for 4 to 6 months before making any decisions about its effectiveness.

3. Maybe we should be looking more closely at this interaction and trying to understand exactly why glucose metabolism and serotonin transport are so closely related? Nature made our brains that way for a reason. Sometimes throwing a medication at the problem we can see keeps us from seeing and understanding the problem we need to see.

I still think anyone who is diagnosed with depression should automatically get a referral to a mental health-specializing dietitian. There are a myriad of things that can be added to a treatment plan that can often keep this from even being something we have to discuss.

Gonçalves P, Araújo JR, Martel F. The effect of high glucose on SERT, the human plasmalemmal serotonin transporter. Nutr Neurosci. 2008 Dec;11(6):244-50.

Wednesday, December 3, 2008

And I thought I was happy after eating at Delhi Palace because the food was so good!


Turmeric is a spice commonly used in Indian cooking that is gaining attention for its health properties. Curcumin, the ingredient in turmeric that provides its yellow color, is thought to be a very powerful antioxidant and anticancer agent.

In Alzheimer's patients, not only can it prevent the accumulation of destructive beta-amyloid proteins, but it is thought to even break up already existing plaques (when I saw this, it made me wonder if this is why the oldest man in the world always seems to be living in some small Indian village.)

Now it's looking like curcumin may also have antidepressant properties. When tested on rats, it had activities mimicking that found in three different categories of antidepressants--monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, and dopamine reuptake inhibitors. Specific medications it was compared to included fluoxetine (Prozac), venlafaxine (Effexor), and bupropion (Wellbutrin).

When rats were already on medication, curcumin seemed to enhance the activity of the medication. Which has me thinking that psychiatrists should be handing out coupons to the closest Indian restaurant along with their medication scripts.

It appears that curcumin absorption is better in the presence of piperidine, a component of black pepper. Curry powder, readily available in most grocery stores, is a combination of coriander, cumin, black pepper, white pepper, turmeric and chillies). Not a bad item to keep stocked in your mental health cooking arsenal.

If you like to cook, Indian food is fun and easy. To get you started, here's a link to some curry recipes. Be sure you cook with olive or canola oil to get the best brain bang for your buck.

Kulkarni SK, Bhutani MK, Bishnoi M. Antidepressant activity of curcumin: involvement of serotonin and dopamine system. Psychopharmacology (Berl). 2008 Dec;201(3):435-42. Epub 2008 Sep 3.

Yang, F; Lim GP; Begum AN; Ubeda OJ; Simmons MR; Ambegaokar SS; Chen PP; Kayed R; Glabe CG; Frautschy SA; Cole GM (February 2005).
Curcumin inhibits formation of amyloid beta oligomers and fibrils, binds plaques, and reduces amyloid in vivo. Journal of Biological Chemistry (American Society for Biochemistry and Molecular Biology) 280 (7): 5892–901.

Friday, November 28, 2008

N-acetyl-L-cysteine: use with hope, use with caution


N-acetyl-L-cysteine is an up and coming supplement, which is gaining popularity among body builders. What's interesting is that it's also showing promise as a natural antidepressant.

It makes sense that it would work for both, since NAC is an antioxidant. In the case of exercise, it helps to repair the damage created in the process of metabolizing energy to fuel the exercise. When it comes to depression, it helps to slow down the oxidative process that has been destroying neurons.

Other potential mental health issues it is showing promise for include: bipolar disorder, schizophrenia, and obsessive-compulsive disorder. It may also help with polycystic ovary syndrome, another issue I specialize in treating.

NAC is to be treated with respect, however. In mice, in large doses it has been found to increase blood pressure in the lungs and right ventricle of the heart, creating symptoms similar to what is seen in animals subjected to an oxygen-deprived environment for 3 weeks.

While this supplement may have some very useful potential, it is important to work with a professional who knows how to dose it in order to maximize your benefit from it without putting yourself at risk. The guy at the corner bodybuilding store, who makes more money, the more you use, is likely not this person. A registered dietitian with specific training ins sports nutrition is your better bet.

Ferreira FF, Biojone C, Joca SR, Guimarães FS. Antidepressant-like effects of N-acetyl-L-cysteine in rats. Behav Pharmacol. 2008 Oct;19(7):747-50

Wednesday, November 26, 2008

Zinc KO's Prozac in the fight against depression


Zinc is an essential mineral that can cause depression when it is deficient. In a recent study, scientists produced depression in a population of rats by creating a zinc deficiency. They went one step further and tried to reverse the depression with an antidepressant. Turns out, the rats did not respond to the medication.

