A nutritionist's perspective on psychiatric medications and some of their effects.

We made a top 50 list!

2009-05-13T20:10:00.000-07:00

Wow, it's been awhile since I posted...I've been busy with another blog. I look forward to more regular posting here soon!

In the meantime, I just received word that we received inclusion in a "top 50" list of dietitian blogs. I consider that a wonderful compliment, given the number of blogs out there focusing on nutrition.

If you'd like to read and learn more about our colleagues, here is the link to the list:

http://radiologytechnicianschools.net/top-50-dietician-blogs/

Omega-3's in a Powder: You Saw It Here First

2009-03-16T11:31:00.001-07:00

Hello everyone,

Just wanted to share an article you may have seen on MS-NBC.

The main ingredient in our sponsor's Omega-3 Brain Booster is the Ocean Nutrition product featured in this article. If you'd like to try it, you will receive a 10% discount on your first purchase if you click this link and use the coupon code "neuron" when you order.

I was thrilled to see this article and to know we'd brought this information to all of you long before MS-NBC had even heard of it!

What Stresses You Most--Your Weight Or The Economy?

2009-03-12T10:24:00.000-07:00

This request comes from good friend Marsha Hudnall, up in beautiful Vermont.

If you have a moment and some inclination take the survey and share with friends/colleagues/whatever.

**********************************************************************************
We're trying to get as many responses to our survey as possible, and one way to do that is to get other blogs to mention it. Would you consider asking your readers to take the survey, or sending it to people you know?

What creates the most stress for you -- your weight or the economy? Please take our survey.

Thanks!
Marsha

Marsha Hudnall, MS, RD, CD
Director
Green Mountain at Fox Run
a women's retreat for healthy living without dieting
www.fitwoman.com
www.aweightlifted.blogs.com
http://twitter.com/MarshaHudnall

In honor of National Registered Dietitian Day

2009-03-10T19:00:00.000-07:00

Today, my post is devoted to a special project promoting registered dietitians. I am cohosting, with dietitian Renata Mangrum, the first-ever Registered Dietitian blogfest, aimed at showcasing to the Internet-surfing public the many things dietitians do and can do to help you with your quest for help. Listed below my entry is a list of links to other blogs written by other dietitians that you can visit to see the many things my friends and colleagues do within this profession.

I started this blog when I noticed, over time, that a vast amount of research regarding the relationship between nutrition and mental health existed in the National Library of Medicine database...but it wasn't making it to the public. My guess is that is because nutritional answers to brain and nervous system problems are not nearly as profitable to spend money marketing as medications.

That doesn't mean there is not a need to get this information to where it is needed--the screens of blog readers like you!

I was surprised and excited to see how quickly blog traffic to this publication grew. One of my favorite things to do is to read research and find items to share with all of you.

I can't think of anything better I could be devoting my work and my career to. I hope you enjoy our blog...and I hope you enjoy getting to know some of the many colleagues participating in our blogfest today!

Warmest regards,

Monika M. Woolsey, MS, RD

No, fish oil isn't as multipurpose as Windex...it's still about overall lifestyle

2009-03-09T08:23:00.000-07:00

I am devoting this blog post to my friends who think I've gone fish oil overboard! I write and talk about fish oil so much, it seems, they've gotten the impression that maybe I've forgotten about all of the other things that determine health. One of my neighbors constantly teases me about the fact that I believe in and promote fish oil like the guy who uses Windex for everything in the movie My Big Fat Greek Wedding. Colleague Karen Siegel (Houston registered dietitian and licensed acupuncturist) sent me the following article.

Note that the recommendations at the end of this quote are the same recommendations commonly made for diabetes prevention--and you HAVE seen in this blog, that I have written on the connection between diabetes and Alzheimer's disease.

It's not that I think fish oil can replace a healthy lifestyle, it's that I see so many people who pretty much have the right idea, and not balancing omega-3's is the piece that keeps them from being completely on the right train.

Though I do believe fish oil is important, this article perfectly sums up how I do feel: by no means is fish oil a "bad habit eraser"! You've got to live a healthful life, and when you do that, fish oil may help decrease your health risk.

Oh, BTW, that neighbor who teases me? She told me the other day she secretly went to Costco and got the pills...and her hair and nails have started to become longer and stronger.

Dangour AD, Allen E, Elbourne D, Fletcher A, Richards M, Uauy R. Fish Consumption and Cognitive Function among Older People in the UK: Baseline Data from the Opal Study. J Nutr Health Aging. 2009;13(3):198-202.

A UK study has cast doubt on claims that eating oily fish can protect against dementia in old age.

Data from a trial of more than 800 older people initially showed that those who eat plenty of oily fish seem to have better cognitive function.

But factors such as education and mood explained most of the link.

Researchers need to clarify what, if any, benefits fish oil has on the ageing brain, they wrote in the Journal of Nutrition, Health and Ageing.

In recent years, there has been increasing interest in diet as a way of preventing dementia.

It's not at all clear that healthy older people get any benefit from eating fish oil

Dr Alan Dangour, study leader
Much focus has been on omega 3 fatty acids found in oily fish, such as salmon and mackerel.

And there are biological reasons, backed by tests in the laboratory, why in theory, these fatty acids would be neuroprotective.

The latest study found a significant association between eating a couple of portions of fish a week and better scores on tests of cognitive function.

But when the researchers, from the London School of Hygiene and Tropical Medicine, took into account education and psychological health the association almost disappeared.

Healthy

Experts advise eating a couple of portions of fish a week, with at least one being an oily fish, because there are proven benefits on the heart.

Study leader Dr Alan Dangour said claims about the benefits of oily fish in warding of dementia in older people seemed to have been oversold.

"The evidence on this has always been sporadic.

"What this shows is there is a link between people who eat oily fish and better cognitive function, but if you adjust for education and mood this relationship goes, so it's not at all clear that healthy older people get any benefit from eating fish oil."

The evidence collected by Dr Dangour was for a study due to report later this year comparing fish oil supplements with placebo.

He added that this randomised, controlled study should provide clarification.

Neil Hunt, chief executive of the Alzheimer's Society, said: "One of the best ways to reduce your risk of dementia is by eating a Mediterranean diet rich in fruit, vegetables, grains, fish and poultry.

"However, we still do not know which components of this sort of diet help the most.

"Unfortunately this study does not add to our understanding.

"Once age, sex and education are accounted for the research does not show any significant benefit of regularly eating oily fish."

Why weight loss experts fail their clients--Part 2

2009-03-07T08:17:00.000-08:00

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.

The American Heart Association Needs to Check Its Omega-3 Math

2009-03-02T19:25:00.000-08:00

I have heard the following recommendations made by the American Heart Association repeatedly for years now. And I hear them parroted everywhere by well-intended medical experts who, it seems, did not stop to check the math on which the recommendations are based:

Population Recommendation
Patients without documented coronary heart disease (CHD)
Eat a variety of (preferably fatty) fish at least twice a week.
Include oils and foods rich in alpha-linolenic acid (flaxseed, canola
and soybean oils; flaxseed and walnuts).

Patients with documented CHD Consume about 1 g of EPA+DHA per day,
preferably from fatty fish. EPA+DHA in capsule form could be
considered in consultation with the physician.

Patients who need to lower triglycerides 2 to 4 grams of EPA+DHA per
day provided as capsules under a physician's care.

Patients taking more than 3 grams of omega-3 fatty acids from
capsules should do so only under a physician's care. High intakes
could cause excessive bleeding in some people.

Evidence from prospective secondary prevention studies suggests that
taking EPA+DHA ranging from 0.5 to 1.8 grams per day (either as fatty
fish or supplements) significantly reduces deaths from heart disease
and all causes. For alpha-linolenic acid, a total intake of 1.5–3
grams per day seems beneficial.

I couldn't sit back anymore. Ellen Reiss Goldfarb, RD, a member of my inCYST Network for Women With PCOS collaborated with me on hopefully setting the record straight. We hope it helps, especially to get a mathematically-correct set of recommendations out to the public so they can go grocery shopping with a better sense of empowerment.

Regarding the omega-3 recommendations recently discussed, you all may want to consider that there are several contradictions within that make it very difficult (maybe even impossible) for the average American to follow them. As dietitians, it is important that we understand this math so that we help, not confuse or hurt, people who look to us for advice.

First of all, we are telling people that they are not to eat more than 3 grams of omega-3's per day unless they are under a physician's care. However, if you try to get 1.8 mg of combined EPA + DHA combined, in the form of food first, 3 ounces of Alaskan salmon, which contains 384 mg of EPA plus DHA, would have to be eaten in a DAILY QUANTITY OF 14 ounces in order to get there. Are you really saying that if you're eating enough fish to get the amount of omega-3's we recommend, that the MD has to manage it??? You are unnecessarily putting yourself out of business if you are!!!

Secondly, given those numbers for salmon, the densest seafood source of omega-3's, there is no way eating fish just a few times a week is going to get you to the level of omega-3 intake these recommendations are making. It is so frustrating watching colleagues parrot these recommendations and wondering if we're the only ones who've actually sat down and done this math..

We also went to three popular fish oil brands and calculated out how many pills you would need to get the upper level of DHA + EPA recommended. Two of those, Nordic Naturals and Carlson's, if taken at the level needed to get there, would also place your client at levels you say a physician needs to manage.

Realistically and honestly, how many of you are really doing that?

With regards to bleeding, in all of our collective years actively recommending fish oil, only one client encountered a bleeding problem. The people at greatest risk for that are people who are on medications such as coumadin...and if you work closely with a physician who "gets it"--the dose of that medication can be dropped as EPA levels rise and help normalize blood clotting function. Always start low, titrate up, look closely for symptoms in people not on contraindicated medicatoins and let the MD check blood levels in people who are...and work very hard to minimize omega-6 intake. You'll get a lot more bang out of your omega-3 buck if you focus on the omega 6 to omega 3 ratio than if you only think about one.

If you don't know how to use omega-3's to promote health, you may actually CREATE health risks for your clients, which I don't think any of you want to do.

Here are the numbers from our calculations for your reference.

EPA + DHA, total mg
3 ounces salmon 384 mg
Nordic Naturals 550 mg
Carlson's 500 mg
Barlean's 600 mg

Total omega-3 content
3 ounces salmon 3250 mg
Nordic Naturals 690 mg
Carlson's 600 mg
Barlean's 780 mg

Amount needed to meet n-3's needed to meet upper DHA + EPA recommendation/total omega-3 content of that amount
3 ounces salmon 14 oz DAILY/15.2 total gms n-3
Nordic Naturals 3.27 capsules/3.6 gm total n-3
Carlson's 3.6 capsules/6.0 gm total n-3
Barlean's 3.0 capsules/2.3 gm total n-3

Monika M. Woolsey, MS, RD
Ellen Reiss Goldfarb, RD

Why weight loss experts fail their clients--Part 1

2009-03-02T08:51:00.000-08:00

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.

Nutritional compounds with promise in Alzheimer's syndrome

2009-02-27T03:35:00.000-08:00

Anyone experiencing Alzheimer's disease firsthand probably has wondered if there is any extra "edge" they might obtain for their own risk from nutritional supplementation. A group of researchers recently reported that a combination supplement reduced the levels of already existing specific oxidative marker levels by 57% and prevented the reappearance of new molecules.

The supplement used in this study contained the following compounds: alpha-lipoic acid, acetyl-l-carnitine, glycerophosphocoline, docosahexaenoic acid (DHA), and phosphatidylserine.

I don't know about you, but this is one condition I'd rather not give a head start to my brain, and one I'm happy to be proactive when it comes to my current supplemental choices.

Suchy J, Chan A, Shea TB. Dietary supplementation with a combination of alpha-lipoic acid, acetyl-L-carnitine, glycerophosphocoline, docosahexaenoic acid, and phosphatidylserine reduces oxidative damage to murine brain and improves cognitive performance. Nutr Res. 2009 Jan;29(1):70-4.

Is your chia pet a hidden nutritional surprise?

2009-02-25T05:21:00.000-08:00

Risperidone (Risperdal) is a common antipsychotic medication that was recently investigated for its influence on omega-3 fatty acid metabolism.

Rats were placed on two different diets, one containing alpha-linolenic acid (ALA) and one that was ALA-deficient. Then both groups were administered a dose of risperidone.

This research design was used because ALA can be converted to docosahexaenoic acid (DHA), and the purpose of the study was to evaluate the influence of risperidone on this conversion.

In rats not fed ALA, there was a significant increase in tissue DHA in the presence of risperidone, suggesting that this medication helps to increase the conversion of ALA to DHA. When there was ALA in the diet, this was not observed, suggesting that when there is enough ALA available, there is no need for any augmentation of pre-existing mechanisms.

Some questions and comments:

1. This will be an interesting line of research to follow...to determine whether schizophrenia is related to nutritional imbalances and/or deficiencies, whether there might be different types of schizophrenia, some nutritionally instigated and aggravated, others not.

2. Seems that a dietary strategy of increased ALA isn't a bad idea if you struggle with schizophrenia.

3. At this point, it is NOT rational to assume that increasing dietary ALA will eliminate the need for antipsychotic medications.

4. At the same time, it doesn't make sense to use a prescription medication to correct a nutritionally-relevant problem.

If you balance the diet and focus on adequate ALA, the amount of medication you might actually need might decrease, therefore reducing the risk of metabolic side effects.

For those who are interested, foods that are good sources of ALA include: canola oil, whole soybeans, walnuts, salva (chia), ground flaxseeds, and flaxseed oil.

McNamara RK, Able JA, Jandacek R, Rider T, Tso P. Chronic risperidone treatment preferentially increases rat erythrocyte and prefrontal cortex omega-3 fatty acid composition: Evidence for augmented biosynthesis. Schizophr Res. 2009 Feb;107(2-3):150-7. Epub 2008 Nov 7.

Diet and Parkinson's disease

2009-02-24T01:10:00.000-08:00

I've been studying nutrition and the brain for awhile now, and it's clear I'm a big fan of omega-3 fatty acids. It's only been recently that their role in Parkinson's disease prevention is becoming clear.

Oxidative stress, or aging, is to the brain what rust is to your car. In Parkinson's disease, oxidation appears to significantly affect the brain systems regulating dopamine.

In this study, rat brain tissue was exposed to several by-products of fatty acids found in the brain, docosahexaenoic acid and arachidonic acid. It turned out that the arachidonic acid--derived compound was the most toxic to brain cells.

Arachidonic acid is derived from two main sources, certain dietary oils, and meats. It's fairly easy to identify the oils that promote arachidonic acid production. They tend to be those, which in English, begin with the letters "S" and "C"; soybean, safflower, sunflower, sesame, corn, cottonseed...the only exception would be canola. These oils have been unloaded into the food supply in recent years and as they have, many diseases, not just Parkinson's, have been on the upswing. Start reading your labels!

Arachidonic acid is also found in meat. So if you are eating large portions of meat instead of balancing your protein with other types of food, your diet may be out of balance and promoting inflammation/oxidation/aging, particularly in the nervous system. Some rules to follow which you've heard before, for other reasons, include: eat more seafood and less red meat, eat more vegetarian meals, and limit your meat portions to the size of the palm of your hand without the fingers.

Parkinson's is not a problem to be taken lightly. If you have ever known someone who has had to deal with the tremors and deterioration in quality of life...you know what I mean. Some very simple dietary choices may help you to delay or prevent having to personally deal with this challenging diagnosis.

Liu X, Yamada N, Maruyama W, Osawa T. Formation of dopamine adducts derived from brain polyunsaturated fatty acids: mechanism for Parkinson disease. J Biol Chem. 2008 Dec 12;283(50):34887-95. Epub 2008 Oct 15.

Are "vegetarians" at risk for depression?

2009-02-20T06:03:00.000-08:00

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.

Iron and restless legs

2009-02-18T00:57:00.000-08:00

It is becoming more well known that iron status and restless legs are connected. Many times when I share restless legs information on my Facebook page, someone will comment with a reminder of this connection.

I love that we're making a nutritional connection with such an uncomfortable problem.

However, it is important to remember, as was confirmed in a recent article reviewing numerous accepted treatments for restless legs, that iron supplementation is most likely to help the condition if there is a standing iron deficiency. If iron status is adequate, "topping off", so to speak, isn't going to fix the problem.

So....

...if you've got restless legs and you haven't checked your iron status, might be a good idea.

...if your iron levels are low, try an iron supplement.

However...

...if your iron status is fine, and/or you've tried the iron and your legs are still moving,

...consider that there are other options that may provide more relief.

Nutrition is a great place to start, and being well-nourished before trying medication is always a great strategy, but don't stop there if it doesn't turn out to be the answer.

Yes, the solution can be worse than the problem

2009-02-16T00:34:00.000-08:00

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]

More on zinc and depression

2009-02-09T11:40:00.000-08:00

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.

A little red meat may help your depression

2009-02-06T11:25:00.000-08:00

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.

Your medications and your genes

2009-02-04T11:54:00.000-08:00

DNA and genetics are not my areas of specialty but I found this study very interesting and wanted to share it. Anyone who does have expertise on this...please respond!

Alprazolam (Xanax), a popular tranquilizer, was recently reported to "intercalate" with DNA. I'm providing a link to a Wikipedia piece on what intercalation is...in short, I gather it means that somehow Xanax incorporates itself into the structure of DNA itself. Which would mean, that it potentially changes how the DNA expresses itself. This finding prompted the research to issue caution about the random use of Xanax.

Makes me wonder when I see all these medications that are associated with weight gain, if other medications have the same ability? And it also makes me wonder if other compounds, even certain foods, might also affect DNA structure and function.

It's a whole lot more complex than "eat less and exercise more"...which is why I love reporting on this specialty so much! There is always something new and different to share that provides a potential answer to someone doing a Google search.

Saha B, Mukherjee A, Santra CR, Chattopadhyay A, Ghosh AN, Choudhuri U, Karmakar P. Alprazolam intercalates into DNA. J Biomol Struct Dyn. 2009 Feb;26(4):421-30.

Do we need a kindler, gentler football?

2009-01-28T09:09:00.000-08:00

I'm going to let the New York Times do the talking today. I hate to see stories like this, because every time I do.....I wonder how we could use some simple nutritional therapies to minimize the chances of this kind of tragedy? I don't think it's all about nutrition, but I do think a good chunk of it might be.

http://www.nytimes.com/2009/01/28/sports/football/28brain.html?th&emc=th

Here's hoping some day, someone in a place to take action on that sentiment, has the money and the connections to actually do so.

Alzheimer's, sleep, and diabetes--three very interesting amigos

2009-01-27T00:01:00.000-08:00

I didn't realize until reading this abstract that Alzheimer's disease affects sleep patterns as well as memory. It makes sense, since adequate sleep is necessary in order to retain memory of information gained during the day.

The medication reviewed in this article is galantamine (Reminyl), and the authors suggest that it is important to time medication administration in order to gain maximum effectiveness and sleep. And, that certain medications help (and interfere with) sleep more than others.

Disrupted sleep can worsen diabetes. Since many people with Alzheimer's also have diabetes--in fact, the two diseases are starting to be recognized as being very strongly linked to each other--this connection between sleep and medication can be very important to understand.

My guess is that if you are on this blog looking for information about Alzheimer's, it is a loved one, not you, that the information is for. Here is the bottom line:
1. If your loved one had problems with sleep before being recommended or placed on medication, it might be a good idea to check with the prescribing physician to be sure this was taken into account when choosing which Alzheimer's medication to prescribe.
2. If your loved one has developed changes in sleep habits since starting an Alzheimer's medication, be sure to let the prescribing physician know.
3. If your loved one's diabetes has become worse despite diligent attention to medications and food intake, consider the influence of sleep or lack thereof.
4. Be sure to ask your physician and/or pharmacist if there is a time of day your particular medication needs to be taken for maximum effectiveness.

Nieoullon A, Bentué-Ferrer D, Bordet R, Tsolaki M, Förstl H. Importance of circadian rhythmicity in the cholinergic treatment of Alzheimer's disease: focus on galantamine*. Curr Med Res Opin. 2008 Dec;24(12):3357-67.

Which came first...the hair or the hormones?

2009-01-16T05:25:00.000-08:00

This abstract caught my eye because I also have a blog about polycystic ovary syndrome (PCOS) and finasteride is sometimes used to treat the hirsutism (hair growth in women) that this syndrome often causes. It has now been observed to have antipsychotic properties and is being proposed as a treatment for psychosis.

Antipsychotics are increasingly being used to treat depression, and at least 85% of women with PCOS have some kind of anxiety, depression, or other mood disorder associated with this diagnosis. If you have PCOS, please do not jump to the assumption that I am saying you are psychotic. What I am trying to point out here is that there is a huge mind-body connection in the syndrome that is often ignored. Physicians can be so compartmentalized with their treatments that they focus on the acne, the hair, the infertility...and completely ignore the moods, the mood swings, the associated disrupted eating patterns...and then they and their patients wonder why treatment is not successful.

I am posting this abstract to challenge anyone who treats PCOS to figure out what is going on in the brain of the woman with PCOS since it is, after all, the brain that controls hormones. Rather than mess with hormones and create even more problems, why aren't we going to the source and looking THERE for potential solutions? Let's make this the day we shift our thinking.

Bortolato M, Frau R, Orrù M, Bourov Y, Marrosu F, Mereu G, Devoto P, Gessa GL. Antipsychotic-like properties of 5-alpha-reductase inhibitors. Neuropsychopharmacology. 2008 Dec;33(13):3146-56. Epub 2008 Mar 19.

I chose the photo I did not to be funny, demeaning, or hurtful. I did it for the benefit of those who truly do not understand what many women go through because of their PCOS. Hair growth can be devastating and lead to horrible issues with self-image. Long ago it was often called "diabetes of the bearded ladies". If you can imagine what it's like to look in the mirror and feel as though you're losing your femininity, often at a time when you're trying to conceive and desiring to be attractive to your partner...it's a situation deserving of much more attention than it often gets by physicians.

Factors potentiating the risk of mirtazapine-associated restless legs syndrome.

2009-01-14T05:06:00.000-08:00

Restless leg syndrome (RLS) is a very annoying condition. I know, because I get it when I'm under stress. It strikes when I'm relaxing; my legs begin to move on their own as if I am a puppet and they are attached to strings.

Restless legs is officially classified as a sleep disorder. Those involuntary movements interfere with restful sleep. You can see the vicious cycle that can get started, as poor sleep can make a day more stressful, which can exacerbate restless legs, etc., etc.

So this article about risk factors for restless legs syndrome caught my eye on a recent cruise through the National Library of Medicine database.

In 181 records reviewed over a 3 1/2 year period, in individuals taking the antidepressant mirtazapine (Remeron), eight percent reported having RLS, tending to start within a few days of beginning mirtazapine therapy. This trend seemed to be more frequent if, in addition to mirtazapine, the individual was using tramadol and/or dopamine-blocking agents.

Be sure to let your physician know if you've noticed this syndrome developing. There are alternatives, pharmacological and non pharmacological, that won't steal your sleep in the name of making you feel better.

Kim SW, Shin IS, Kim JM, Park KH, Youn T, Yoon JS. Factors potentiating the risk of mirtazapine-associated restless legs syndrome. Hum Psychopharmacol. 2008 Oct;23(7):615-20.

Let's not play around with our adolescents!

2009-01-12T06:10:00.000-08:00

Methylphenidate (Ritalin) is a very common, in fact the most common, choice for treating attention deficit-hyperactivity disorder (ADHD). One of its major effects is to interfere with social interaction so that people with ADHD are not overly intrusive or disrespectful of normal social boundaries with others. A recent study of methylphenidate in adolescent rats showed that not only did this medication accomplish that goal, it interfered with social and play behaviors considered to be normal for these rats at this developmental stage. In other words, methylphenidate somewhat overshot the mark when it came to inhibiting pre-medicated behaviors.

Of course, to a parent who is frustrated and tired from managing a child whose behaviors have not demonstrated appropriate boundaries, this can be a welcome change. However, social interactions and recreational activities are important for teaching skills important to a productive adult life. Chemically denying a child these learning opportunities may create more problems later in life, when that child does not have the social skills that promote successful relationships, careers, and stress management.

I of course believe there are many options to consider before medication, and they are discussed elsewhere in this blog. If you do believe methylphenidate is the only rational solution to your child's situation, I would at least recommend closely observing your child's social behavior. If s/he has become a wallflower and swung completely in the opposite direction, at least discuss this change with the prescribing caregiver. There ARE other medications and options that can help set your child up for a successful adulthood...which is one of the primary responsibilities of responsible parenthood.

Vanderschuren LJ, Trezza V, Griffioen-Roose S, Schiepers OJ, Van Leeuwen N, De Vries TJ, Schoffelmeer AN. Methylphenidate disrupts social play behavior in adolescent rats. Neuropsychopharmacology. 2008 Nov;33(12):2946-56. Epub 2008 Feb 27.

Sweet dreams for fewer migraines

2009-01-09T05:24:00.000-08:00

If you've ever had a migraine, you know they're debilitating. I get them. When they come, my vision gets squirrely, my thinking gets fuzzy, and all I want to do is sleep. I'm completely useless for as long as one chooses to stick around.

I've tried the pharmaceutical options, and while they worked, I always wished that there was a natural solution. For me, that solution came with changing my work situation, moderating caffeine intake, stress management, and incorporating yoga into my activity routine. When I found this article, I realized that I've also been better to myself when it comes to sleep, and not cutting myself short in that department. Maybe that's part of the reason I rarely have migraines anymore.

The scientists in this study gave a 3 mg dose of melatonin to 22 children who complained of regular migraine or tension-type headaches. By the time the study was over, 3 months later, 2/3 of the subjects reported a decrease in headache frequency of 50%, and 4 subjects reported having no headaches at all.

Of course, you can go out and buy some melatonin. But what I'd recommend, first of all, is taking a good hard look at your sleep habits. Are you giving yourself at least 7 hours of sleep a night? Or are you hooked on late night TV? Are you sitting in bed with your laptop surfing the net when you should be dreaming?

It's an easy solution for a serious and unpleasant problem. Take care of your head--and your head won't have to hit you where it hurts to get your attention.

Miano S, Parisi P, Pelliccia A, Luchetti A, Paolino MC, Villa MP. Melatonin to prevent migraine or tension-type headache in children. Neurol Sci. 2008 Sep;29(4):285-7. Epub 2008 Sep 20.

Thanks to all of you and Happy 2009!

2009-01-01T05:00:00.000-08:00

Hello readers,

I had no idea whatsoever that my random posts about mental health would gain so much readership. In one short year this blog has grown from a reader here and there to 1300 readers from 112 countries, and 1600 page views per month.

Thank you so much for your interest!

I can tell by the comments you take the time to post, that you are all sincerely desiring to take control of your health. I understand the responsibility that goes with that kind of trust, given the diagnoses and medications I address when I write. I hope as 2009 progresses that I continue to write about meaningful topics that give you inspiration and tangible ideas for actions you can take in your respective lives.

Please do let me know how I can improve on this blog, and please comment where you see fit. This blog is a community effort, steered by the interests of you, the readers.

Happy New Year everyone!

Eat your veggies and sleep!

2008-12-23T08:07:00.001-08:00

I've become fascinated with sleep. How much we need it. How little we value it. And what happens to our health when we don't get it. Sometimes I wonder if we should be obsessed with sleep and not worried about what we eat.

Now the two worlds have collided!

It has been found that melatonin is a component of some vegetables. Some Japanese researchers gave a group of women high amounts of six specific vegetables. Another group of women was asked to avoid these same vegetables during the same time period. The women who consumed the vegetables had higher amounts of melatonin by-products in their urine.

Melatonin, as you know from reading this blog, is a sleep enhancing hormone and a very powerful antioxidant.

Of course, the very first thing most people will ask on reading this, is "what vegetables?"

I don't think the power in this study comes from the melatonin content of the vegetables. Melatonin is a highly unstable compound and it would be challenging to have it stay intact in a compound that is harvested, stored, chopped, and cooked before eating.

What may be happening here, is that vegetables are great sources of antioxidants. And since melatonin appears to be the ultimate antioxidant, it is called to duty when other antioxidants are in short supply and cannot do their job. If your melatonin is on cleanup duty, it can't be used to help you sleep!

The melatonin in the urine, I'm guessing, came from the fact that melatonin was allowed to function as melatonin, and not changed as it was used as an antioxidant.

So...the strategy appears to be, to eat as many different vegetables as you can in order to have maximum antioxidant power. And that will give you a better chance at getting a good night's sleep.

I know that it's difficult not to yawn if you see someone else yawning, so on behalf of helping you feel sleepy, here's a wonderful blog a friend told me about yesterday!
It's called Cute Things Falling Asleep.

Oba S, Nakamura K, Sahashi Y, Hattori A, Nagata C. Consumption of vegetables alters morning urinary 6-sulfatoxymelatonin concentration. J Pineal Res. 2008 Aug;45(1):17-23. Epub 2008 Jan 15.

Some updates on fish oil

2008-12-17T07:03:00.000-08:00

This article is from the following link:

It pretty much answers any questions I'd answer about fish oil so this morning Nutraingredients and ConsumerLab get credit for having built the best mousetrap!

ConsumerLab releases omega-3 test results
By Lorraine Heller, 05-Aug-2008

Related topics: Industry, Nutritional lipids and oils, Cardiovascular health, Cognitive and mental function

Independent product tester ConsumerLab.com has given the thumbs up to almost 50 omega-3 dietary supplements and functional foods for delivering on dosage and being contaminant-free.

The report, released today, is the group’s most comprehensive analysis of fish oils to date, said ConsumerLab president Tod Cooperman. The large majority (85 percent) of visitors to the organization's site are consumers looking for independent information on which products to purchase.

A total of 50 omega-3 fish oil supplements, foods and beverages were tested for contaminants and dosage (including two marketed for pets). Out of these, 23 were randomly selected by ConsumerLab to provide a “snapshot” of the market based on popular products found at different retail outlets. The other 27 products were tested at the request of their manufacturers, through ConsumerLab’s Voluntary Certification Program.

According to the results, all products met their label claims in regard to EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) levels, with levels ranging from16 mg in a yogurt product to 1,000mg in a single pill.

In addition, all of the products tested were free of contaminants common in fish, including mercury, lead and PCBs. These contaminants have been associated with fish oil supplements in the past, and Consumerlab suggested cleaner fish stocks as well as improved processing had contributed to the glowing report card.

Not approved

All products tested bar one supplement brand and one product for pets received an approval rating from ConsumerLab.

The supplement brand that did not pass was Kirkland Signature Enteric Coated Fish Oil 1700 mg Concentrated Fish Oil. This, said ConsumerLab, was found to contain the level of EPA and DHA that it claimed, but it failed the enteric-coating test because it released its fish oil too early.

In accordance with ConsumerLab’s certification program guidelines, the group is able to announce the positive test results of brands that are volunteered by their manufacturers, but any negative results remain confidential.

Cooperman would not confirm if any of the omega-3 products provided for testing by their manufacturers failed the approval rating, but said that a clear indication of the state of the industry can be received from the 23 randomly selected products tested by the group.

In addition, he noted that the report clearly identifies which products were volunteered, and which were selected.

Questions raised

The report also took issue with some food and drink products that claimed to provide portions of a daily intake of omega-3s, when such a value has yet to be established.

According to ConsumerLab, fortified foods and beverages including Tropicana with Omega-3, Silk Soymilk Plus Omega-3 DHA, Yoplait Kids Yogurt with DHA, and the Aristo nutrition bar stated on labels that they supplied certain percentages of the ‘Daily Value’ of 160 mg for EPA and DHA.

“These statements are incorrect,” said ConsumerLab. “A Daily Value has not been established for EPA and/or DHA. Silk Soymilk Plus Omega-3 DHA also touted "400 mg beneficial Omega-3" above its Nutrition Facts panel, but only at the bottom of the other side of the carton did it note, in tiny letters, that just 32 mg of the total omega-3 is DHA. Testing found the remainder to be ALA.”

The160mg daily benchmark value was provided by the Institute of Medicine (IOM) in its Dietary Reference Intakes for Macronutrients, published in 2002. However, other organizations, such as the International Society for the Study of Fatty Acids and Lipids and the American Dietetic Association, recommend a minimum combined intake of 500 mg/day EPA and DHA to support heart health.

According to Robert Orr, president and CEO of leading omega-3 supplier Ocean Nutrition and also chair of GOED (the Global Organization for EPA and DHA Omega-3) said this highlights the need for national guidelines for omega-3 intake.

The issue is not so much which levels are currently being thrown around as reference levels, but the need to establish an RDI, he suggested. “The focus needs to be on the fact that there is a huge dietary deficiency,” he told NutraIngredients-USA.com earlier today.

Brands tested

Brands included in the ConsumerLab report are: Advocare, Aristo, Berkley & Jensen (BJ’s), Carlson, Coromega, CVS, Eniva, GNC, Health from the Sea, Iceland Health, Integrative Therapeutics, Jarrow, Great American Products, Healthy Hide, Kirkland (Costco), Lipiderm, Mega Smarts, Minami, Mommy’s Bliss, Natural Factors, Nature Made, Nature’s Bounty, Nature’s Sunshine, New Chapter, Nordic Naturals, Now, Nutramax, Nutri-Supreme, OmegaBrite, Omega-Gel, Origin (Target), PharmAssure, Pharmanex, Pure Encapsulations, Puritan’s Pride, Shaklee, Silk (WhiteWave), Spring Valley (Wal-Mart) Sundown, Swanson, Tropicana, Twinlab, USANA, Vital Oils, Vitamin Shoppe, Vitamin World, Wegmans, Weil, and Yoplait.

Being a banana brain just might be a good thing

2008-12-15T10:21:00.000-08:00

Pyridoxine, a form of vitamin B6, is important for brain and nervous system function. It is needed for the chemical reactions that produce several neurotransmitters, including serotonin, dopamine, and norepinephrine. A recent study found that a therapeutic dose of pyridoxine administered to mice decreased their depressive-type behaviors. The response was similar to what was seen when these mice were given imipramine (Tofranil). When the two compounds were administered together, pyridoxine did NOT increase the effectiveness of imipramine.

Bottom line? Before meds, be sure your diet is balanced in the nutrients your brain needs to properly function.

The table below is from the National Institutes of Health, and it lists your best food sources of pyridoxine.

Table of Food Sources of Vitamin B6
Food Milligrams (mg) per serving % DV*
Ready-to-eat cereal, 100% fortified, ¾ c 2.00 100
Potato, Baked, flesh and skin, 1 medium 0.70 35
Banana, raw, 1 medium 0.68 34
Garbanzo beans, canned, ½ c 0.57 30
Chicken breast, meat only, cooked, ½ breast 0.52 25
Ready-to-eat cereal, 25% fortified, ¾ c 0.50 25
Oatmeal, instant, fortified, 1 packet 0.42 20
Pork loin, lean only, cooked, 3 oz 0.42 20
Roast beef, eye of round, cooked, 3 oz 0.32 15
Trout, rainbow, cooked, 3 oz 0.29 15
Sunflower seeds, kernels, dry roasted, 1 oz 0.23 10
Spinach, frozen, cooked, ½ c 0.14 8
Tomato juice, canned, 6 oz 0.20 10
Avocado, raw, sliced, ½ cup 0.20 10
Salmon, Sockeye, cooked, 3 oz 0.19 10
Tuna, canned in water, drained solids, 3 oz 0.18 10
Wheat bran, crude or unprocessed, ¼ c 0.18 10
Peanut butter, smooth, 2 Tbs. 0.15 8
Walnuts, English/Persian, 1 oz 0.15 8
Soybeans, green, boiled, drained, ½ c 0.05 2
Lima beans, frozen, cooked, drained, ½ c 0.10 6

* DV = Daily Value. DVs are reference numbers based on the Recommended Dietary Allowance (RDA). They were developed to help consumers determine if a food contains a lot or a little of a specific nutrient. The DV for vitamin B6 is 2.0 milligrams (mg). The percent DV (%DV) listed on the nutrition facts panel of food labels tells you what percentage of the DV is provided in one serving. Percent DVs are based on a 2,000 calorie diet. Your Daily Values may be higher or lower depending on your calorie needs. Foods that provide lower percentages of the DV also contribute to a healthful diet.

Amara RO, Aburawi SM. Pyridoxine effect on the antidepressant action of imipramine in albino mice. Saudi Med J. 2008 Nov;29(11):1554-7.

Qnexa--The next frontier in weight management drugs--or is it?

2008-12-11T18:28:00.000-08:00

Below my pontificating you will see a press release for a new weight loss medication, Qnexa.

My initial impressions:

1. This looks like the new twist on the old "phen-fen," phentermine being the common ingredient in both, with the problem compound, fenfluramine, being replaced with topiramate (Topamax). Topiramate is a mood stabilizing drug that has been found to have weight loss effects in some people and has been used in an off-label fashion for this purpose.

2. For the record, I've collected a bunch of references on potential side effects reported with topiramate, including: kidney stones, reduced testosterone in males, dry mouth, nausea, reduced sweating, body temperature regulation (which could become an issue if you're following directions and exercising more), cerebellar cognitive affective syndrome, and delusional parasitosis. (That's when you have the creepy feeling that bugs are crawling all over you when none are there.) References are provided below.

3. People aren't overweight because they have phentermine or topiramate deficiencies. Obesity is a huge target for drug research because there's such a huge market--it's a gold mine for anyone who can create and patent a medication that can stay on the market without its negative side effects forcing it to be yanked. My concern is once this med is used in large numbers some of these side effects are going to become huge problems.

4. Just beware if you decide to try this medication when it becomes available. It's not 100% foolproof. Anyone who prescribes you this medication without advising you of these potential problems may not fully understand how this medication works. And that's your red flag of a potential problem. Be informed!

Otoom S, Batieneh H, Hassan Z, Daoud A. Effects of long-term use Topiramate on fertility and growth parameter in adult male rats. Neuro Endocrinol Lett. 2004 Oct;25(5):351-5.