Makes me wonder about another relationship. The fact that medical schools often give as little as one hour of nutrition to medical students in a four year curriculum. Could that be why, the first thing physicians think of when a patient is depressed, is to use the therapy on which semester-long courses are created, rather than to recommend something mentioned in passing in that long lost hour?

If you want to do something about your own zinc intake, remember that the highest levels of the best absorbed kind of zinc is found in protein-based choices such as beef, lamb, pork, crabmeat, turkey, chicken, lobster, clams and salmon. If you're vegan, your best bets are milk and cheese, yeast, peanuts, beans, and wholegrain cereals, brown rice, whole wheat bread, potato and yogurt.

Interestingly, pumpkin seeds are a great source of zinc. I keep running across pumpkin seeds for a lot of different pieces I'm writing these days. They just might be one of those foods you should never let yourself run out of. Trail mix, anyone?

Tassabehji NM, Corniola RS, Alshingiti A, Levenson CW. Zinc deficiency induces depression-like symptoms in adult rats. Physiol Behav. 2008 Oct 20;95(3):365-9. Epub 2008 Jul 3.

Wednesday, November 19, 2008

Biochemical and brain differences in bipolar disorder--that nutrition might be able to help


These guys think like me. Instead of coming up with a pill that fixes what appears to be wrong on the outside...why not start on the inside and figure out what's really causing the problem?

This group of researchers started out looking at tissue samples of people who had had depression. What they discovered was that these individuals had low levels of docosahexaenoic acid (DHA, if you read this blog you know that's fish oil and marine algae) in their red blood cells and their cortices. The cortex is the part of the brain that does logical, rational problem solving.

They decided to poke around some brains that had been under the influence of bipolar disorder in their time and discovered that there were several abnormalities. As with depressin, DHA levels were low. Arachidonic acid and stearic acid levels were also low. Brains of individuals who had been on mood stabilizing or antipsychotic medications were not as deficient. The deficiencies appeared to be more severe if alcohol abuse had been an issue.

It's not clear whether or not the issue is totally dietary, or if there is some kind of abnormal metabolic process that alters fatty acid ratios, but it does seem that researchers in this area are leaning toward the possibility that nutrition is extremely important to brain function--as well as to the management of psychiatric disorders.

It causes me to wonder why dietary controls are not a standard protocol in psychotropic drug studies, but that's a topic for another blog post. I'm sure you'll see that soon!

McNamara RK, Jandacek R, Rider T, Tso P, Stanford KE, Hahn CG, Richtand NM. Deficits in docosahexaenoic acid and associated elevations in the metabolism of arachidonic acid and saturated fatty acids in the postmortem orbitofrontal cortex of patients with bipolar disorder. Psychiatry Res. 2008 Sep 30;160(3):285-99. Epub 2008 Aug 20.

Oh! Why the graphic? Just some random thinking...all this writing about fish, and brains, and fish for brain health kind of has me wondering...if fish might not be more intelligent than we give them credit for, if fish ever get depressed...and if there is such a thing as a manic salmon?

Monday, November 17, 2008

Pregnant women and psychotropic medications really don't mix


What I hate about this study is that we even have to study whether or not a pregnant woman should be given psychotropic medications during pregnancy. It disturbs me that this many studies surrounding this question are showing up in Pub Med. My common sense would tell me absolutely not, without even having to do the research. However, I guess there are some situations where it is more dangerous to have a pregnant woman's psychopathology left completely untreated for an entire 9 months. So, despite my personal feelings, I'll share the findings.

Pregnant mice were given fluoxetine (Prozac) throughout their pregnancy and kept on the medication until their pups were weaned. The pups were then given other medications and their responses to those medications were evaluated. The effects seemed to be more significant in the female offspring, who did not seem to have normal responses related to dopamine function. (Dopamine is important for impulse control, which influences potential for chemical dependencies and troubles such as addictions, gambling, shoplifting, and carbohydrate bingeing). The researchers also suggested that if this relationship existed in humans, daughters of women who took Prozac during pregnancy may not effectively respond to certain medications later in life. Two important classes of medications this might include are Parkinson's medications and antipsychotics, both of which attempt to correct problems in dopamine systems.