Sharief M, Viteri C, Ben-Menachem E, Weber M, Reife R, Pledger G, Karim R. Double-blind, placebo-controlled study of topiramate in patients with refractory partial epilepsy. Epilepsy Res 1996 Nov;25(3): 217-24.

Incecik F, Herguner MO, Altunbasak S. Topiramate associated hypohidrosis and hyperthermia. Indian Pediatr. 2008 Mar;45(3):238-40.

Cerminara C, Seri S, Bombardieri R, Pinci M, Curatolo P. Hypohidrosis during topiramate treatment: a rare and reversible side effect. Pediatr Neurol 2006 May;34(5):392-4.

Baillieux H, Verslegers W, Paquier P, De Deyn PP, Mariën P. Cerebellar cognitive affective syndrome associated with topiramate. Clin Neurol Neurosurg. 2008 May;110(5):496-9.

Fleury V, Wayte J, Kiley M. Topiramate-induced delusional parasitosis. J Clin Neurosci. 2008 May;15(5):597-9.

Vega D, Maalouf NM, Sakhaee K. Increased propensity for calcium phosphate kidney stones with topiramate use. Expert Opin Drug Saf 2007 Sep;6(5):547-57.

Koçer A, Dikici S, Atakay S, Okuyucu E. Serum Uric Acid and Lipid Levels While Taking Topiramate for Migraine. Headache. 2007 Dec 27.

Qnexa Meets Primary Endpoint by Demonstrating Superior Weight Loss over
Components and Placebo in the 28-Week Equate Study (OB-301)

Subjects on Full-Dose Qnexa Attained an Average Weight Loss of 9.2% with
66% Achieving 5% or Greater Weight Loss

MOUNTAIN VIEW, Calif.--(BUSINESS WIRE)--Dec 11, 2008 - VIVUS, Inc.
(NASDAQ: VVUS), a pharmaceutical company dedicated to the development
and commercialization of novel therapeutic products, today announced
positive results from the EQUATE study (OB-301), a 28-week, phase 3
obesity trial conducted at 32 sites with QnexaTM, an investigational
drug. The EQUATE study met the primary endpoint by demonstrating
superior weight loss with both the full-dose and mid-dose of Qnexa, as
compared to the individual components and placebo. Subjects treated with
full-dose and mid-dose Qnexa had an average weight loss of 9.2% and 8.5%
respectively, as compared to weight loss of 1.7% reported in the placebo
group (ITT LOCF p<0.0001). Average weight loss was 19.8 pounds and 18.2
pounds in the treatment arms as compared to 3.3 pounds in the placebo
group. Qnexa was well-tolerated, with no drug-related serious adverse
events in the study.

"The results from the EQUATE trial once again confirmed our belief in
Qnexa. In addition to hitting the primary endpoints of the study with
the full-dose, we were also able to show excellent results with the
mid-dose of Qnexa," commented Leland Wilson, president and chief
executive officer of VIVUS. "The EQUATE study is the first of three
studies in the Qnexa phase 3 obesity program. Data from the EQUIP and
CONQUER studies, which combined enrolled over 3,750 subjects, is
expected in mid-2009."

The EQUATE study included 756 obese subjects (599 females and 157 males)
across 32 centers in the United States. The average baseline BMI of the
study population was 36.3 kg/ m2 and baseline weight was 223 pounds. The
proportion of patients losing 5% or more of their initial body weight
was 66% for full-dose, 62% for mid-dose and 15% for placebo (p<0.0001).
The proportion of patients losing 10% or more of their initial body
weight was 41% for full-dose, 39% for mid-dose and 7% for the placebo
group (p<0.0001).

The most common drug-related adverse events reported for the full-dose,
mid-dose and placebo group were paresthesia (20%, 15%, 3%), dry mouth
(18%, 12%, 0%), altered taste (15%, 8%, 0%) and constipation (11%, 6%,
6%). Reported drug related adverse events for depression and altered
mood were minimal (1.9%, 0.9% and 1.8% respectively) . Moreover,
individual depression assessments for each subject, as measured by
PHQ-9, demonstrated statistically significant improvements (p<0.05) from
baseline for both Qnexa treatment groups. Overall average completion
rate for the Qnexa treatment group was 71%.

Subjects in the EQUATE study had a 4-week dose titration period followed
by 24 weeks of treatment. The study was a randomized, double-blind,
placebo-controlled, 7-arm, prospective trial with subjects randomized to
receive once-a-day treatment with mid-dose Qnexa (7.5 mg phentermine/ 46
mg topiramate CR), full-dose Qnexa (15 mg phentermine/ 92 mg topiramate
CR), the respective phentermine and topiramate constituents, or placebo.
Subjects were asked to follow a hypocaloric diet representing a
500-calorie/ day deficit and advised to implement a simple lifestyle
modification program.

About the Qnexa Phase 3 Obesity Program

In addition to the EQUATE study, the phase 3 Qnexa program includes two
pivotal, double-blind, placebo-controlled, multi-center studies that
will compare the efficacy and safety of Qnexa to placebo during a
56-week treatment period. The first year long study, known as EQUIP
(OB-302), has enrolled approximately 1,250 morbidly obese adult subjects
with a Body Mass Index (BMI) of 35 or greater with or without controlled
co-morbidities. The second trial, known as CONQUER (OB-303), has
enrolled overweight and obese adult subjects with BMIs from 27 to 45 and
at least two co-morbid conditions, such as hypertension, dyslipidemia
and type 2 diabetes. The co-primary endpoints for these studies are the
mean percent weight loss and the percentage of subjects achieving a
weight loss of five percent or more. Results from these studies are
expected mid-2009. In total the phase 3 program has enrolled
approximately 4,500 subjects.

VIVUS R&D Day December 12, 2008

As previously announced, VIVUS will host a Research and Development Day
Event on Friday, December 12, 2008 at 8:00 a.m. ET in New York City.
Additional details on the data released today will be presented.

To access the webcast of this event, please visit:
http://phx.corporat e-ir.net/ phoenix.zhtml? p=irol-eventDeta ils&c=79161& ev
entID=2046581 or VIVUS' Investors site at http://www.vivus. com. Replay
will also be available on demand from the website at the conclusion of
the program and will run through December 31, 2008.

If you are interested in attending, please contact Brian Korb at The
Trout Group at 646 378 2923 or bkorb@troutgroup. com.

About VIVUS

VIVUS, Inc. is a pharmaceutical company dedicated to the development and
commercialization of novel therapeutic products. The current portfolio
includes investigational product candidates addressing obesity, diabetes
and sexual health. The investigational pipeline includes: QnexaTM, which
is in phase 3, for the treatment of obesity and has completed a phase 2
study for the treatment of type 2 diabetes; avanafil, for which a phase
2 study has been completed for the treatment of erectile dysfunction
("ED") and LuramistTM (Testosterone MDTS(r)), for which a phase 2 study
has been completed for the treatment of Hypoactive Sexual Desire
Disorder ("HSDD"). MUSE(r) is approved and currently on the market for
the treatment of ED. For more information on clinical trials and
products, please visit the company's web site at http://www.vivus. com/.

Certain statements in this press release are forward-looking within the
meaning of the Private Securities Litigation Reform Act of 1995. These
statements may be identified by the use of forward-looking words such as
"anticipate, " "believe," "forecast," "estimated" and "intend," among
others. These forward-looking statements are based on VIVUS' current
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VIVUS does not undertake an obligation to update or revise any
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periodic reports filed with the Securities and Exchange Commission.

Safely using eicosapentaenoic acid (fish oil) for schizophrenia

2008-12-10T08:33:00.000-08:00

Fish oil, primarily eicosapentaenoic acid (EPA) is gaining popularity as a natural treatment for schizophrenia. (Before I continue, just want to say I have to be very careful with this post because I don't want to encourage anyone who needs to be on antipsychotics to read that I'm saying to discontinue them--I AM NOT!)

Because of this popularity, a prominent group of schizophrenia researchers in the UK decided to evaluate whether or not therapeutic doses of EPA produced any safety issues for its users. They divided 84 individuals with schizophrenia into two groups; one group received 2 grams EPA per day along with their antipsychotic, the other received a placebo along with their medication.

Those individuals receiving EPA experienced a trend toward decreased total cholesterol and HDL. Weight tended to increase. And their bleeding time increased, meaning it took longer for their blood to clot when they cut themselves.

Here are some thoughts to take away from this study.

1. 2 grams daily of EPA is a very high dose. Most over the counter capsules have about 10% of that amount. This was a very specific protocol unlikely to be randomly adopted by the average person.

2. If you have ever had any issues with blood clotting, or are on any type of medication that affects clotting time, such as Coumadin, it is very important to work with your prescribing physician in order to coordinate appropriate dosages of medications and supplements.

3. I'm not working with critically ill schizophrenics on an outpatient basis, so I have the liberty of starting low and upping doses to evaluate for tolerance. I tend to work with a mixture of dietary fats and fish oils and not use such a specific, directed protocol. I feel much safer with that. But I am always on the lookout for the kinds of reactions that this study produced.

4. What is not known is whether or not all the subjects were on the same antipsychotic, or for how long before starting this study. Each antipsychotic has a slightly different effect on lipids, weight, and hormones, and that information would likely affect the results that were reported.

Overall, I'd say the most important finding in this study was the effect of super-high doses of EPA on clotting time. Because EPA has been getting more attention for its potential in treating bipolar disorder and schizophrenia, it is showing up more and more as a single supplement rather than as a component of fish oil. There is a tendency to use the "more is better" approach and to assume that if it's natural, and it's over the counter, it's safe. That may or may not be true with EPA, and it should be used judiciously.

Emsley R, Niehaus DJ, Oosthuizen PP, Koen L, Ascott-Evans B, Chiliza B, van Rensburg SJ, Smit RM. Safety of the omega-3 fatty acid, eicosapentaenoic acid (EPA) in psychiatric patients: Results from a randomized, placebo-controlled trial. Psychiatry Res. 2008 Dec 15;161(3):284-91. Epub 2008 Oct 29.

Another "because" to put on my long list of reasons to eat hummous

2008-12-08T05:09:00.000-08:00

All of my clients know that of all the foods on the famous internet glycemic index list, hummous is the one that scores the most favorable. It's got garbanzo beans, a great high protein/carb combo food, olive oil, a healthy fat...and in many cases, tahini, which is also packed with health potential.

Tahini is a paste made from sesame seeds, and sesame seeds contain a compound called sesamin. Sesamin has been found to help take vegetarian omega-3's and convert them into the omega-3's more commonly associated with fish oil. This conversion almost always exists to some degree, but nutritionists have always questioned whether the conversion is efficient enough to provide adequate DHA and EPA for human needs.

One interesting disclaimer I should add here...this conversion was tested in salmon as a potential way to increase the DHA content of salmon. The process has yet to be proven in humans. Even so, it doesn't seem like it would hurt to add a little bit of sesame seed to your own program. It's when sesame OIL is extracted from seeds and used in large quantities that you can override the benefits with potential disadvantages.

I don't know if I'm ready to say if you eat hummous you can stop eating fish, but I can say that hummous definitely helps to improve your omega-3 balance, and it's certainly a most tasty way of doing it!

For some more ideas on how to get more sesame seeds onto your plate, check out one of my favorite websites, World's Healthiest Foods.

Trattner S, Ruyter B, Ostbye TK, Gjøen T, Zlabek V, Kamal-Eldin A, Pickova J. Sesamin Increases Alpha-Linolenic Acid Conversion to Docosahexaenoic Acid in Atlantic Salmon (Salmo salar L.) Hepatocytes: Role of Altered Gene Expression. Lipids. 2008 Nov;43(11):999-1008. Epub 2008 Sep 11.

Which came first, the high glucose or the depression?

2008-12-05T05:09:00.000-08:00

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.

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

2008-12-03T04:36:00.000-08:00

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.

Information for aviation professionals

2008-12-01T07:09:00.000-08:00

If any of you know anyone who is a flight attendant or a pilot, I wanted to let you know I've launched a new endeavor to address their specific needs. In all the years I've done my work, this profession consistently stands out as one at great risk for health issues...and when mental health issues hit they can end an aviator's career.

My partner in this business and I want to provide ideas and support to help lengthen some of those careers and enrich the lives of those who sacrifice much so we can get where we need to. We'll be covering everything from eating well to conquering sleep disorders to stress management.

If you are interested, or know someone who might be, please check us out!

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

2008-11-28T06:12:00.000-08:00

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

Zinc KO's Prozac in the fight against depression

2008-11-26T06:29:00.000-08:00

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.

I coulda had a V8--er--fish oil pill

2008-11-24T10:24:00.000-08:00

There's a part of me that knows that as long as science continues to do things the way it does things, I have journalistic job security.

But the heart inside me really wishes they'd get it so I could trash this blog and head for an isolated Costa Rican beach until I find another pressing issue to blog about.

What I mean by "getting it" is that the reason we're so sick as a culture is not because we're not taking enough medicine, or that we haven't created the perfect medicine. It's because the perfect medicine is sitting right under our noses and we refuse to acknowledge it because it won't give the people who make money off of people being sick...a patent or a respectable profit margin.

Someone who sees things the same way finally got his words into a peer-reviewed journal.

He reports that you can reduce the incidence of heart attack if you get people to take, in combination,
a statin medication,
three different blood pressure medications,
a folic acid supplement, and
an aspirin.

This brave new concoction has been called the "polypill". Yikes! It doesn't take long even for someone who hates math to figure out how many people THAT marketing...um..."treatment" approach employs.

In the words of the author delivering this breaking news,

Unlike the proposed "polypill", EFAs are endogenous molecules present in almost all tissues, have no significant or few side effects, can be taken orally for long periods of time even by pregnant women, lactating mothers, and infants, children, and adults; and have been known to reduce the incidence cardiovascular diseases including stroke.

I propose that a rational combination of omega-3 and omega-6 fatty acids and the co-factors that are necessary for their appropriate action/metabolism is as beneficial as that of the combined use of a statin, thiazide, a beta blocker, and an angiotensin converting enzyme (ACE) inhibitor, folic acid, and aspirin. Furthermore, appropriate combination of omega-3 and omega-6 fatty acids may even show additional benefits in the form of protection from depression, schizophrenia, Alzheimer's disease, and enhances cognitive function; and serve as endogenous anti-inflammatory molecules; and could be administered from childhood for life long.

Sigh...wonder how many pharmaceutical company trash cans that brilliant idea ended up in?

Fortunately, you can decide if you want to support your own health with this idea. It is available over the counter. It's totally up to you.

Das UN. Essential fatty acids and their metabolites could function as endogenous HMG-CoA reductase and ACE enzyme inhibitors, anti-arrhythmic, anti-hypertensive, anti-atherosclerotic, anti-inflammatory, cytoprotective, and cardioprotective molecules. Lipids Health Dis. 2008 Oct 15;7:37.

Fatty aspirin: a new perspective in the prevention of dementia of Alzheimer's type?

2008-11-21T06:30:00.000-08:00

One of the reasons many nutritional therapies don't get much research attention is that research studies need to be funded. And the biggest bank accounts to be accessed for those funds are those held by companies who can get a return on their investment for supporting that research. In other words, if a company can invest research in a project that results in a chemical that can be patented and sold at a profit, there's a motivation to spend money in that way.

You can't patent a salmon.

And if you saw the way my pecan farming friends managed their businesses here in Arizona...a few pecans here, a bed and breakfast there...not really multi-million dollar enterprises.

So it makes sense that some of the best answers to medical problems are likely not going to show up in medical journals. For all their good intent and peer reviews, these journals are often promotional venues for the companies funding the studies they report on. Those promotions just aren't formatted as advertisements.

But I always wonder when reading all these studies, why the Reese's Peanut Butter Cup Effect hasn't happened. What I mean by that is, if there is a little bit of (very strong) evidence to support natural remedies such as fish oil and herbs, why these drug companies don't come up with combinations of supplements and medications that (1) increase the effectiveness of the treatment, (2) reduce the side effects that minimize drug compliance, like weight gain, and (3) engage the interest of people who don't necessarily want to take medications but might consider them if the natural remedies they DO trust were somehow incorporated into the treatment? Just like the old, "You got chocolate in my peanut butter" ads.

Here is a reference for such a combo, a "fatty aspirin", or fish oil-aspirin combination, that could be used to delay the development of Alzheimer's disease.

OK, in that case I can't say you heard it here first, but when you guys start coming up with fatty antipsychotics, fatty antidepressants, yadayada...and you know it's eventually going to happen...you know where to send the royalty check!

Pomponi M, Di Gioia A, Bria P, Pomponi MF. Fatty aspirin: a new perspective in the prevention of dementia of Alzheimer's type? Curr Alzheimer Res. 2008 Oct;5(5):422-31.

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

2008-11-19T05:30:00.000-08:00

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?

Pregnant women and psychotropic medications really don't mix

2008-11-17T06:30:00.000-08:00

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.

An alternative to that nasty CPAP machine

2008-11-14T07:40:00.000-08:00

A recent USA Today article reported that the use of continuous positive airway pressure (CPAP) machines is up 96% nationwide since 2004.

I'm not sure if that means our sleep quality has plummeted in just 4 short years, or if the pharmaceutical and medical equipment industries have recognized what I've recognized...that we're sleeping a whole lot less than we used to...and should. Problem is, these industries appear to be viewing this alarming trend as an amazing profit center instead of a huge problem we need to solve in less invasive ways...and they've gone after it full force.

I do know that people with mental health issues are more prone to sleep disorders. So anyone reading this blog is likely to be high-risk for having this kind of problem.

I don't know about you, but heading off to bed every night feeling like I've just left the wardrobe room for "Top Gun" doesn't sound like a long-term solution for sleep apnea. As the USA Today article states, sleep disorders are associated with a whole host of other serious problems. So they cannot be ignored. But I just can't accept that these awful masks should be the first line of treatment, or the only option offered to patients, especially those who travel frequently.

Enter the dental profession!

Diane Whelan, my partner on this blog, recently introduced me to Dr. Michael Simmons, a dentist near her, who offers some interesting and more viable options. Dr. Simmons is the Director of Pre-doctoral studies in Dental Sleep Medicine at UCLA, so the topic of sleep disorders is a focus of his practice.

Dr. Simmons provides a CPAP option called Oral Appliance Therapy, or OAT. The device is similar to a retainer, worn at night to help reposition the tongue, which serves to open the airway. The American Academy of Sleep Medicine actually considers OAT to be the best alternative treatment to CPAP for mild to moderate obstructive sleep apnea.

There are over-the-counter devices purported to be equally effective, but Dr. Simmons advises that studies are showing that in order for these devices to be effective, custom fitting by a trained dentist needs to be part of the protocol. A one-size-fits-all device is not likely to help.

For blog readers who also happen to be struggling with infertility, it seems as though removing the mask might help enhance the romance a bit. :)

Given a choice between schlepping with a bulky CPAP machine or slipping a simple dental device into your mouth, I'd be willing to bet a dentist like Dr. Simmons can be a great investment in your own career longevity.

Proper screening, fitting, and followup for OAT requires about 4 visits. You can contact Dr. Simmons at the link above for information on pricing, appointments, etc.

Weight change in Parkinson and Alzheimer patients taking atypical antipsychotic drugs.

2008-11-12T06:00:00.000-08:00

As much trouble as I have with indiscriminate use of antipsychotic medications, I do think they have important uses in certain situations, and that we have to be very careful about overgeneralizing their negative aspects.

For example, these medications are increasingly being used to help control side effects in some serious illnesses such as Parkinson's disease and Alzheimer's disease. In some cases, especially when not managing these side effects can make things hard to manage for these individuals' caregivers (who are often family in a home situation), it is important to balance considerations about overall quality of care, caregiver sanity and health, and weight. Each situation is different, and there are no easy answers.

Sixty-one Parkinson's patients on either quetiapine (Seroquel) or clozapine (Clozaril) for at least six months were compared to 28 Alzheimer's patients in similar situations. The weight changes, though small, were statistically significant. Parkinson's patients trended toward weight loss compared to controls, and Alzheimer's patients trended toward weight gain.

It may not be that these medications cause weight changes in one direction or the other...but rather, they foster metabolism moving in a direction that genetic tendency long ago pre-programmed. It is important to not be afraid of a medication that can help ease the life of the caregiver. Of course, judicious use and close monitoring are always the caveats that go with any medication decision. Alzheimer's patients seem to be prone to developing diabetes and that should not be ignored.

I was glad to see this study attempt to parse out exactly what these medications do and why. That's a great use of scientific minds.

Sitburana O, Rountree S, Ondo WG. Weight change in Parkinson and Alzheimer patients taking atypical antipsychotic drugs. J Neurol Sci. 2008 Sep 15;272(1-2):77-82. Epub 2008 Jun 16.

Smoking reduces serum levels of lamotrigine.

2008-11-11T14:17:00.001-08:00

If you smoke, and you are using seizure medications, take notice--smoking was shown in a recent study to reduce blood levels of lamotrigine (Lamictal). That means that, in order for the medication to be effective in a smoker, you need more of it.

The obvious solution here...is to quit smoking. You'll save money on cigarettes as well as medication. Hopefully at some level any smokers reading this will file this information into their "reasons to quit" pile and eventually think about doing so!

Reinsberger C, Dorn T, Krämer G. Smoking reduces serum levels of lamotrigine. Seizure. 2008 Oct;17(7):651-3.

Television, epilepsy, and children

2008-11-10T06:30:00.000-08:00

When I first read the title to this abstract I knew I had to use it in the blog. Here scientists have determined that television exposure can cause epilepsy in some children...and instead of working to minimize exposure to the trigger, they're looking for a pill that allows the child to continue the behavior causing the problem.

I could tell you what medication was found to be most effective, but that would make me part of the problem. If you're a parent who knows your kid's brain doesn't tolerate television...get rid of the television and teach him how to otherwise spend his free time! Here's a concept, interact with him like parents used to do in the old days.

That's kind of how we do things anymore, isn't it?

We know too much food can cause weight gain, but rather than stop eating...we spend billions of dollars looking for ways to allow us to, quite literally, have our cake and eat it too.

We know we need a minimum amount of sleep in order to properly function. But in this day and age of 24 hour schedules, a whole new pharmaceutical specialty has sprung up, medications that drive wakefulness in people who simply need to make more time for sleep.

Instead of suggesting to the parents of these children that they might best be encouraged to learn to play the piano, play a sport, or, God forbid...READ...we want to figure out how to medicate the kids so they stay on our revenue-generating map.

I give up. But what I would like to request, if we're going to encourage studies like this one and call it science, is that we at least make the study designs interesting for the reader.

I mean, if kids who probably shouldn't be watching television are allowed to watch television anyway because they're another important profit niche for certain drug manufacturers, wouldn't it be more important to know whether Sesame Street or Spongebob Squarepants is more effective at creating seizures? Seems to me that kind of information could be really important when it comes to marketing plans. Not just for the drug companies but all those companies who love to use those programs to sell junk to kids, who need to hold on to their audience.

The best part is going to be when Bert and Ernie are called to testify in court. Now THAT will be television worth watching.

Etemadifar M, Raoufi M, Maghzi AH, Ebrahimi A, Kaji-Esfahani M, Mousavi SA. Television-provoked epilepsy in children: a follow-up survey from isfahan, iran. Arch Iran Med. 2008 Nov;11(6):649-53.

Your brain loves lipoic acid!

2008-11-07T06:00:00.000-08:00

I'm primarily a food first, supplements second kind of person. However, lipoic acid is a supplement I love to recommend. It's not something that you can readily find in food, but it does a whole lot of good, especially in the brain.

It can delay and prevent Alzheimer's disease, and dementia, in a variety of ways. It helps to increase acetylcholine levels. Acetylcholine is the neurotransmitter in charge of memory function. It helps to bind free radicals, preventing them from doing damage. It prevents the formation of proteins associated with inflammation.

Not a bad friend, is it?

The amount given in the two studies evaluating lipoic acid's effect on the brain was 600 mg per day.

Lipoic acid is also unique in that it has the ability to make other antioxidants more powerful. The authors of the article reviewed here suggested that in combination with curcumin, EGCG (active ingredient in green tea), and DHA (in fish oil and marine algae), lipoic acid could be a very powerful warrior in the fight against degenerative brain disease.

Hmmmm...anyone for some fish curry, with a green tea chaser?

Maczurek A, Hager K, Kenklies M, Sharman M, Martins R, Engel J, Carlson DA, Münch G. Lipoic acid as an anti-inflammatory and neuroprotective treatment for Alzheimer's disease. Adv Drug Deliv Rev. 2008 Oct-Nov;60(13-14):1463-70. Epub 2008 Jul 4.

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

2008-11-05T06:00:00.000-08:00

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.

Aging brains and medicine

2008-11-03T10:54:00.000-08:00

How medications work at different points in life can be a very important consideration. I see many, many studies looking at the viability of antidepressant therapy in the elderly. Recently there seems to be a flurry of research looking at how to medicate (note I did not use the word "treat") depression when it occurs as a comorbidity with diagnoses such as stroke or Alzheimer's disease.

In this study, the naturalistic finding was that as rats (and probably humans, too) age, the rate at which they are able to generate new neurons declines. The survival rate of those new cells starts to deteriorate as well.

The good news is that the response to fluoxetine (Prozac) was the same across the board.

The bad news is, that in none of the groups, even the young rats who had a better ability to make new neurons, did fluoxetine enhance that ability.

Hmmm...is it just me, or does it make sense that if a medication is going to work, it needs some brain cells to work on?

Cowen DS, Takase LF, Fornal CA, Jacobs BL. Age-dependent decline in hippocampal neurogenesis is not altered by chronic treatment with fluoxetine. Brain Res. 2008 Sep 4;1228:14-9. Epub 2008 Jun 24.

Sneak peek at new drug booklet

2008-10-31T13:59:00.000-07:00

Here is a sample page from the newly released booklet, This Is Your Brain On Psych Drugs. You can order this booklet by clicking here.

This study gives new meaning to the term, "mama's boy"...

2008-10-31T06:43:00.000-07:00

Several years ago I was diagnosed with uterine fibroids. For all of my medical knowledge and connections, I was very distressed to learn that the treatments for this very common gynecological condition seemed to be very crude and invasive. There really wasn't much research into gentle, natural, or nutritional solutions. Every physician I spoke to just wanted to give me a hysterectomy, despite my young age. Some couldn't figure out why I wouldn't consent, given the fact I was not going to have children and my uterus was, therefore, essentially useless and unnecessary.

When I shared my situation with another female friend, she immediately said, "Well, if it was men who got fibroids on THEIR reproductive organs, you can guarantee there would be a gazillion dollars devoted to researching any possible way to treat them without removing the affected body part!"

Ever since, when I see some kind of gender inequity in medicine, I think of that conversation and remind myself that, unfortunately, sometimes men have to hurt in a unique and most unexpected place in order for them to think more creatively about how they treat women, personally and clinically.

This study is about depression and not fibroids, but it makes my point. Something I find very frustrating with my work in polycystic ovary syndrome is the reluctance on the part of some endocrinologists who treat the disorder to acknowledge the extreme anxiety, depression, and mood swings this disorder promotes. Even though 85% of the over 1,000 women who answered a survey on my website reported at least one of these problems, there are physicians who will flat out say depression is not part of the disorder. Or, rather than trying to understand what may be driving the depression, they simply write a script for an antidepressant.

Well...here's what might happen if you treat depression so superficially. Female rats were treated, throughout pregnancy and lactation, with fluoxetine (Prozac). Later on, the sexual behavior of their male offspring was observed. They appeared to have less incentive to participate in sexual activity. This lack of libido wasn't coming from any measurable, explainable change in hormones, these guys just didn't seem to want any.

With all due respect, knowing that fish oil/omega-3 fatty acids are a great option for depression as well as promoting libido, this kind of problem simply shouldn't be something we have to encounter or research. Except to identify and define precisely why we shouldn't be encountering or researching it.

Oh! And if you're male and you're feeling a little uncomfortable while reading this, you've just experienced what every woman in history has felt when she was told she had to have a hysterectomy that may have been unnecessary. Welcome to the world of medicine without compassion.

Gouvêa TS, Morimoto HK, de Faria MJ, Moreira EG, Gerardin DC. Maternal exposure to the antidepressant fluoxetine impairs sexual motivation in adult male mice. Pharmacol Biochem Behav. 2008 Sep;90(3):416-9. Epub 2008 Apr 4.

2008-10-30T07:23:00.001-07:00

Be sure to vote! No one knows what's best for you but YOU.

"Going up in smoke: tobacco smoking is associated with worse treatment outcomes in mania."

2008-10-29T06:23:00.000-07:00

Bipolar disorder, to me, is a fascinating disorder. It seems to affect some very intelligent and creative people, and that, I believe, is precisely why it is so hard to treat. The manic episodes it can produce can be part of the thrill of having the disorder. I've had more than one client who accepted medical treatment for bipolar disorder complain that the medication took away the "edge". People started to ask if anything was wrong. We kind of like manic people for their charisma, for the creative performances, work output, etc., that they give us. And, because mania is a natural kind of high, giving it up can be somewhat of a chemical straight jacket.

However, bipolar disorder is also neurodegenerative. Meaning if it progresses unchecked, all that extra brain energy that's requiring oxidation of glucose to fuel all those charismatic neurons is also creating a process that's not unlike a "rusting out" of the brain. So, if we want to preserve the creativity and contributions of people born with this kind of hardwiring, we have to work harder to understand the hardwiring, and develop medications that don't leave people feeling zombied. Plus, we have to encourage lifestyle choices that promote longevity.

One of the worst risk factors, it appears, (in other words, a group of people we now know we have to work extra hard to learn how to help), is people with bipolar disorder who smoke. In this study, what was found was that the subjects who smoked did not respond as well to the medications they were given.

What is really interesting about this study, is that the medications tested happened to be antipsychotics that have been found to be helpful in some cases of bipolar disorder. No traditional mood stabilizers, such as lithium, were used. I wish that had been included in this study, because this study may not be saying that bipolar smokers have worse treatment outcomes, as much as it says when a patient is diagnosed with bipolar disorder who smokes, they may do better with a different category of medication.

Our patients depend on us to be diligent with scientific process and not let our bias interfere with their well-being.

Berk M, Ng F, Wang WV, Tohen M, Lubman DI, Vieta E, Dodd S. Going up in smoke: tobacco smoking is associated with worse treatment outcomes in mania. J Affect Disord. 2008 Sep;110(1-2):126-34. Epub 2008 Feb 15.

New booklet: This Is Your Brain On Psych Drugs

2008-10-28T10:38:00.000-07:00

As this blog grows, it is harder to read in a logical, stepwise fashion. So, I've taken the information from the most commonly read posts and compiled a 26 page booklet that summarizes this information.

If you'd like ordering information, it is available at this link.

I was prompted to do this by seeing the information be so widely read, and so to those of you who have done this, thank you so much for the inspiration!

Which came first? Who's on first? Medications and weight gain

2008-10-27T06:30:00.000-07:00

As I mentioned in a recent post, olanzapine (Zyprexa) is strongly correlated with weight gain. It's no ordinary kind of weight gain, it's the kind that is associated with hyperlipidemia, diabetes, and even diabetic ketoacidosis. Because of this, it is a popular drug for researchers to study, with regards to its nutritional and metabolic implications. My own fact sheet lists almost 300 references with regard to these interactions.

Now, researchers are starting to look at whether or not certain genetic profiles are more likely to induce weight gain when using this drug. And it turns out, how the leptin gene is expressed may be significantly affecting how a person responds to this medication. Leptin is a hormone that helps to regulate body weight, metabolism, and even reproductive function.

What is interesting is that as I read the research, there are also studies coming out suggesting that the people who best respond to some of these medications may also be the ones who experience the most weight gain when using them. And the whammy there is that the people who experience the most weight gain when using the drugs, are the ones most likely to have low compliance with regard to using them. A medical "Who's on first?" dilemma.

It's fascinating that the brain, weight, and metabolism are all so intricately linked. It certainly means there will be plenty of information for me to blog about, way into the future.

I very much look forward to that!

Srivastava V, Deshpande SN, Nimgaonkar VL, Lerer B, Thelma B. Genetic correlates of olanzapine-induced weight gain in schizophrenia subjects from north India: role of metabolic pathway genes. Pharmacogenomics. 2008 Aug;9(8):1055-68.

Kuzman MR, Medved V, Bozina N, Hotujac L, Sain I, Bilusic H. The influence of 5-HT(2C) and MDR1 genetic polymorphisms on antipsychotic-induced weight gain in female schizophrenic patients. Psychiatry Res. 2008 Sep 30;160(3):308-15. Epub 2008 Aug 20.

A Chinese herb with antidepressant activity

2008-10-24T06:40:00.000-07:00

I love Chinese medicine and think there is a lot of potential with its options to treat conditions Western medicine simply doesn't manage very well. It's challenging to share this specialty in an evidence-based blog like this one, because much of the research that is reported, uses terminology that is not meaningful to a Western-trained practitioner like myself. So I was grateful that this group of Chinese researchers took the time to study an aspect of their practice, as well as report on it, in a way that is meaningful and potentially useful to their Western colleagues and friends.

These researchers investigated the activity of xiaobuxin-tang (XBXT), which is a traditional Chinese herb that has been used as an antidepressant in China for centuries. Previously, these researchers discovered that XBXT improves the serotonin balance as well as the behavior of chronically stressed rats with depression. In this particular study, the researchers demonstrated that XBXT stimulates neuron development in the hippocampus, the brain's memory center. (Hippocampal neurons tend to degenerate and die in the throes of depression.) Levels of compounds associated with neuron formation, such as brain-derived neurotropic factor (BDNF), were also increased in the presence of XBXT.

The overall activity of XBXT was compared to that of the antidepressant imipramine.

This little guy here felt so good on XBXT he's still celebrating eight months into the year of the rat!

An L, Zhang YZ, Yu NJ, Liu XM, Zhao N, Yuan L, Chen HX, Li YF. The total flavonoids extracted from Xiaobuxin-Tang up-regulate the decreased hippocampal neurogenesis and neurotrophic molecules expression in chronically stressed rats. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Aug 1;32(6):1484-90.

My new alternative to medication

2008-10-23T08:39:00.000-07:00

I know a lot of you are coming to this blog looking for information about your medication. I wanted to share with you my experience last night that got me thinking about therapy and medication.

I have a friend who has been inviting me to join her in tango class. My interest in this dance started a few years ago when I took a Spanish class at the local community college and I had to do an oral report on Argentina. It's become my goal to get down there someday, and in the meantime to learn to tango so I can have more fun when I get there.

So I finally went to the class last night. It was so...much...fun!!! A big part of the dance is not so much the choreography as it is letting loose and just experiencing the music. In fact, a big portion of the class we were assigned by the instructor to just close our eyes and "feel" the music.

I have learned from learning other styles of partner dance, that it is impossible to participate if you bring any kind of control issues to the floor. Dance is all about partnership. Listening to your partner's unspoken communication, and working with that energy to create beautiful movements. Tango is no different. You have to listen to the music, sense your partner's energy, and within all of that input, together, spontaneously express yourselves in a compatible way as you move across the floor.

If you have any self-consciousness whatsoever, you ruin the flow. One partner I tried to dance with was so caught up with what I was doing wrong and what I needed to correct so that his experience would improve that I found myself not even trying to work with him. With others, things just flowed.

The lesson flew by, and way too soon, it was time to go. My friend and I lingered in the parking lot and I told her it seemed that couples who took the time to learn to dance together would probably have better relationships. Because everything that you have to do on the dance floor to succeed, is everything you need to do in life to succeed. It's a lot of give and take, losing a sense of who's right and who's wrong...and about just being yourself. Tango, as are other dances, is completely about knowing how much to let another person into your space and where boundaries need to be defined. That's pretty much what life is about, too.

Isn't that what therapy is about? Not that counseling doesn't have its place, but sometimes you just have to stop talking about how you want to live your life...and just do it.

Hopefully one of these days I will be posting a photo of myself from Buenos Aires, rose in my teeth, tangoing the Argentinian night away!

Mental health and the presidency

2008-10-21T06:32:00.000-07:00

Several years ago a teenage client of mine had her first manic episode in the middle of her school day. Her behavior was bizarre enough that most people thought she was high on meth. I ended up intervening, getting her to the hospital, insisting on a urine test which I knew would be negative, and eventually getting her the proper diagnosis and help.

Most people I know who would be diagnosed with bipolar disorder would be angry, they'd be paralyzed, they wouldn't accept the diagnosis. And they would go around for the rest of their lives, not managing the diagnosis, and likely as a result, not realizing their full potential.

Not this teen. She showed up at her next appointment with a list of names. She decided to do an Internet search to see if any famous people had been diagnosed with bipolar disorder. On her list were some remarkable names, including Abraham Lincoln and Winston Churchhill. She said to me, "I decided that if Abraham Lincoln can be bipolar and do incredible things....so can I."

And that is what this remarkable woman has done ever since her diagnosis.

Her exercise intrigued me, and I've since become interested in reading biographies of American Presidents, not so much to learn the facts of the eras in which they led, but to learn more about their personalities. I began to see that many of them, in the documents and legacies they left, left some great clues for us regarding their personalities and mental functioning.

I recently surfed the Internet to see if anyone else had written about this, and learned that a few years ago, some researchers at Duke University actually did. They propose that about half of our presidents have actually had diagnosable mental disorders, if you use the criteria in the Diagnostic and Statistical Manual of Mental Disorders. The incidence cited is about what is found in the general population, so mental illness is not anything more common or rarer in our country's leaders.