So, MY take on this is that given the fact that fish oil is such a powerful antidepressant and it is important to have enough of it during pregnancy for both mother and baby, perhaps we're learning that we should lean more in that direction on behalf of the two individuals involved in a pregnancy.

My CONCERN is that a drug company R and D person is likely to read the very same study and think, "Hmmm...if we get started right now, we can have a new drug ready for all those babies coming down the pike whose dopamine systems aren't responding to anything we can currently script."

We'll see which direction this information takes science. I sure hope it's the one involving fewer trips to the pharmacy in 20 years.

Favaro PN, Costa LC, Moreira EG. Maternal fluoxetine treatment decreases behavioral response to dopaminergic drugs in female pups. Neurotoxicol Teratol. 2008 Nov-Dec;30(6):487-94. Epub 2008 May 14.

Wednesday, November 5, 2008

Folic acid and brain health--don't forget it!


As my last post discussed, depression is not just about mood. It's about the integrity of neurons and the systems that support them. One very strong connection that research is increasingly supporting, is the link between depression and inflammation. Inflammatory markers commonly used to identify heart disease, such as homocysteine, are being correlated as well with depression.

Here, 27 subjects were divided into two groups. One group was given fluoxetine (Prozac) and folic acid, while the other was given fluoxetine and placebo. (Folic acid was given because it has been shown to help prevent elevated homocysteine.) Another 15 subjects were given nothing at all, for a basis of comparison.

As happens in cardiovascular studies using folate as an intervention, plasma homocysteine levels dropped with folate supplementation. The interesting finding, however, was that when subjects took the Hamilton Depression Rating Score, those who had received the folate showed greater improvement than those who only received the fluoxetine. There was no significant difference in serotonin levels, so the researchers concluded that folate was not affecting the mechanism by which fluoxetine works.

So the bottom line seems to be...you can't just fix depression with a pill. How you take care of yourself (i.e., how you choose to eat) can be a crucial factor in whether or not your brain works at its absolute best.

If you want to add more folate to your diet, here are your best food choices: fortified breakfast cereal, whole wheat products, meat, beans, liver, eggs, sunflower seeds, asparagus, leafy green vegetables, oranges, strawberries, melons.

Resler G, Lavie R, Campos J, Mata S, Urbina M, García A, Apitz R, Lima L. Effect of folic acid combined with fluoxetine in patients with major depression on plasma homocysteine and vitamin B12, and serotonin levels in lymphocytes. Neuroimmunomodulation. 2008;15(3):145-52. Epub 2008 Aug 21.

Tuesday, October 14, 2008

Fish and dementia


I've talked a lot about how fish develops brain power. It also helps you hang onto the brain power you have! In a French study, 1214 seniors without dementia were followed for 4 years. During that time, 65 of them developed dementia. It was found that the higher the person's eicosapentaenoic acid (EPA) level, the lower the risk of dementia. Factors that could have explained this trend that were factored out included: age, education, diabetes, and vitamin E levels. EPA appeared to be a more significant determinant in this population than did the "other" fish oil, docosahexaenoic acid, or DHA.

When individuals also had depression, it appears as total fatty acid ratios also became important. High ratios of the omega-6 fatty acids to omega-3 fatty acids were also important in risk determination.

One thing to take away from this study: Omega-3's are important for preserving brain integrity. Secondly, balancing the right kind of fats and limiting the potentially destructive ones (omega-6's, if you've been reading this blog that means the "S" and "C" oils), is important for managing mood and preventing depression.

Samieri C, Féart C, Letenneur L, Dartigues JF, Pérès K, Auriacombe S, Peuchant E, Delcourt C, Barberger-Gateau P. Low plasma eicosapentaenoic acid and depressive symptomatology are independent predictors of dementia risk. Am J Clin Nutr. 2008 Sep;88(3):714-21.

Wednesday, October 1, 2008

Effect of fish-oil supplementation on mental well-being in older subjects: a randomized, double-blind, placebo-controlled trial.


We hear all the time that fish oil is good for mood. So why did this study here not come to that conclusion?

302 seniors (independently living) were divided into 3 groups. The first group was dosed 1800 daily milligrams of EPA and DHA, the second group 400 milligrams, and the third group received placebo capsules. Before being given the capsules, and 13 and 26 weeks into the study, plasma concentrations of EPA and DHA as well as responses to several psychological tests were measured. Even though the fish oil significantly increased EPA and DHA concentration in the two dosed groups (by 238% in the high dose and 51% in the low dose), responses to the questionnaires were not significantly different. Why is that? There are probably several reasons.