Some of the examples they provide:

Ulysses S. Grant struggled with social phobia and alcohol abuse. This combination makes sense, since if you have trouble being around people and your job has a lot of people wanting to be around you...you're going to need some self-soothing at the end of a long day.
Howard Taft had sleep apnea and often fell asleep in meetings. Sleep apnea is correlated with depression.
Abraham Lincoln is thought to have been bipolar. One account I read said his depressive bouts were so severe he would not even allow himself to carry a pocket knife.
Franklin Pierce witnessed the violent death of his son in a railway accident just before he assumed office, and he suffered from symptoms indicating depression or post-traumatic stress during his term. The study noted that his associates described Pierce of being a different person than the one who had energetically campaigned for office.
Richard Nixon abused alcohol.
Calvin Coolidge reportedly had social phobia, and experienced depression after his son died
Thomas Jefferson's behavior was consistent with social phobia.
Theodore Roosevelt and Lyndon Johnson both are believed to have had bipolar disorder. (I read both their bios last summer and was struck with (1) the amount that Roosevelt accomplished during his term and (2) the extreme behavior that Johnson was allowed to act out in such a prominent position. It was like no one knew what to do with him, and he intimidated his way all the way up to the top. Just this week Johnson's bio was on PBS. If you're interested in this topic, get a hold of a copy. It's fascinating to watch his contemporaries describe his energy, his complexity, and his mood swings in the detail they did without ever using the words "manic" or "bipolar")
John Quincy Adams had clinical depression. (I recently read this bio and throughout, his writings reflected a despair that he was not accomplishing much with his life.)
Rutherford B. Hayes, James Garfield , and Dwight D. Eisenhower all appear to have had depression.
Franklin Pierce did, too, along with alcohol issues.
Woodrow Wilson lived with generalized anxiety disorder.
Ronald Reagan had Alzheimer's disease, which may have started to manifest during his service.

Contemporaries of several of these men even expressed, likely in observing behaviors related to these conditions, early on, that they may never achieve anything noteworthy in their lives.

MY COMMENTS

1. Wow! My client is part of a distinguished list of people who proved themselves to be very important to our country and our heritage. I love to use this list with clients who have not had the courage to admit their diagnosis, for fear of being stigmatized. Having a mental health diagnosis is clearly not about lacking intelligence or capability to achieve great and wonderful things. And it's important to note, mental health diagnoses do not discriminate. They reach across those party lines and affect individuals regardless of their political bent.

2. I wasn't surprised to find this article. When I worked in a treatment center there seemed to be a disproportionate percentage of our population coming from what I used to call the "Big P" professions: Performers, Politicians, Psychologists (and related therapists and social workers), and Preachers (people in ministry-related work). I can't tell you why it played out that way, except for maybe the first two categories are people who use public attention as a way to convince themselves they're really ok and a way to distract from inner turmoil...and the latter as people who seek out professions looking for answers they haven't yet found. I won't get a Nobel Prize for that theory, and honestly, I'm just surmising.

And for anyone reading this who works in one of the "Big P" professions, please take my observation as a compliment. The most intelligent, creative, inspiring people I know are my clients. I think these variations on cognitive function are what drive our inventions, our art, our newest and greatest ideas. It's when we stigmatize people who have them and make them feel something is wrong with them that we prevent them from achieving their true potential.

3. I must qualify before saying anything here, I'm seriously considering not voting for President for the first time ever since I've voted. I'm simply not enthusiastic about either option this time around...so this is not at all a hint at my political leaning. But what I must say is that it distresses me very much that the party that supposedly is mental health-friendly seems to think it is ok as part of campaign strategy to needle the other party's candidate because he is "hot-headed".

I see the same personality, but coming from someone who was a POW, my first inclination is to think it's likely part of some understandable post-traumatic stress disorder. I don't think that someone who has PTSD and isn't managing it appropriately should be given responsibilities that his level of cognitive functioning are not able to manage. However, neither do I think it is responsible, especially if you call yourself mental health-friendly, to bully someone and then use the resulting response as a weakness to capitalize on for personal gain. Especially not when respecting and taking better care of veterans, a whole host of which are returning from Iraq with PTSD, is a prominent campaign issue.

I'm not sure I want to know what our country would be like had Thomas Jefferson and Theodore Roosevelt not served us, and therefore, I choose to refrain from jumping to the gun about anyone's mental state and fitness for a job I certainly wouldn't want to have myself.

As it is clearly illustrated in this Duke article, having a mental health diagnosis does not preclude one from greatness. Having a mental health diagnosis and not appropriately managing it, or treating someone as if they are a lesser person for having one...are the problems we'd be best to work at solving.

Davidson JR, Connor KM, Swartz M. Mental illness in U.S. Presidents between 1776 and 1974: a review of biographical sources. J Nerv Ment Dis. 2006 Jan;194(1):47-51.

Oh, the tangled web we weave, when science we manipulate in order for profits to achieve...

2008-10-20T06:00:00.000-07:00

Oh, this story just won't go away.

Years ago, when olanzapine (Zyprexa) was fairly new to the market, my colleagues started commenting that they noticed huge weight gains (like 40-50 pounds) in short time intervals (like a month). No matter where we attempted to get information, Lilly, this drug's manufacturer, insisted that this drug did not increase weight gain.

I had the opportunity to meet one of Lilly's lead marketing guys at a national conference. We exchanged cards and when I got home I emailed him with a proposal that the team of nutritionists I was training in the area of psychotropic medications and hormone imbalances, work with Lilly to create a diabetes management educational program targeted specifically at psychiatrists, who were not specialized in this area but who appeared to need support in order to use these new medications in safe and appropriate ways.

I received an email in return, carbon copied to quite a few people at Lilly, stating that "weight gain on our medication is an unscientific rumor". (I now call this correspondence my "60 Minutes E-mail").

It wasn't 6 months before Lilly was required to put a black box warning on this very medication regarding its potential to cause diabetes. Apparently the timing of my original email struck a raw nerve.

What really bothered me about this whole situation was at the very time Lilly was insisting that that this drug did not cause weight gain, they were marketing it to eating disorder specialists as a treatment option for anorexia nervosa.

Yes, you heard me correctly. Lilly apparently wanted us to believe that the drug doesn't cause weight gain if you use it in people who don't want to gain weight, but it is very effective in causing weight gain in people who desperately need to gain weight.

Fast forward to last Friday. I'm scanning new research abstracts in Pub Med and right next to each other I see these two titles:

Olanzapine in the treatment of low body weight and obsessive thinking in women with anorexia nervosa: a randomized, double-blind, placebo-controlled trial.

Olanzapine (LY170053, 2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno[2,3-b][1,5] benzodiazepine), but not the novel atypical antipsychotic ST2472 (9-piperazin-1-ylpyrrolo[2,1-b][1,3]benzothiazepine), chronic administration induces weight gain, hyperphagia, and metabolic dysregulation in mice.

There is also, in Pub Med, research to suggest that this medication may trigger binge eating disorder.

So apparently, the newest, quickest way to cure anorexia is to replace it with another eating disorder. Never mind that it creates hormone imbalances that are strongly documented and have mandated a warning be placed on this drug.

I thought when we helped people with anorexia, they were supposed to be healthy in all respects. Not just normal weight with a risk of developing diabetes. Which, by the way, is starting to be associated with Alzheimer's disease.

Insert huge, frustrated, sigh...

Bissada H, Tasca GA, Barber AM, Bradwejn J. Olanzapine in the treatment of low body weight and obsessive thinking in women with anorexia nervosa: a randomized, double-blind, placebo-controlled trial. Am J Psychiatry. 2008 Oct;165(10):1281-8. Epub 2008 Jun 16.

Coccurello R, Caprioli A, Conti R, Ghirardi O, Borsini F, Carminati P, Moles A. Olanzapine (LY170053, 2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno[2,3-b][1,5] benzodiazepine), but not the novel atypical antipsychotic ST2472 (9-piperazin-1-ylpyrrolo[2,1-b][1,3]benzothiazepine), chronic administration induces weight gain, hyperphagia, and metabolic dysregulation in mice. J Pharmacol Exp Ther. 2008 Sep;326(3):905-11. Epub 2008 Jun 20.

Theisen FM, Linden A, König IR, Martin M, Remschmidt H, Hebebrand J. Spectrum of binge eating symptomatology in patients treated with clozapine and olanzapine. J Neural Transm. 2003 Jan;110(1):111-21.

Gebhardt S, Haberhausen M, Krieg JC, Remschmidt H, Heinzel-Gutenbrunner M, Hebebrand J, Theisen FM. Clozapine/olanzapine-induced recurrence or deterioration of binge eating-related eating disorders. J Neural Transm. 2007;114(8):1091-5. Epub 2007 Mar 20.

Kluge M, Schuld A, Himmerich H, Dalal M, Schacht A, Wehmeier PM, Hinze-Selch D, Kraus T, Dittmann RW, Pollmächer T. Clozapine and olanzapine are associated with food craving and binge eating: results from a randomized double-blind study. J Clin Psychopharmacol. 2007 Dec;27(6):662-6.

Do we really need to do this kind of stuff in the name of science?

2008-10-17T10:32:00.000-07:00

I read scientific research an average of 2 hours a day. I see some pretty strange things. Today I encountered the horrible.

Mexican scientists interested in whether or not melatonin could lessen the damaging effects of a caustic burn, induced such a burn in the esophagi (plural for esophagus) of rats. Their rationale was that caustic ingestion (you know, things like drinking Liquid Plumr) is a serious life-threatening event in children.

I don't understand why, since melatonin is a naturally occurring substance, they couldn't just do the research using children who had already, accidentally, ingested something caustic? Since the purpose of the research is supposedly to help these children, wouldn't the research be best conducted on the population it is intended to help?

This is just cruel. I almost didn't post this because I didn't want to reward this kind of sadistic thinking by giving it attention. But at some point you just have to stand up and say, "That's just wrong."

Oh, by the way, the melatonin worked. So while these guys were busy in their lab burning rat throats in order to get a publication, Mexican children who could have benefited from being subjects in the study...sat in the hospital with burnt throats and no melatonin to help them. Go figure.

Larios-Arceo F, Ortiz GG, Huerta M, Leal-Cortés C, Saldaña JA, Bitzer-Quintero OK, Rodríguez-Reynoso S. Protective effects of melatonin against caustic esophageal burn injury in rats. J Pineal Res. 2008 Sep;45(2):219-23. Epub 2008 Mar 26.

Monkeys with no memories and the marijuana munchies

2008-10-16T11:02:00.000-07:00

Endocannabinoids are chemicals we make that are important in many functions, including cognitive thought, and memory. When our internal endocannabinoid levels are low, we also start to crave sugar. (THC, the active ingredient in marijuana, is also a cannabinoid, and using it messes with our cannabinoid system, giving us the munchies).

In this study, endocannabinoid levels were evaluated in the prefrontal cortex area of 23 pairs of brain cadavers of people with schizophrenia and normal age and gender matched comparisons. Messenger RNA levels for endocannabinoid production were lower in the schizophrenic brains.

Eighteen brains of macaque monkeys who had been exposed long-term to one of two antipsychotics, haloperidol (Haldol) or olanzapine (Zyprexa), were compared to brains that had never been exposed to these medications. There was no significant difference in their endocannabinoid levels. So even though the medication was helping some aspect of the schizophrenia, it was not correcting the endocannabinoid imbalance.

That might provide one reason why it might be hard for schizophrenics to stay compliant with their medication--they're not being given a medication that helps their brains remember to take it.

As a nutritionist, I also see an important "next study". Knowing that omega-3 fatty acids DO improve cognition and memory, I wonder what would happen if that supplementation was added to the protocol?

It also explains why these clients have such an appetite for sweets, and the kind of foods that further degrade the brain. It's coming from a pretty entrenched biological mechanism.

Eggan SM, Hashimoto T, Lewis DA. Reduced cortical cannabinoid 1 receptor messenger RNA and protein expression in schizophrenia. Arch Gen Psychiatry. 2008 Jul;65(7):772-84.

OK, I managed to keep a straight face until now, which I wanted to do since schizophrenia is an entirely serious topic and people with the disease deserve my respect. Completely. But do you know how hard it was to word this study without using the distracting phrase "monkey brain"? I figured this guy must have been a subject, given his predilection for popsicles.

Fish and dementia

2008-10-14T09:08:00.000-07:00

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.

Trans fat information

2008-10-11T12:47:00.000-07:00

Yes, I've been a little quiet lately. I've been traveling, and also ramping up to re-launch my newsletter, After the Diet. This next issue is about food policy, which I really want to get out before the election.

Don't fret, I did my best to be nonpartisan! The goal was mainly to illustrate how the things we believe about food and the foods that show up in our food supply are related to deals cut on Capitol Hill. I do my best to stay right down the middle. My obligation is to help anyone who can benefit from my expertise, since diabetes, infertility, depression, you name it, affect Democrats, Republicans, Libertarians, and Independents.

It matters not to me HOW you vote, it matters THAT you vote, and that when you do, your vote is informed.

So I researched some issues related to foods and put them together in a newsletter.

The graphic you see is a handout, included in that newsletter, that I developed on trans-fats, since they've recently been making a lot of news and I see clients misusing this information since they don't understand it.

If you're interested in any of the following:
--why wild salmon isn't really wild
--why the United States sued Mexico to import high-fructose corn syrup
--how flooding in Iowa may be raising the price of shrimp
--why catfish is not so easy to find in your grocery store
--what food-related legislation was actually co-sponsored by (!) John McCain and
John Kerry
--what FDA warning is potentially reducing the IQ of babies
--what one simple change Americans could make to collectively save $18,630,000,000
then you might be interested in subscribing to my newsletter.

I'm already working on the next edition, which will cover the following topics:

Melatonin: The Ultimate Antioxidant?

Dietary Aspects of Melatonin Balance

Sleep, Weight, Insulin Resistance, and Aging

Why Do Pilots Have Shortened Lifespans?

Is It Attention Deficit Disorder? Or Is It Sleep Deprivation?

It's a really fun publication and I'd love to have you subscribe!

I promise, once I get this issue out, there's lots and lots to blog about.

Stay tuned!

The effects of omega-3 fatty acids monotherapy in Alzheimer's disease and mild cognitive impairment:

2008-10-03T06:00:00.000-07:00

In my last post, I suggested that despite the findings of one study, it was still a good idea to supplement omega-3 fatty acids in the diet. Here is one study supporting my argument.

Forty-six seniors with mild to moderate Alzheimer's disease were given either a dose of omega-3's of 1.8 grams per day (roughly equivalent to what was provided in the previously mentioned study) or placebo. A 24-week, randomized, double-blind placebo-controlled study was carried out to test the feasibility of using omega-3 polyunsaturated fatty acids (PUFAs) monotherapy in people with cognitive impairment and to explore its effects on cognitive function and general clinical condition in these participants. Seventy-six participants completed the study. Those who received the omega-3's showed better improvement on a clinician-based assessment of symptoms. The change was more significant in those individuals with mild cognitive impairment than it was in those diagnosed with Alzheimer's disease.

The changes were more significant, also, in persons with higher concentrations of eicosapentaenoic acid (EPA) in their red blood cells.

And, as I suggested, study design is an important determinant of outcome. In the words of the researchers, "Further studies should be considered with a larger-sample size, diet registration, higher dosages, comparisons between different combinations of PUFAs, and greater homogeneity of participants, especially those with mild Alzheimer's disease and mild cognitive impairment."

I am excited to see what studies like this teach us about minimizing the devastating effects of diseases of aging, such as dementia and Alzheimer's disease!

Chiu CC, Su KP, Cheng TC, Liu HC, Chang CJ, Dewey ME, Stewart R, Huang SY. The effects of omega-3 fatty acids monotherapy in Alzheimer's disease and mild cognitive impairment: a preliminary randomized double-blind placebo-controlled study. Prog Neuropsychopharmacol Biol Psychiatry. 2008 Aug 1;32(6):1538-44. Epub 2008 May 25.

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

2008-10-01T06:00:00.000-07:00

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.

What happens in your brain when you have bipolar disorder

2008-09-29T09:07:00.000-07:00

I love studies like this. They help substantiate that diagnoses such as bipolar disorder are not just "behavioral problems." They come with true biochemical imbalances, that sometimes even affect the tissue structure of the brain. Hopefully, the more studies like this are done, the less people with bipolar disorder will be looked down upon by society, and will be able to get the care they need that truly corrects these imbalances.

In this study, the fatty acid composition of the orbitofrontal cortex was studied in 10 patients with bipolar disorder. Compared to 19 cortices in individuals who did not have bipolar disorder. (This was performed in post-mortem, or after all the patients had died.)

Those individuals who had had bipolar disorder had higher concentrations of arachidonic acid and lower concentrations of docosahexaenoic acid (DHA) than those who had not. In both populations, there was also a trend toward higher arachidonic acid concentration and lower DHA concentration that was related to the degree of alcohol consumption.

A little visit over to Wikipedia gave me this information about the orbitofrontal cortex: Destruction...typically leads to a pattern of disinhibited behaviour. Examples include swearing excessively, hypersexuality, poor social interaction, compulsive gambling, excessive alcohol / smoking / drug use, and poor empathising ability. Disinhibited behaviour by patients with some forms of frontotemporal dementia is thought to be caused by degeneration of the OFC[8]. Patients with damage to the OFC tend to make rash decisions, and typically manage their finances poorly.

Sometimes it's easy to make judgments about a person's behavior and assume the person can just change them if they want to. It's reality that sometimes the problem is truly biological and that changing the nutritional status and/or the biochemistry of the brain is what is needed in order to help change behaviors.

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.

Omega-3's for schizophrenia

2008-09-26T06:00:00.000-07:00

DHA is commonly the omega-3 of the fish oils that gets the most attention for use in mental health conditions. However, EPA is gaining quite a reputation of its own. In this study, 24 patients presenting with their first episode of psychosis were treated with EPA for 12 weeks. Just before and at the end of this interval, brain scans were done to look for changes. Increases in glutathione and decreases in negative symptoms were observed as a result of EPA treatment.

Glutathione is a chemical that helps to prevent cell death, so its increase means EPA helps to preserve brain tissue. Because glutathione is not something that is easily administed via diet or supplementation, it's good to know there are other avenues for increasing its concentrations in populations at risk for greater rates of cell death, such as people with schizophrenia.

Berger GE, Wood SJ, Wellard RM, Proffitt TM, McConchie M, Amminger GP, Jackson GD, Velakoulis D, Pantelis C, McGorry PD. Ethyl-eicosapentaenoic acid in first-episode psychosis. A 1H-MRS study. Neuropsychopharmacology. 2008 Sep;33(10):2467-73. Epub 2008 Jan 16.

Why you can't just take a pill to feel better

2008-09-24T06:00:00.000-07:00

Ohhh...I hate to say it, but we've become so lazy as a society. Evidence abounds that food, activity, stress management, and sleep choices can significantly affect overall health. But if given the option to try these or pay money for a pill or a medical procedure, the average American will tend to opt for the more passive option. Here's why those who make that choice may be selling themselves short.

Both omega-3 fatty acids and exercise have been found to improve brain function and keep brain tissue young.

A group of researchers is reporting that when the two are combined, compounds common in healthy, regenerating brain tissue (brain derived neurotrophic factor, or BDNF, for example) are higher than when only one of those options is applied. It seems as though the two play off of each other and each makes the other more effective.

Sorry, guys, there's no such thing as a way out of exercise and all the great things it does for you! :)

Wu A, Ying Z, Gomez-Pinilla F. Docosahexaenoic acid dietary supplementation enhances the effects of exercise on synaptic plasticity and cognition. Neuroscience. 2008 Aug 26;155(3):751-9.

A natural antipsychotic?

2008-09-22T06:00:00.000-07:00

l-Stepholidine is a chemical derived from the Chinese herb Stephania. Since it had been found to have dopamine activity similar to that seen in atypical antipsychotics, it was tested and compared to the activity of haloperidol (Haldol) and clozapine (Clozaril). Scientists predicted its activity would more closely resemble clozapine. Indeed, when tested, it did mimic clozapine. The one downside researchers did report was that it was eliminated fairly rapidly from the body, which would make it challenging to use as a long-term therapeutic agent for treating schizophrenia.

What is stepholidine? It is a naturally occurring chemical, extracted from Stephania intermedia, a Chinese herb. I like to find pictures of herbs to share in this blog, but unfortunately, even Google can't pull anything up on this one.

I think this is exciting news, but being that this is very new information, I certainly am not recommending that anyone stop using a prescribed antipsychotic and head for Chinatown! I do promise, if anything new comes up, I'll be sure to share it in this blog along with references.

Natesan S, Reckless GE, Barlow KB, Odontiadis J, Nobrega JN, Baker GB, George SR, Mamo D, Kapur S. The antipsychotic potential of l-stepholidine--a naturally occurring dopamine receptor D1 agonist and D2 antagonist. Psychopharmacology (Berl). 2008 Aug;199(2):275-89.

When it takes more than a minute to describe how many medications you're taking...time to take a closer look.

2008-09-19T20:07:00.001-07:00

Yesterday I was lunching with a dear friend, who mentioned that one of HIS friends has started to have problems with diabetes. I knew this friend also has Alzheimer's disease, so, knowing that many brain and nervous system-targeted medications can provoke insulin resistance and diabetes, I started asking questions about this person's medications.

We called the friend we were discussing for a complete list. Sure enough, in the battery of medications he had been prescribed...was valproic acid, or Depakote. Depakote is well documented to promote the development of metabolic syndrome--a cluster of problems including hypertension, insulin resistance, diabetes, and high cholesterol. Much of the research in this area has focused on women, because polycystic ovary syndrome, a feminine variant of metabolic syndrome, is also correlated with Depakote use. If you're looking for research on the effects of Depakote in men, it's there, it's just a little harder to find.

New research is suggesting that there is a link between diabetes and Alzheimer's disease. Some researchers even call it diabetes of the brain, and there is some evidence to suggest that diabetes medications such as metformin can help delay the progression of Alzheimer's syndrome.

So here we have a guy who has been prescribed a seizure medication, which has likely provoked his problems with diabetes, which is likely worsening his Alzheimer's disease...and what do you know? It seems as though now that he is on galantamine (Reminyl) for his Alzheimer's disease, he's started noticing tremors. I'd bet money on the possibility that the seizure meds are adjusted upward as a result.

So you can see where I'm going. Not only does this keep this poor guy's physicians busy, it pads the pockets of more than one pharmaceutical company, in progressively more expensive chunks.

My friend asked me what I would do? Well, I must qualify that I am not a prescribing medical doctor. I am a registered dietitian who studies the brain and nervous system. But this is where I'd go.

1. Based on the evidence that seizure disorders respond well to omega-3 fatty acids, I'd up those to a DHA equivalent of 1000 mg per day.
2. To help those omega-3's be most effective, I'd teach this person my "S" and "C" rule (avoid, as much as possible, all fats and oils beginning with the letters "S" and "C"...canola being the only exception). I know my friend and his friend eat out quite a bit and it likely is a significant source of these oils.
3. If you reduce the seizure and tremor activity, you reduce the need for seizure medication, and minimizing medications is always very important.
4. I would consider an alternative seizure medication with less potential for disrupting hormone balance. The one that I have seen repeatedly and successfully used in women to achieve this is lamotrigine (Lamictal). Of course, there may be a reason we do not know of that this would not be appropriate, but if this has not been considered it's certainly worth a try.
5. Less Depakote (or potentially no Depakote) potentially also means less insulin resistance, which provides the possibility that the Alzheimer's medication could be reduced. Again, less meds....fewer side effects.
6. Finally, acetyl l-carnitine has been shown to effectively reduce symptoms of diabetes as well as Alzheimer's disease. It also improves cholesterol profiles. And...it has repeatedly and specifically been found to effectively counter the negative side effects of Depakote. I have seen this cited so often recently I can't understand why it is not automatic for any physician prescribing Depakote to simultaneously recommend carnitine.

This trend, of treating one symptom, letting side effects develop, then treating them with other meds that create other side effects, which eventually build vicious cycles of ever-increasing doses of medications...in recent years...has spiraled out of control. The field of nutritional psychiatry is just out of the starting gate. But I'm hooked on its potential. Hopefully in this case, and for others who find this blog, we can help back our friends out of these pharmaceutical corners, save them some money, and improve their overall quality of life.

Luef G, Abraham I, Trinka E, Alge A, Windisch J, Daxenbichler G, Unterberger I, Seppi K, Lechleitner M, Kramer G, Bauer G. Hyperandrogenism, postprandial hyperinsulinism and the risk of PCOS in a cross sectional study of women with epilepsy treated with valproate. Epilepsy Res 2002 Jan;48(1-2):91-102.

Tan H, Orbak Z, Kantarci M, Kocak N, Karaca L. Valproate-induced insulin resistance in prepubertal girls with epilepsy. J Pediatr Endocrinol Metab 2005 Oct;18(10):985-9.

Aydin K, Serdaroglu A, Okuyaz C, Bideci A, Gucuyener K. Serum insulin, leptin, and neuropeptide y levels in epileptic children treated with valproate. J Child Neurol 2005 Oct;20(10):848-51.

Pylvanen V, Pakarinen A,Kniop M, Isojarvi J. Insulin-related metabolic changes during treatment with valproate in patients with epilepsy. Epilepsy Behav 2006 May;8(3):643-8.

Isojarvi JI, Laatikainen TJ, Pakarinen AJ, Juntunen KT, Myllyla VV. Polycystic ovaries and hyperandrogenism in women taking valproate for epilepsy. N Engl J Med 1993 Nov 4;329(19):1383-8.

Rasgon NL, Reynolds MF, Elman S, Saad M, Frye MA, Bauer M, Altshuler LL. Longitudinal evaluation of reproductive function in women treated for bipolar disorder. J Affect Disord 2005 Dec;89(1-3):217-25.

Roste LS, Tauboll E, Morkrid L, Bjornenak T, Saetre ER, Morland T, Gjerstad L. Antiepileptic drugs alter reproductive endocrine hormones in men with epilepsy. Eur J Neurol. 2005 Feb;12(2):118-24.

Pylvanen V, Pakarinen A, Knip M, Isojarvi J. Characterization of insulin secretion in Valproate-treated patients with epilepsy. Epilepsia 2006 Sep;47(9):1460-4. Neurology. 2008 Sep 2;71(10):750-7.

Beeri MS, Schmeidler J, Silverman JM, Gandy S, Wysocki M, Hannigan CM, Purohit DP, Lesser G, Grossman HT, Haroutunian V. Insulin in combination with other diabetes medication is associated with less Alzheimer neuropathology. Prescrire Int. 2007 Oct;16(91):197-8.

McCain KR, Sawyer TS, Spiller HA. Evaluation of centrally acting cholinesterase inhibitor exposures in adults. Ann Pharmacother. 2007 Oct;41(10):1632-7.

López-Pousa S, Garre-Olmo J, Vilalta-Franch J. [Galanthamine versus donepezil in the treatment of Alzheimer's disease] Rev Neurol. 2007 Jun 1-15;44(11):677-84.

Schrauwen E, Ghaemi SN. Galantamine treatment of cognitive impairment in bipolar disorder: four cases. Bipolar Disord. 2006 Apr;8(2):196-9.

Aarsland D, Hutchinson M, Larsen JP. Cognitive, psychiatric and motor response to galantamine in Parkinson's disease with dementia. Int J Geriatr Psychiatry. 2003 Oct;18(10):937-41.

Isojarvie JI, Rattya J, Myllyla VV, Knip M, Ovine R, Pakarinen AJ, Tokay A, Tapaneinen JS. Valproate, lamotrigine, and insulin-mediated risks in women with epilepsy. Ann Neurol 1998 Apr;43(4):446-51.

Ribacoba-Montero R, Martinez-Faedo C, Diaz C, Salas Puig J. [Remission of polycystic ovary syndrome associated with valproic acid in an epileptic female]. Rev Neurol 2003 Apr 1-15;36(7):639-42.

Bruno G, Scaccianoce S, Bonamini M, Patacchioli FR, Cesarino F, Grassini P, Sorrentino E, Angelucci L, Lenzi GL. Acetyl-L-carnitine in Alzheimer disease: a short-term study on CSF neurotransmitters and neuropeptides. Alzheimer Dis Assoc Disord. 1995 Fall;9(3):128-31.

Thal LJ, Carta A, Clarke WR, Ferris SH, Friedland RP, Petersen RC, Pettegrew JW, Pfeiffer E, Raskind MA, Sano M, Tuszynski MH, Woolson RF. A 1-year multicenter placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's disease. Neurology. 1996 Sep;47(3):705-11.

Sano M, Bell K, Cote L, Dooneief G, Lawton A, Legler L, Marder K, Naini A, Stern Y, Mayeux R. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease. FASEB J. 1992 Dec;6(15):3379-86.

Want to get someone's attention? Mess with their head

2008-09-15T08:55:00.000-07:00

In all the years I've been doing this work, I've noticed people gradually tune out messages about fitness, weight management, and exercise...at least the ones with meaningful, important information. Except when it comes to their brains.

This past weekend, for example, I ran a demo booth at a local Whole Foods store for one of my company's sponsors, Organic Bistro. A gentleman and his son stopped by, and I offered them some samples of salmon cakes. The man pretty much went off on me.

"I'm vegan. I'm 51 years old. I'm a professional athlete. Just look at this body. Look at my legs. Do I look like I need your food? If I didn't know what I was doing would I be in this condition?"

I let him rant, and accommodated, interestingly, his wish that his son get a sample of the food that in his mind was not good enough for him.

After he finished, I said to him, "You clearly take very good care of yourself. I'm curious, though, because I'm a sports nutritionist and even athletes seem to not be getting some really important information about nutrition. Did you know that omega-3 fatty acids have been found to delay and possibly prevent the progression of Alzheimer's disease? And that it is possible but not easy to get those omega-3's in a completely vegan diet?"

The man's posture slumped, his voice got quiet, and he said, "My wife has permission, if I ever go there...to shoot me."

Since he'd dug a hole for himself and everyone in the frozen food aisle had been drawn into this interchange because of its decibel level, he couldn't really ask for more information.

So I pulled him aside and suggested that on his own, in the privacy of his own cable connection, that he Google "omega-3" and "Alzheimer's" and draw his own conclusions.

I'm not sure why it is that we're ok with a few extra pounds, we can justify eating that piece of cake even if we've been diagnosed with diabetes and there is a possibility that poor dietary choices might even lead to amputation...or eating those potato chips even though we want a baby and the evidence suggests that trans fats interfere with fertility...

...but you mention the brain and you've got a whole new, motivated audience.

My guess is, that by the time I'd broken down my demo this athlete had already been online learning about Alzheimer's. And hopefully, by now, has been back to Whole Foods for some of those really tasty wild salmon cakes.

Just one gram, that's all it takes!

2008-09-15T08:07:00.000-07:00

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.

Some great information on how to choose the right kind of fish

2008-09-12T06:00:00.000-07:00

One of the most common arguments/questions I receive about fish is whether or not it is safe to eat because of the mercury content.

Rather than reinvent the wheel, I thought I'd share a blog sent to me by Jennifer Wilmes, MS, RD, another fish-friendly dietitian who is trying to get the right information out there.

Hope this frees up some choices for you!

http://www.babygooroo.com/index.php/2008/09/09/gone-fishin/

Can good science really be half full?

2008-09-10T07:53:00.000-07:00

One reason I probably gravitated into science is that I am a very logical thinker. I enjoy following topics such as politics but I don't enjoy debating them because I'm usually thinking, "Why don't these people do outcome measurements with their legislation and report on that when they run for re-election?" Politics simply isn't an evidence-based discipline.

I admit, I can be overly-evidence-based, as evidenced by my prolific referencing in this blog. But that is what I am trained to do as a scientist--come to conclusions based on evidence.

So when a study like this one comes up, I just shake my head. At Cornell, I would have been handed back a paper like this with a big, fat, red "D" on the top. I would have been asked to rewrite my conclusions based on the evidence. These guys got published!

Based on the observation that mirtazapine (Remeron) helped to improve respiratory measurements in stroke patients, a group of scientists decided to try giving Remeron to ten patients, without depression, who had sleep apnea but refused to use a continuous positive airway pressure (CPAP) machine. Editorial note: Those contraptions SUCK...do you blame them?

Here is how they reported their results.

"After 51.9 +/- 8.4 days, the RDI was either reduced (51.9% in "responders" who were identified arbitrarily by a reduction in RDI >/= 25% at any time point of the investigation) or increased (154.4% in "non-responders"). Mirtazapine administration was stopped in the four patients with increased RDI. "

Translation: After an average of 52 days, patients either got better or worse. If you read the fine print where we said we only had 10 subjects in this study, almost half of them got worse.

Mirtazapine may be a probably effective treatment in stroke survivors with obstructive sleep apnea who refuse nasal CPAP treatment. As it may worsen central and mixed sleep apnea, patients who receive mirtazapine to alleviate sleep apnea or to control post-stroke depression with sleep disturbances should be monitored for changes in breathing parameters during sleep.

There is more waffling in that first sentence than I heard in the Democratic and Republican Convention broadcasts combined. Maybe a "probably effective" treatment? If you had cancer and you went in to your doctor and he suggested major surgery, would you be ok with him telling you that maybe this surgery was a "probably effective" strategy? If you were paying $20,000 for an in-vitro fertilization, would you fork that money over if all your doctor had to tell you was that maybe what you were paying him to do was "probably effective"

Translation: We really need to say something good about this medication so we can get published and keep our grant, but it looks like the only way we're going to be able to do that is fill this abstract with long sentences that go in circles and hope readers are in too much of a hurry to do the math.

I used to curse under my breath at those "D"'s my scientific writing professor used to scrawl across the top of my hard-labored assignments. Now I'm grateful he did. Not because it helps me to write this blog, but because when I need to ask for help for any of my own personal medical conditions, I can be much more assertive and judicious about negotiating the course (I'm talking safety as well as effectiveness)of my treatment.

Brunner H. Success and failure of mirtazapine as alternative treatment in elderly stroke patients with sleep apnea-a preliminary open trial. Sleep Breath. 2008 Aug;12(3):281-5. Epub 2008 Mar 28

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

2008-09-08T07:25:00.000-07:00

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.

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

2008-09-02T16:22:00.001-07:00

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.

Why are cats and bipolar disorder showing up in the same blog post?

2008-09-02T10:51:00.001-07:00

I volunteer for two different animal rescue groups here in Phoenix. I like to say that when things get tough with humans, I de-stress with the animals. As my friends in these organizations have realized what I do for a living, I've been presented with some interesting opportunities to combine both interests. You may have seen the post about Norm, the abandoned cat who we eventually lost due to consequences of prolonged and severe malnutrition. Thanks to my nutrition colleagues, I was steered toward a refeeding protocol developed by the World Health Organization used with children in third world countries. It's had limited and successful use in animals. I have submitted it to our vet staff for review, with the hopes that the next time an animal in need comes our way, we won't have to go through the emotional stress of losing it.

Last week, my friend Gerda paid me to consult with her about her cat Yani. I know Yani from the Arizona Animal Welfare League, and Gerda is a PhD candidate at Arizona State University. She is so diligent, she has plotted Yani's weight on a white board and kept his intake records over several months so we can problem solve. (Being the animal lover that she is, she put "anonymous" rather than "Yani" next to his assigned color so he wouldn't develop body image issues over being identified as obese!) So all of the medical and nutritional history I have for him makes this like a dream project in a fancy nutritional lab.

Despite Gerda's best efforts and documentation that Yani's food intake is limited, he continues to gain weight. He is, in turn, exhibiting signs and symptoms of depression. No interest in exercise. Extreme interest in food. Interest in food with any kind of environmental stimulation. I find this fascinating, because I used to work in eating disorders. Humans with eating disorders tend to connect all of their eating issues to some kind of psychological issue--an abuse, a trauma, an emotional issue. But here we have a cat, exhibiting the same behaviors and as far as we know he's not been verbally belittled, he's not had his body image assaulted by reading a few too many issues of Elle or Vogue, and he's certainly not being coerced by food ads on television. (Fortunately for Yani, and my Ivy League-ingrained insistence on maintaining proper scientific method, Gerda is more of a PBS than a Desperate Housewives person.)

So we've started a Facebook group and we're trying to figure out why Yani is getting fat when, thanks to a conscientious kitty mom and dad, he is following all the rules.

It seems, we've learned, that cats don't do well with carbohydrates. Many cat foods have carbohydrate fillers. And in reading cat food labels, I've seen supposedly high-protein foods that are high protein because they contain fillers such as corn gluten and soy protein that any self-respecting cat would never choose on his own. Cats are meat eaters. We've switched Yani primarily to meat, tossed the fillers, and we're experimenting with carnitine, a supplement that has been found to help metabolize fat and has actually been studied in cats.

I am particularly interested in what happens with Yani, because it's been my experience that people with mood disorders also seem to have problems with their weight. Some of it is binge eating, I know, but there just seems to be something metabolic that goes with a mood disorder that causes a proneness to gaining weight. It can even often be seen in the body type--solid center of gravity, proneness to gaining weight around the abdomen, skinny legs, in women, a tendency toward bustiness--it's the most common body type I treat in working with mental illness. I just described the apple shaped body type that is defined as a risk factor for metabolic syndrome, if you're not familiar with it. More and more, my observation is being supported in the literature, that people who have metabolic syndrome tend to have this body type...and to be more prone to mood disorders. This long drawn out dissertation is my attempt to be politically correct at saying that sometimes there is a genetic tendency toward a mood disorder, and that can be strongly linked with problems with weight.

When you see the issue manifest in a cat, who isn't subject to the same kind of emotional conditioning as a human, it really points to the fact that some people are, weight and calorie wise, completely different from others.

Researchers recently looked at the medical records of 161 individuals with bipolar disorder. Over three fourths of them were were overweight, and almost half were obese. High triglycerides, high blood pressure, and diabetes were noted at a rate greater than is observed in the general population. Over half met the criteria for metabolic syndrome.

There was a trend toward even greater incidence among individuals whose bipolar disorder was being managed with second generation antipsychotics (for example, Zyprexa). However, the trend existed whether or not those medications were part of the scenario.

My point? There are many psych meds that get blamed for weight gain. The reality is that they may exacerbate a pre-existing tendency toward weight gain, but they do not cause it. That genetic profile may benefit from a certain kind of diet. Just as Yani cannot blame his weight gain on poor social conditioning and must be encouraged to follow a lifestyle that minimizes his identified genetically-based medical risks, so must people with bipolar and other mood disorders. Weight gain is not necessarily an excuse to not take medications. A well-planned diet may help to minimize weight gain, and that is why it can be helpful to work with a nutritionist specializing in mental health, in conjunction with a psychiatrist who understands the complex interactions of mood, weight, and hormone function.