1. Brain function is about a lot more than just omega-3 balance. Independently living seniors are likely to be eating an overall diet that is deficient in several nutrients. It would have been interesting to see a baseline blood test of other nutrient levels to see if overall nutritional status was correlated with test scores and EPA/DHA response.
2. The background diet of these seniors was not measured, or if it was, it was not reported. If, which is common because of convenience, the group as a whole was eating a lot of pre-prepared and packaged food, the ratio of pro-inflammatory oils to dietary omega-3 content may affect the outcome of the study.

It doesn't mean that just because there was not a mood-based response to these oils that they weren't beneficial. If levels of omega-3's increased dramatically, they most certainly were reducing cardiovascular risk, preventing the development of dementia and Alzheimer's, and improving bone health, to mention a few.

I just wish these researchers would understand the importance of controlling diet in any study that investigates the usefulness of an isolated supplement. Not only will it provide more significant results, it will keep people from mistakenly assuming that a certain nutrient is not of benefit when it actually is.

van de Rest O, Geleijnse JM, Kok FJ, van Staveren WA, Hoefnagels WH, Beekman AT, de Groot LC. Effect of fish-oil supplementation on mental well-being in older subjects: a randomized, double-blind, placebo-controlled trial. Am J Clin Nutr. 2008 Sep;88(3):706-13.

Monday, September 15, 2008

Just one gram, that's all it takes!

A couple of years ago I prescribed fish oil to a client with depression. Her psychologist told her my recommendation was not proven in the research. These days, I'd be able to counter with a lot more hard data.

For example, in one study, 35 depressed adults (about half women, half men) were divided into 3 groups and given 3 different doses of DHA, one of the omega-3 fatty acids found in fish oil. 83% of the group with the lowest dose responded to the DHA with decreased symptoms of depression! Higher doses did not seem to be as effective.

My guess is, there may be a threshold over which adding more therapy into the system exceeds the body's ability to use it. So even with fish oil, more is not better may not be the appropriate approach.

However, I do like knowing that even a little bit of this very available, very inexpensive, nonpharmacological treatment can have profound effects on a common and debilitating issue. It's worth a try!

Mischoulon D, Best-Popescu C, Laposata M, Merens W, Murakami JL, Wu SL, Papakostas GI, Dording CM, Sonawalla SB, Nierenberg AA, Alpert JE, Fava M. A double-blind dose-finding pilot study of docosahexaenoic acid (DHA) for major depressive disorder. Eur Neuropsychopharmacol. 2008 Sep;18(9):639-45. Epub 2008 Jun 6.

Monday, September 8, 2008

Modulation of serotonin transporter function during fetal development causes dilated heart cardiomyopathy and lifelong behavioral abnormalities.


While I've drifted into the topic of antidepressants, I thought I'd share this piece on using them when pregnant. Two different antidepressants, fluoxetine (Prozac) and fluvoxamine (Luvox) were given to pregnant mice. Luvox reportedly did not as easily cross the placenta as Prozac. (This means that Luvox was not as available to the developing baby as Prozac was.)

Most of the rats' babies that were prenatally exposed to Prozac died after birth of a type heart failure known as dilated cardiomyopathy. This is a condition in which the heart becomes enlarged and too weak to pump enough blood to the rest of the body. These rats also showed alterations in serotonin receptor levels in the raphe nucleus, the part of the brain that is in charge of serotonin release. There was also an increased incidence of behaviors in these mice indicating anxiety and depression.

If you are female and you are choosing to treat your depression with an antidepressant, and you are at an age where you can conceive, you may wish to discuss this study with your prescribing caregiver. Your medication decisions are affecting two people, both deserving of consideration.

Noorlander CW, Ververs FF, Nikkels PG, van Echteld CJ, Visser GH, Smidt MP. Modulation of serotonin transporter function during fetal development causes dilated heart cardiomyopathy and lifelong behavioral abnormalities. PLoS ONE. 2008 Jul 23;3(7):e2782.

Sunday, May 25, 2008

I'd like to introduce you to some of my other writing!