Fiedorowicz JG, Palagummi NM, Forman-Hoffman VL, Miller del D, Haynes WG. Elevated prevalence of obesity, metabolic syndrome, and cardiovascular risk factors in bipolar disorder. Ann Clin Psychiatry. 2008 Jul-Sep;20(3):131-7.

Special note: In order to continue to protect Yani's identity and self-image, the photo above is merely a stock photo of a random cat. The photo is included solely for illustrative purposes and is not intended to belittle or poke fun at any animal whose weight exceeds kitty culturally-accepted norms.

Hyperglycemia-induced membrane lipid peroxidation and elevated homocysteine levels are poorly attenuated by exogenous folate in embryonic chick brains

2008-09-01T08:13:00.001-07:00

Today I wanted to share some recent findings about the effects of elevated glucose on a developing baby's nervous system. I often think we start too late when looking for origins of many medical issues. I've learned to start way back in utero when evaluating a situation and trying to sort through what's going on. Here's an example of why that can be important.

A group of chick eggs were injected with glucose. Significant changes were found in the babies that developed from those eggs, including:
--their own hyperglycemia
--elevated oxidative (degenerative) activity in body and brain tissue
--lower body weight
--lower brain weight
There also seems to be lower levels of DHA in babies exposed to hyperglycemia. This may be due to the elevated oxidative activity destroying any DHA that might be there.

You're likely aware that taking folate is pretty much an across the board recommendation to pregnant women. In this study, hyperglycemia seemed to induce a level of oxidation/inflammation that was not significantly helped with a folate supplement.

Bottom line, it's important to eat well not just to avoid weight gain or to keep your blood sugar low to keep your doctor and dietitian happy, but because your baby's brain and body depend on you to do so.

Most of my clients express surprise that healthy eating includes as many tasty foods as it does. So before you write off a visit to the dietitian because you're afraid of what you WON'T be able to eat, consider that it may be your ticket to freedom and guilt relief to work with someone who can introduce you to the many foods that will BENEFIT you and baby!

Cole NW, Weaver KR, Walcher BN, Adams ZF, Miller RR Jr. Hyperglycemia-induced membrane lipid peroxidation and elevated homocysteine levels are poorly attenuated by exogenous folate in embryonic chick brains. Comp Biochem Physiol B Biochem Mol Biol. 2008 Jul;150(3):338-43.

It starts with Mom

2008-08-27T08:38:00.000-07:00

It's so good to be back! I love my morning routine, which involves getting up, checking my email, giving milk to the cats, working out, fixing my coffee, then settling in for an hour or two of reading research that I end up sharing in my blogs. It's been about a month since I've been able to indulge that routine, and I am so glad to be back in the groove! Today I'm going to share some more research about what happens to the brains of developing babies whose mothers don't get enough omega-3 fatty acids. This time we're looking at linolenic acid (ALA), which comes primarily from flaxseed oil and nuts. This omega-3 appears to be important for the metabolism of the neurotransmitter dopamine.

When ALA is deficient, in the hippocampus, levels of enzymes that help to create dopamine from its building blocks drop. There is also a reduction in the number of vesicles that transport the finished product, dopamine, to where it can be released and used as a neurotransmitter. As a result, dopamine levels may back up in the neuron, which the researchers in this study propose may potentially damage the terminals in charge of processing dopamine.

In the cortex and striatum, under these same conditions, there is an increase in dopamine receptor levels. These same researchers propose that this is some sort of compensatory mechanism that allows cells "downstream" from the problem to maximize their ability to capture and use what dopamine is available.

Dopamine is important for impulse control. It is also the focus of much Parkinson's disease research. The D2 receptor mentioned in this study is especially important for managing weight, carbohydrate cravings, and addictions.

Could it be that many of the chronic problems medical professionals deal with and that we as people live with...have their origin before we're even born?

I've been saying for years that the population that needs the focus of our preventive nutrition and medical education is women of childbearing age. If we don't catch problems then, and if we focus on telling them what NOT to eat instead of helping them best eat for two...well, unfortunately, it may end up being job security for anyone whose work uniform includes a lab coat.

Kuperstein F, Eilam R, Yavin E. Altered expression of key dopaminergic regulatory proteins in the postnatal brain following perinatal n-3 fatty acid dietary deficiency. J Neurochem. 2008 Jul;106(2):662-71.

Great news for you readers struggling with infertility!

2008-08-17T22:47:00.000-07:00

I'm going to be a little less active for about a week here, but it's for an important reason that will hopefully serve at least a few of you who regularly visit my blog!

For the past few years I've been training colleagues around the country in some of the practical aspects of using nutrition to help with mental health problems. One of the areas where these issues abound is in fertility treatment. So I've been actively using the same concepts that work for anxiety and depression to help with infertility. The colleagues I've been working with, as we've gained an understanding of how it all fits together, have been reporting some wonderful success stories in clients who had been told they might never have a child of their own.

As we've grown as a network, we've gained the attention of sponsors, and one of those sponsors, Nutrabella, approached me about collaborating with them to contribute to a fertility report that will be appearing in East Coast newspapers this coming Friday--the Washington Post, Wall Street Journal, and Boston Globe, to name a few. Another sponsor, SGJ Consulting, contributed to the project as well. It's been a great team to work with from start to finish!

That kind of opportunity has the potential to reach quite a few people (2.1 million is what has been projected)! So I've been busy making sure we're ready to handle the traffic and that everyone who's been going through my training is ready to take referrals.

If you know of anyone who is struggling with infertility, please tell them we have several resources:
(1) our network's blog,
(2) individual consultations, and
(3) Fertile Intentions (TM), our new couples infertility spa day experience, in Marina del Rey, California.

This is such a great audience with whom to share the message that there are many options outside of medication for helping with stress-related problems.

I'll be back in about a week, hopefully with some exciting updates, and definitely with more comments on nutrition and mental health.

Have a wonderful rest of August in the meantime!

A little about vitamins...and a lot about food and mood

2008-08-15T20:19:00.000-07:00

My friend Diane Whelan and I toured a vitamin factory yesterday. Was that ever interesting! I guess you just assume all those pills show up in all those bottles on their own. I learned so much about what it takes to grow the herbs, extract the active ingredients...even how much it takes to be an international business and sell different formulations to different countries while being in compliance with labeling regulations and varying cultural nutritional needs.

At one point our guide hand-pressed me a personal supplement the old-fashioned way.

Diane works with a product line called Nutrilite. The products are very high quality, and what really struck me as we toured the factory was how proud the employees were of their work.

You can learn more about this product line at this link: http://www.afterthediet.com/whyvitamins.htm

I receive no commission from Nutrilite for sharing this information. I simply like to share good information and products when I do see them.

Below is some great information about food and mood from Nutrilite that you also may enjoy.

You and Your Mood: What’s Food Got to Do with It?
Duke Johnson, M.D.
Medical Director, Nutrilite Center for Optimal Health

Do you head straight for the ice cream after an especially hard day at work? It seems like a no-brainer that your mood affects your food choices. But did you know that food can also affect your mood? There are foods that can give you a boost when you need one.

The food-mood connection
It starts with chemicals in your brain, called neurotransmitters. They act like a one-way command center, telling your brain cells what message to pass on to all the other cells. Two neurotransmitters always send a “pay attention, stay alert” message, while another one always sends a “calm down, relax” message.

Now, consider this: If your diet doesn’t include the right nutrients, your brain won’t make enough neurotransmitters to send messages at optimum levels. And if you eat (or don’t eat) specific nutrients, your brain selectively makes certain neurotransmitters but not others.

Generally speaking, the following nutrients all affect neurotransmitter production:

Proteins.
Carbohydrates.
Vitamins.
Minerals.
For example, if you don’t consume enough food with the right amount of B vitamins, vitamin C, selenium, and magnesium, your body won’t produce or store enough of these critical chemical messengers.

And that’s how the foods you eat (or don’t eat) affect your mood, energy levels, stress, and sleep habits.

And in case you want to know their names, the “high-alert” neurotransmitters are dopamine and norepinephrine. And serotonin has a calming, anxiety-reducing effect.

How to say it:
(emphasize the syllable in bold):

Neurotransmitters: Nurr-oh-trans-mitters.
Dopamine: Dope-a-mean.
Norepinephrine: Nor-eppa-neff-rinn.
Serotonin: Ser-oh-tone-in.
Feeling down?
Eat a small amount of carbs, like whole-grain cereal, whole-wheat pasta, or yogurt with fruit. That stimulates serotonin production, and relaxation and calm will follow.

Want more energy?
But if you’re gearing up for an exam or an interview, you should eat some lean protein with healthy carbs. That will trigger dopamine and norepinephrine, to get your mental juices flowing.

Nutrient
Food
Results
How

Lean protein
Meat, low-fat dairy, and eggs
Increases your alertness and concentration
Increased production and activity of dopamine and norepinephrine

Healthy carbohydrates
Brown rice, plain oatmeal, whole-grain cereals, and fresh fruit
Improves your mood, curbs your food cravings, and helps you sleep
Increased production and activity of serotonin

Omega-3 fats
Salmon, tuna, sardines, anchovies walnuts, and flaxseed

Increased production and activity of serotonin

Brain drainers and brain boosters
Be careful about grabbing chips, crackers, or fast food when you’re feeling down or stressed. It definitely can make you feel better, because processed foods high in sugar and saturated fat give you a burst of energy. But not too much later, you’ll crash and feel irritable and anxious.

And then, to feel better, it’s natural to return to the food and drink that gave you energy … but it’s easy to see where that leads – more sugar and more unhealthy fats, another boost and another crash.

Break this cycle and feel better – in a healthier, more lasting way, by eating these brain boosters, instead:

Brain drainers
Brain boosters

Coffee and a doughnut for breakfast
Oatmeal topped with berries, and a hard-boiled egg

Hamburger, fries, and soda for lunch
Turkey sandwich on whole-grain bread and veggies

Frozen fish nuggets and tater tots for dinner
Grilled salmon, broccoli, brown rice, and a green salad

Comfort foods
Sometimes the only food that will do is the meatloaf and mashed potatoes Mom used to make when you were a kid. Or maybe it’s tomato soup and grilled cheese sandwiches. The strong emotional connection of these comfort foods stimulates release of the “feel good” neurotransmitters.

And to balance out the comfort food, up the nutritional quality. If you want a cookie, make it oatmeal raisin or fruit filled. Buy lower-fat ice cream or single-serve popsicles. Throw some veggies on that pizza.

What you drink matters, too
Do you reach for a cup of java or cola first thing in the morning or a glass of wine in the evening? Caffeine and alcohol can improve your mood, but too much of a good thing can have not-so-good consequences. Three hundred milligrams of caffeine – roughly what you get from three cups of brewed coffee – can increase your alertness and concentration. But more than 300 mg can make you nervous and jittery.

Alcohol has its pros and cons, too. Two drinks a day for men and one for women is linked to a lower risk of heart disease, but more than that may lead to weight gain, difficulty sleeping, and decreased powers of concentration. Too much alcohol also makes it easier to choose foods that don’t support a good mood.

Eat well to feel good
Feed your brain the best food you can! Choose a balanced diet of lean protein, healthy carbs, and omega-3 fats. Make sure to take a multivitamin that delivers the right blend of vitamins, minerals, and phytonutrients. Add regular exercise, enough sleep, and decisions that fit your lifestyle priorities. And you’ve got a no-brainer recipe for mastering your mood.

So tell me again....WHY are we telling pregnant women to avoid eating fish?

2008-08-11T12:20:00.000-07:00

This is one of those issues that simply drives me crazy. The Food and Drug Administration, several years ago, because of mercury content, identified four fish that might be harmful to consume during pregnancy. Those four fish were king mackerel, tilefish, swordfish, and shark.

For the recored, in 26 years of doing this work, I have yet to EVER have ANYONE at ANY point in their life tell me in a diet recall that they eat mackerel (too fishy), shark (eeeuuw!!!), or tilefish (what the heck is a tilefish?). Swordfish is a rare item that comes up.

Let's count those again. Four fish. Mackerel. Shark. Tilefish. Swordfish.

In the time that this warning has come out, consumption of ALL fish has decreased, by about one sixth (17%).

Why have we overgeneralized? Because scary headlines are what sell newspapers and news broadcasts. And when newspapers sell and news shows are watched, newspapers and television stations make more money from advertising.

Did you know, that the losses associated with this preventative measure may outweigh the benefits? According to the Harvard Review, if pregnant women were to eat the same amount of fish they normally do, but replaced fish high in mercury with fish low in mercury, cognitive development benefits could be achieved with virtually no nutritional losses. When those cognitive development benefits are taken into consideration, if those women were to cut their fish consumption by one-sixth, exactly what has happened, the nutritional benefit derived drops by 80%.

A new study suggests that omega-3 deficiency during pregnancy may have effects years later. A group of researchers who had reported that supplementing pregnant and lactating women with omega-3 fatty acids during pregnancy resulted in higher IQ scores in their children 4 years after birth, retested the same children at 7 years. The women in this study either took 10 ml of cod liver oil or corn oil from the 18th week of pregnancy until 3 months after their babies were born. Mothers with high levels of plasma ALA and DHA (two omega-3 fatty acids) had children who better learned information, organized it, and later used it in practical situations.

Again...'splain me why we're telling pregnant women to be afraid of fish?

http://www.hno.harvard.edu/gazette/2005/10.20/26-merc.html

Helland IB, Smith L, Blomén B, Saarem K, Saugstad OD, Drevon CA. Effect of supplementing pregnant and lactating mothers with n-3 very-long-chain fatty acids on children's IQ and body mass index at 7 years of age. Pediatrics. 2008 Aug;122(2):e472-9.

Carnitine supplementation enhances Depakote activity

2008-08-06T08:00:00.000-07:00

For the last few months I've been reading carnitine research (there's a boatload of it and it's completely kept me out of trouble!)

It is pretty well documented that people taking valproic acid (Depakote) have a problem maintaining carnitine levels. To the point where, after doing this research, I have no problem saying that anyone on Depakote should automatically be placed on L-carnitine as well.

Anyway, I just found an article reporting that carnitine supplementation in conjunction with Depakote use enhanced the levels of Depakote in the brain. In other words, if you use carnitine while using Depakote, you won't need as much Depakote. And if you're not using as much Depakote, you're not as likely to experience the side effects that make people not want to comply with the regimen, such as weight gain, infertility, acne, yadayadayada.

Monika's Bottom Line
Doctors should have a carnitine chip inserted in the medication-prescribing region of the brain that does not allow them to script this med without also scripting this supplement.

Sakemi K, Takada G. Effect of carnitine on valproic acid concentrations in serum, brain, and liver. Pediatr Neurol. 1998 Apr;18(4):331-3.

Topamax and kidneys...these two will probably never be BFF's

2008-08-04T08:53:00.000-07:00

I've noticed in looking at my blog statistics that a previous entry on kidney stones resulting from topiramate (Topamax) use continues to be one of my most visited pages on this blog. So when I found more information about this medication and its effect on kidneys I wanted to be sure to share it.

Within 5 days of starting topiramate, the six subjects in this study experienced an average drop of calcium in their urine of about 31% and of citrate by about 40%. When calcium and citrate are not showing up in the urine, it's likely because it's accumulating elsewhere. Like in kidney stones.

Interestingly, increasing the topiramate dose seemed to improve calcium readings and to worsen citrate readings. Meaning you might get less of one kind of kidney stone and more of another.

The authors of this study said that the degree of reduction of urinary citrate was profound enough to be compared to the clinical presentation of renal tubular acidosis. This is a condition in which the body's pH is shifted to an unhealthy level, promoting important changes such as bone demineralization. And THIS will cause rickets in children and osteomalacia in adults. These are not things you will see or feel in those first few days. You need to measure them clinically.

I would strongly recommend, if you and your physician have concluded that the absolute only way to manage your bipolar disorder, your migraine, or your epilepsy, is with topiramate, that you closely monitor your urinary metabolites to be sure you're not doing more harm than good.

And if you're one of those souls who's been convinced that it might be nice to try topiramate to see if it helps you lose weight, consider that you might not just be
losing fat, you might also be losing bone. What's the point of being thin if you have to be sick when you get there?

The only way to know is to monitor. Please don't stick your head in the sand and hope it's not happening to you.

Warner BW, LaGrange CA, Tucker T, Bensalem-Owen M, Pais VM Jr. Induction of progressive profound hypocitraturia with increasing doses of topiramate. Urology. 2008 Jul;72(1):29-32; discussion 32-3.

I found a photo of a kidney stone on the 'net. Imagine trying how it feels to pass something this big through an opening about as big as a piece of cooked pasta. Now you know why I'm trying to get your attention!

This topic hit home for me and because of that I want to pass along a very important warning

2008-08-01T07:46:00.000-07:00

Hello everyone,

Last night I attended a memorial service for a neighbor. A month ago she committed suicide, in a very violent fashion. Most of us were dumbfounded, as this neighbor, to all of us, was a healer, kind, loving, always smiling. What most of us did not know, until last night, as her daughter spoke, was that our friend struggled with bipolar disorder. She had been on many different medications, and apparently had a rotation going of different medications. The issue seemed to be that she would develop a tolerance to one regime, so she would rotate through different cocktails as one set lost its effect.

Apparently, on her own, she decided to wean herself off the medications. No supervision from her doctor.

I wonder if this is how she got herself into trouble.

I do my best in this blog to stay neutral, and let you, the readers, decide if medication is for you, or if you'd rather choose an alternative option. I still feel that way.

However, what I do want to insist on, after this personal experience, is that if you are on medications, that you do not manage the use of these medications, or even alternative options, on your own. Whether it's in a bottle or from a plant or a food, when you use chemicals to alter your brain chemistry, you alter your brain chemistry. Once the compound is in your body, regardless of its origin, you really don't have any control over where, when, and how this compound is going to work.

Please do not operate on the assumption that because you are "getting off meds", that what you are doing is safe. It can be, but only if done correctly. Please do not assume that because what you are taking is organic and/or was not sold to you by a pharmaceutical company, that you're in good hands. You may...or you may not be.

It can be very hard to reach out for help when the problem you have is a mental health issue. I lived just yards from this neighbor, she knew what I did for a living, and never once did she ask me for any information. But the important thing to remember about a mental health issue is that it affects how you think, reason, feel, and act. Even if you feel that you're in control, it's always important to have at least one human sounding board to depend on when making decisions affecting how your brain functions.

I don't want any of you to ever think I said anything to encourage you to endanger yourself. If I present new information that you think might be helpful, please download it and share it with your provider. Don't act on it alone. I want all of you to be around as long as I can come up with new and helpful information to post on this blog.

Fifty Ways to Boost Your Energy Without Caffeine

2008-07-30T17:25:00.000-07:00

Here's a great piece by Christina Laun at the Nursing Online Education Database:

http://noedb.org/library/features/50_ways_to_boost_your_energy_without_caffeine

I am continually concerned about the number of people I'm seeing on sleep medications who have never been given information about natural options. This article is a great place to get you started thinking.