I've been a little quiet here, haven't I? Here in Phoenix we had a wacky weather week, starting out in the triple digits and then plummeting to the point where I had to turn my heat on a couple of mornings. Knowing just what kind of scorching rebound is just around the corner, and knowing I'll be hiding out inside, working to avoid the heat, I decided to drop the work for a few days, get some great long runs in on those wonderfully cool mornings, and hole up with a few reads that had absolutely nothing to do with neurons, medications, or medical diagnoses. If you're looking for a novel that will start you out laughing, then catch you completely by surprise with the premise that suddenly shows up mid-book, check out Life of Pi. I sat down with my morning coffee today and I only looked up because one of my cats jumped on the sofa to remind me I'd forgotten her lunchtime treat. Great way to spend a lazy Sunday!

Anyway...

...I have also been non-blogging because I've been updating some of my consumer booklets. I thought I'd share a couple of sample pages from the three most popular here in case any of you are interested.

Polycystic Ovary Syndrome
I do most of my work with polycystic ovary syndrome (PCOS), the #1 cause of infertility in the US, which is related to several mental health issues and often exacerbated with the administration of psychiatric medications. Here is a sample from the 30 page booklet:

















Depression
I decided to write this booklet because most information I found about depression was, well....depressing! Most of it focused on external reasons for being depressed, and very little educated about hormones, neurons, and the disease process that depression truly is. I wanted to empower people with depression to view their diagnosis as something as neutral to discuss as high blood pressure, not something to be embarrassed about. I also wanted to share a lot of ideas for preventing or recovering from depression that did not involve prescription medications.

These .jpg files are coming out a little small, but if you copy them and enlarge them you can hopefully see them.
















Post-traumatic Stress Disorder

This booklet came about after 9/11. I felt very helpless sitting all the way out here in Phoenix when one college classmate had to make her way down 75 flights of stairs to safety, while another was conducting a meeting in the Pentagon when the building was hit. This was initially part of my own grief process, but it's turned out to be useful to people with PTSD from a number of different causes.

An interesting note about the booklet: I originally wanted to use clip arts depicting different cultures from all around the world as a way to communicate togetherness during a crisis. However, I could not find a single clip art of a Muslim in traditional dress participating in a modern day activity. I figured that using the art that I found would only make things worse...so I came up with "Plan B", which was to engage my nephews in the illustration work. I think it was meant to be illustrated by them all along, because the most frequent comment I get about the book is that the children's art really softens the message and makes it a lot easier to read about something that is very hard to experience, let alone discuss.

What we would do without the children in our world!

Here is a sample page:


This last one is my absolute favorite, but it's a little difficult to market. I never feel it's appropriate to try to sell something to a person who's in pain...so I have this one on my website in the hopes that friends and loved ones will find it.
If you know people who you think might benefit, perhaps you can let them know about it.

All of these items can be ordered in my bookstore, at
http://yhst-34497545168533.stores.yahoo.net/consumer-publications.html

I hope you all are enjoying your holiday and doing as much socializing and non-work as I am...I need to finish up my novel tomorrow, and then it's back to reading and writing about research.

See you later in the week!

Friday, May 2, 2008

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.

Wednesday, April 30, 2008

Can a pill really cure stress?

It used to be that when I met people, and they asked what I did for a living, that I told them I was a nutritionist. Until a few years ago, on a flight back from an eating disorder conference in Washington, DC. I had the window seat and my boss had the aisle seat. The woman in the middle appeared to be excited about her trip to Phoenix, and wanted to chat things up with the two of us. She started with me.

"Are you from Phoenix or DC?"

"I'm on my way home from a conference."

"What was the conference about?"

"Eating disorders. I work in a treatment center."

Without any closure, she physically picked herself up, turned toward my boss, and started the same conversation a second time...only to discover that it went in the exact same direction. She turned her body away from my boss and sat rigidly, staring at the back of the seat in front of her.

Airlines still served meals back then, and when the three of us received ours, I realized that the seating pattern that evening was an anorexic's worst nightmare. It was clear from the way she was manipulating her food, moving it around to look like she'd eaten more than she had, and picking as much fat off of her sandwich as she could, that this young woman had a pretty serious eating disorder.

I felt for her. I knew in the right setting, at the appropriate time, having the two of us to share perspective and compassion with could have been a gift. But not on that day.

I don't talk about eating disorders anymore unless I'm prompted to. I tell people I specialize in stress-related disease. That is, if I'm in the mood to talk. I can't get people to stop talking when they learn that this is my area of interest!

It's the exact same specialty, just a different spin. I help people who manage their stress in ways that can get them into trouble. No one wants to admit they have an eating disorder. But e-v-e-r-y-o-n-e wants a place to unload their stress!

I get to help a lot more people by focusing on the stress instead of its resulting dysfunction. Apparently the drug companies have figured this out, too. (But did you have to read this far into this blog post to figure that out---have you ever seen an ad on the evening news for a drug that successfully helps with bulimia? Erectile dysfunction--yeah, we got a pill for that. Urinary incontinence--yeah, we can help you with that. Starving yourself to death? Sorry, we're just not comfortable going there...too personal!)

It's been proposed for awhile that depression often results when the stress hormone system doesn't properly regulate itself and stress hormones are oversecreted. Scientists recently injected stress hormones into mice and then evaluated what kind of changes they observed. They discovered that stress hormones reduce the ability of the hippocampus (brain's memory center) to generate new cells, which, understandably, over time, reduced hippocampal volume. Acute exposure to stress hormones created more of a "depressed" response in these mice, while prolonged exposure seemed to elicit an "anxious" presentation.

Antidepressant medications administered at the same time the stress hormones were administered prevented these changes.

OK, but instead of waiting until stress is at a point where it's doing damage...what about reducing stress from the source? What about taking on fewer responsibilities? Setting boundaries? Prioritizing sleep? Developing a support system, especially one outside of your work connections? Picking up a hobby? Not buying into the mentality that the harder you work and the less you sleep and the more e-mails you have...the better person you are?

I'm not arguing that the meds aren't a valuable tool. But I do know that people who push themselves to the point where they need medication to undo what stress has done have been out there for a long time pushing themselves before they finally admit maybe they need to do something about it. What about all the oxidative stress and aging and other physical damage that happened on the road to Prozac? We're able to measure some of the things we can reverse with medication...but I sure hope that doesn't leave us falsely reassured that everything we did to ourselves because we didn't want to relax a little bit more can be fixed when we get to that item on our "to do" list.

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.

Monday, April 28, 2008

There's something fishy about depression treatment...

Here's the study I've been looking for. There are plenty of studies showing the effectiveness of antidepressant medications. And there are plenty of studies showing the effectiveness of fish oil in treating depression. But no one had compared the two. Until now.

In Iran, researchers compared the separate relative effectiveness of eicosapentaenoic acid (EPA), one of the chemicals commonly referred to as fish oil, and fluoxetine (Prozac). What they found was that EPA was equally as effective as fluoxetine, in an 8 week trial, in reducing symptoms of depression. The most superior outcome was found in subjects who received both EPA and fluoxetine.

If you're wanting to try this at home, as always, discuss this with your physician. The risk of using fish oil in conjunction with antidepressants is almost always outweighed by the potential benefits--however, it is not advised that you discontinue any prescription medications you are on without consulting with the prescribing party.

A word about EPA. There is a lot of confusion about what it means to use fish oil. Most products available in the grocery store that are labeled as containing "omega-3 fatty acids" actually contain ALA, a great omega-3 but not the one that has been associated with improved mental health. If you're using omega-3 eggs, or vegan (marine algae-based) omega-3's, you're getting DHA, not EPA. That primarily comes from fish. Even though you will read that there are conversions to EPA from both ALA and DHA, the efficiency of these conversions is great and likely not enough to achieve results such as were seen in this study.

If your diet is high in pro-inflammatory oils (those "S" and "C" oils you see me routinely discuss in this blog), it will be harder to get effects described in this study. You're going to need to tweak your diet in order to get the most bang for your buck. And, realistically, that means you're going to have to get rid of most processed foods and salad dressings.

But, for those individuals motivated to make these changes, the results can be profound. I see it routinely in my private counseling. It is certainly my first recommended item of action when someone is trying to reduce the number of medications they are on.

Finally, for physicians who prescribe antidepressants, this study suggests that if you do so without strong nutritional guidance as well, you're not as helpful to your patients as you have the potential to be. It's not just about pills. Your patients did not become depressed because they were antidepressant-deficient!

Jazayeri S, Tehrani-Doost M, Keshavarz SA, Hosseini M, Djazayery A, Amini H, Jalali M, Peet M. Comparison of therapeutic effects of omega-3 fatty acid eicosapentaenoic acid and fluoxetine, separately and in combination, in major depressive disorder. Aust N Z J Psychiatry. 2008 Mar;42(3):192-8.