Lamotrigine may cause cleft palate

2008-07-28T11:06:00.000-07:00

It is very important for women of childbearing age to know how medications they may be on might affect the health of their children. I've posted the statistics before regarding the percentage of births resulting from unintended pregnancies, so this warning goes out to ALL women, not just those intentionally trying to conceive.

In this case, the issue is Lamictal (lamotrigine). I work a lot with polycystic ovary syndrome. This is a medication often used with women needing anticonvulsants because it is one of the few in that category that does not seem to wreak havoc on the management of that syndrome. So the population I work with the most is especially sensitive to the risk I describe here.

The medical records of 684 women who had taken lamotrigine during pregnancy were reviewed for the incidence of birth defects. These results were compared to trends in children born to women who had not taken this medication during their pregnancy. The incidence of cleft palate-type birth defects was 10.4 times greater in the lamotrigine-exposed infants than it was in the non-exposed infants. The exposure noted to be most important was that which occurred in the first trimester of pregnancy.

Just be aware, if you're female and there is any chance at all that you might conceive, that you would benefit from working closely with any physician prescribing you any medication at all, for any reason, to be sure there is no unconsidered risk lurking beneath the issue being focused on with the writing of a prescription.

Holmes LB, Baldwin EJ, Smith CR, Habecker E, Glassman L, Wong SL, Wyszynski DF. Increased frequency of isolated cleft palate in infants exposed to lamotrigine during pregnancy. Neurology. 2008 May 27;70(22 Pt 2):2152-8. Epub 2008 Apr 30.

Life-threatening constipation associated with clozaril

2008-07-26T08:33:00.001-07:00

This one is short, and sweet, and there is no need for me to paraphrase what the authors report. The one thing I will point out is that even in combination with a laxative, clozapine was not productive in this case. Persons taking clozaril may not be the best historians or the most assertive regarding medication complications and side effects, so it is important to be thorough from evaluation all the way through treatment in order to prevent problems.

OBJECTIVE: The aim of this paper was to describe the association of clozapine with life-threatening constipation. METHOD: Case report. RESULTS: A 53-year-old man presented to the emergency department with severe abdominal pain and bilious vomiting after being on clozapine for over a year for schizoaffective disorder. Surgery revealed severe faecal impaction in the large and small bowel. Clozapine was ceased. There were significant difficulties in the subsequent psychiatric management. Clozapine was gradually reintroduced with concurrent laxative administration, which resulted in another episode of severe constipation with faecal impaction. CONCLUSIONS: Clozapine can be associated with potentially life-threatening constipation. Psychiatrists, especially consultation liaison psychiatrists, physicians, surgeons and radiologists, should be aware of the seriousness of clozapine-induced constipation and its potentially fatal complications.

Rege S, Lafferty T. Life-threatening constipation associated with clozapine. Australas Psychiatry. 2008 Jun;16(3):216-9.

Mixing old and new to create something better

2008-07-23T11:34:00.000-07:00

I've got friends on both sides of the medication issue reading this blog. Some are vehemently anti-medication, while others are suspicious of natural alternatives. My desire is to make this as balanced a blog as possible, and fair to both sides. Maybe that's the Libra in me...maybe it's just that I think there are positive and negative aspects of each approach, and there are safety issues with each approach. It's not so important WHAT treatment is used, as it is WHY and HOW.

I really like this study because it integrates both schools of treatment in a promising way.

Two of the medications I write a lot about, olanzapine (Zyprexa) and clozapine (Clozaril), are notorious for their effects on blood lipids, weight gain, and diabetes risk. I'm not a big fan of either, but I do know because I work with a very skilled psychiatrist in town who completely supports my nutritional and complementary suggestions, that there are simply some people who need the medication in order to be safe to self and others. And because of that, they are simply at risk of metabolic syndrome-related side effects. I am always looking for ways that high-risk-of-side-effects medications can be used in combination with therapies that minimize the actual dose that needs to be used.

Gingko biloba is primarily recognized for its use in preserving memory. However, it was also recently tested on 42 patients with refractory schizophrenia who were maintained on stable doses of clozapine. A dose of 120 mg per day helped to reduce the negative symptoms of schizophrenia. It did not, however, reduce psychopathology symptoms.

So what's the point of taking it if it didn't reduce the medication need? I have read study after study after study over the years and it is clear, people stop taking medications when they don't like the side effects. If you can help push the balance of effects of a medication over to the positive, you might just increase compliance. And compliance to a medication regime means, potentially, better quality of life.

Who would have thought that beautiful tree with the funny shaped leaves had such a great little secret in its biochemistry?

Doruk A, Uzun O, Ozşahin A. A placebo-controlled study of extract of ginkgo biloba added to clozapine in patients with treatment-resistant schizophrenia. Int Clin Psychopharmacol. 2008 Jul;23(4):223-7.

Do you need medication...or do you need to de-clutter?

2008-07-21T15:58:00.000-07:00

We are a sleepless nation. Practically every client I have counseled over the past 6 months has complained of fatigue and some type of disturbed sleep pattern. There is a lot of money, in other words, for whoever can figure out how to put the "zzzzzz's" back into the average American's life.

One group of researchers was hopeful that atomoxetine, (Strattera), a drug approved for attention deficit-hyperactivity disorder, would do the trick. What the researchers found was that this medication helped to decrease the sleepiness related to poor sleep, but it didn't improve the metabolic parameters associated with sleep disorders.

I think an important take away message here is that, like it or not, we need to sleep, and we suffer without it.

Years ago, I was the nutritionist for Apple Computers at their headquarters in Cupertino, California. Clients used to come in to see me about their weight gain, and invariably they'd tell me about the 128 hour work week they'd just completed, or the 3 hour one way commute to work, or the jaunt to Tokyo then Sydney and back to Cupertino in time to report to the boss on Monday morning. And then they wondered why they felt so horrible, why their concentration wasn't what it used to be, and why they were gaining weight.

You can't just put a bandaid on sleepiness and assume that it makes things better. You get sleepy for a reason. Melatonin levels rise when it's time to do some internal housecleaning. If you've been busy, stressed, thinking, etc., etc., etc, you've been oxidizing brain cells. You need melatonin to clear out the clutter. If you don't give your brain that melatonin one-on-one time...the things the brain can do when it's not cluttered with stress remnants, just can't get done.

Think of how long it takes to get a simple task done when you walk into your office and there are piles of papers everywhere. You have to sort through everything, clean out a work space, think about what you're going to do...and you spend a lot of extra time digging through the piles to find the papers you need to do what you need to do.

Your brain is no different. If you let the hormonal housemaid come in and organize things for you, your hormones function, you can actually be in a good mood, you can finish tasks more quickly, and you can be more creative.

So don't think of being sleepy as something annoying that you need to fix with a "fix"...you're not feeling sleepy because you're caffeine deficient or running low on Red Bull. You're sleepy because your brain's trying to tell you to log off of life for a few hours and refresh.

Bart Sangal R, Sangal JM, Thorp K. Atomoxetine improves sleepiness and global severity of illness but not the respiratory disturbance index in mild to moderate obstructive sleep apnea with sleepiness. Sleep Med. 2008 Jul;9(5):506-10. Epub 2007 Sep 27.

Sometimes it's what you CAN'T see that you should be paying attention to

2008-07-15T18:59:00.000-07:00

I've been in this field for many years. Back when I started, and was learning about diabetes, I was taught that the best way to measure whether or not a diabetic had good blood glucose control, was to monitor blood glucose. When records looked good, we assumed all was good. Diabetics knew better. They often manipulated their diet and knew how to eat around the readings, and could straighten out a few days before a doctor's appointment with healthy readings.

These days, the glycosylated hemoglobin test is considered a more accurate assessment. It can give the practitioner an idea of what goes on, on average, all of the time. And people who are not compliant between doctor visits can't manipulate the science behind how the test does its job.

What I've learned from this, is that sometimes, even though things look good on the surface, there are problems underneath. And we should never assume that there are no problems just because we can't see them.

Enter epilepsy.

It has been known for quite awhile that certain antiepileptic medications can deplete the body of carnitine, a nutrient that is needed for healthy weight maintenance and to protect the brain against aging. In fact, older studies recommend supplementing carnitine in persons on medications such as valproic acid (Depakote) in order to minimize problems associated with carnitine deficiency.

Researchers recently compared carnitine levels in children on three other medications (vigabatrin or Sabril*, lamotrigine or Lamictal, and topiramate or Topamax). Clinically the only group with significantly lower carnitine levels were those on valproic acid.

If the conclusion of this study was that carnitine levels were not compromised by the other three medications, that would have been logical. However, the researchers also stated that because there were no apparent symptoms related to carnitine deficiency, that doing anything about it may not be necessary.

I happen to have spent the last few months going through several hundred pages of abstracts on carnitine, and with all due respect, I must disagree. I've got dozens of papers suggesting that carnitine is important to protect the brain against oxidation; in fact, it's been proposed by numerous researchers to be a potentially important agent in the fight against Alzheimer's disease.

With all the research I'm having to wade through, I cannot believe that it is not standard practice to recommend carnitine supplementation to anyone receiving valproic acid for any reason. My list of references is very, very long and I'm only up to the year 1992. If you happen to be reading this and would like me to spend another post detailing these references when I am finished, I would be happy to do so. Simply reply to this post so I know you'd like the information.

Just because we can't see everything happening in the brain...doesn't mean we shouldn't be doing anything about the things that we do know and can do something about.

Zelnik N, Isler N, Goez H, Shiffer M, David M, Shahar E. Vigabatrin, lamotrigine, topiramate and serum carnitine levels. Pediatr Neurol. 2008 Jul;39(1):18-21.

*Sabril is sold in Canada.

Hello and an update

2008-07-15T18:01:00.000-07:00

My posting has been somewhat erratic and for that I apologize. Sometimes life throws us curve balls that need to be honored. In this case...the curve ball was Norm.

I met Norm through my volunteer work in the cattery at the Arizona Animal Welfare League. All spring I've been seeing cats we've rescued from homes abandoned due to foreclosure. Every single one of these cases has been horribly sad...but I wasn't sure what simple me could do about it. Then I met Norm. Norm was left in a home here in Phoenix on June 1--no air conditioning, no food, only toilet water. Someone finally found him in that home on June 26, about as close to death as any living being can get and still breathe. He was so weak, he could not even stand on his own. He's needed two surgeries because his dehydration was so bad his intestines started to stick to each other and cause blockages that prevented him from keeping food down.

I was so upset when I learned of this case I couldn't sleep. I looked online and learned that in my county alone, there are currently over 30,000 foreclosed homes. All I could think about was how many other animals were out there in need of rescue? I didn't care about the overwhelming number. I just cared that someone try to do something.

Then, out of the blue, I found a small link online about a group of real estate professionals who had started a 501(c)(3) organization designed to rescue animals in just these kinds of situations. Long story short, I am now on the board and we're completely focused on lining up foster homes and donations so we can start to do the difficult work of rounding up animals who need us.

If you're interested in helping or donating, our website is soon to go live. You'll find it if you go to Lost Our Home Pet Foundation. In the meantime, you can send donations to 8105 E. Rita Drive, Scottsdale, AZ, or call Jodi Polanski at 480-688-7899 if you have a home to open as a foster.

And Norm? Well, he's been with us for about 3 weeks now, and the clinic staff say when he's completely renourished he's going to weigh about 10 pounds. Right now, after food and IV for 3 weeks, he's only just over 5 pounds. That gives you an idea of just how sick he was when he came into our lives. The main issue right now is that Norm is so playful he's not sitting still the way he ideally would in order to gain all that weight back. But the important thing is, his spirit is back, alive and well, and he's inspired a whole lot of people to step up and work together to prevent such future tragedies.

Now I can get back to the work of posting more information on this blog!

Saying No to Psychotropic Drugs

2008-07-12T18:28:00.001-07:00

By-line:

This post was contributed by Heather Johnson, who writes on the subject of online lpn schools. She invites your feedback at heatherjohnson2323 at gmail dot com.

Saying No to Psychotropic Drugs

Depression can happen to even the hardiest of us, depending on the circumstances we’re in. While most of us bounce back to normalcy in a short period of time, others have a harder time of coping, and are often labeled by society as mentally ill and prescribed psychotropic drugs by doctors in the psychiatric field. These drugs often do more harm than good, and have come under harsh criticism as being promoted indiscriminately by psychiatrists to fill the coffers of the drug manufacturers.

The side-effects of psychotropic drugs:

In the last five years, more than 60 warnings have been issued by international drug regulatory agencies about the medical side-effects that arise when psychotropic drugs are used, especially by those under the age of 18 – suicidal tendencies, increased hostility, diabetes, heart problems, strokes, depression, anxiety, disinterest, hallucinations, mood and personality swings, sleep disorders, delusions, lack of concentration, increased heart rate, confusion, increased nocturnal urination, agitation, irritability, mania, tissue damage, imbalance of hormones, diminished sex drive, nightmares and trembling to name just a few.

Can we treat depression without psychotropic drugs?

The answer to the above question is yes, we can. By:

• Treating the cause and not the symptoms: A good physician is able to treat depression as well as if not better than a psychiatrist by identifying the underlying cause behind the feeling of intense sadness and negative emotions, and providing relevant treatment. Often the cause of depression is a sudden trauma, loss of a loved one or just loneliness.
• Checking general medical health first: A thorough medical examination often reveals that most patients suffer depression as a side effect of a greater problem, such as intense headaches and other pains caused by tumors or other chronic diseases and conditions. Treating those diseases will often solve the problem.
• Examining the drugs and antibiotics the patient is on: Some antidepressant pills cause depression while prolonged usage of antibiotics causes a weakening of the immune system leading to fatigue and anxiety disorders. Eliminating these drugs from the patient’s medication routine in a systematic and proper manner helps in the treatment of depression.
• Checking the food habits of the patient: Foods that are low in good fatty acids and rich in complex carbohydrates often cause depression. Children with attention deficit hyperactivity disorder (for which psychotropic drugs are normally prescribed) are usually found to be on a diet low in fatty acids and iron and high in sugar. Some foods cause allergies which in turn cause depression.
• Checking for conditions: Some conditions like extremely low blood sugar levels, thyroid problems and adrenal fatigue cause depression. Treating these conditions rids the patient of the somber mood.
• Following a pattern of good health: Eating healthy and nutritious food, getting enough physical exercise and sleeping well is often enough to treat depression at times. A mild sedative may be prescribed if sleep is elusive at first.

Very often, we find that mental healing is effectively accomplished with a combination of patience, tolerance and kindness. Trained medical personnel need to be committed to the patient’s well-being instead of immediately resorting to drugs or treatment by shock and incarceration.

A word of warning: It is not safe to stop psychotropic drugs abruptly without medical supervision or advice; the associated risks include side-effects and withdrawal symptoms.

More on cell phones--update

2008-07-09T11:31:00.000-07:00

I am moving this post up with an update--it was a very unfunny hoax created by the Bluetooth people. I apologize for inadvertently passing it along as truth.

If you liked my recent post on cell phones...you'll love this video:

http://www.koreus.com/video/telephone-portable-mais-popcorn.html

Maybe you shouldn't try this at home

2008-07-07T13:18:00.000-07:00

Lisdexamfetamine (Vyvanse) is a relatively new drug. Literature on this medication began to appear in Pub Med about a year ago. It is classified as a "prodrug," which means that it is taken in an inactive form, which then becomes active in the body.

According to the first reviews written about lisdexamfetamine, it supposedly has less abuse potential than dextroamphetamine (Dexedrine, and in combination with other compounds, Adderall), two other medications popular for treating attention deficit-hyperactivity disorder.

However, that doesn't mean toxicity is not an issue. In the words of the researchers themselves, this is what happened when lisdexamfetamine was given to a group of rats:

In an acute study, LDX doses of 60 mg/kg and higher caused increased motor activity. At 1000 mg/kg, one rat died and another was euthanized. In a 7-day repeat-dose study, all rats dosed with LDX (14 per dose group for each sex) showed increased activity; 10 male rats and 11 female rats at 300 mg/kg/day and 3 female rats at 100 mg/kg/day were euthanized because of self-mutilation and 1 male rat at 300 mg/kg/day was found dead. In a 28-day study, only rats at 80 mg/kg showed signs of self-mutilation and thin body condition. In both the 7- and 28-day studies, LDX caused significant changes in some blood chemistry parameters (e.g. blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase) and organ weights (e.g. particularly heart, liver, brain, and spleen).

Self-mutilation is absolutely not a benign or neutral side effect.

"...the apparent lethal dose of LDX in rats is more than five times higher than the LD(50) of orally administered d-amphetamine, supporting a putative protective effect of conjugating amphetamine with lysine."

OK, whew! Apparently since rats were less self-destructive on this medication than they were on dextroamphetamine, they were good to go with the marketing!

Now, an article is showing up in Pub Med with the following title:

Poison Centers Detect an Unexpectedly Frequent Number of Adverse Drug Reactions to Lisdexamfetamine.

And the first sentence of MedLine Plus fact sheet on this medication is, "Lisdexamfetamine can be habit-forming." This about a medication that is supposedly designed to reduce abuse potential!

I cannot access the article online, but as soon as I can get the text, I'll be sure to share it.

Because of the toxicity issue, I want to post known side effects, as listed on MedLine Plus' fact sheet. If you experience any of these, consult your prescribing physician immediately:

restlessness
mood swings
irritability
difficulty falling asleep or staying asleep
uncontrollable shaking of a part of the body
dizziness
headache
dry mouth
stomach pain
nausea
vomiting
loss of appetite
weight loss
fever
fast or pounding heartbeat
chest pain
shortness of breath
fainting
seizures
hallucinating (seeing things or hearing voices that do not exist)
aggression
frenzied, abnormally excited mood
seizures
tics
blisters
rash

I am having a hard time with a medication that was supposed to be a kindler, gentler form of a very potent--and popular--medication having some seemingly serious problems that for some reason...are just buried in the literature.

Faraone SV, Upadhyaya HP. The effect of stimulant treatment for ADHD on later substance abuse and the potential for medication misuse, abuse, and diversion. J Clin Psychiatry. 2007 Nov;68(11):e28.

Blick SK, Keating GM. Lisdexamfetamine. Paediatr Drugs. 2007;9(2):129-35; discussion 136-8.

Biederman J, Krishnan S, Zhang Y, McGough JJ, Findling RL. Efficacy and tolerability of lisdexamfetamine dimesylate (NRP-104) in children with attention-deficit/hyperactivity disorder: a phase III, multicenter, randomized, double-blind, forced-dose, parallel-group study. Clin Ther. 2007 Mar;29(3):450-63.

Krishnan S, Montcrief S. Toxicity profile of lisdexamfetamine dimesylate in three independent rat toxicology studies. Basic Clin Pharmacol Toxicol. 2007 Oct;101(4):231-40.

Spiller HA, Griffith JRK, Anderson DL, Weber JA, Aleguas A. Poison Centers Detect an Unexpectedly Frequent Number of Adverse Drug Reactions to Lisdexamfetamine. Ann Pharmacother. 2008 Jul 1.

http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a607047.html

Antidepressants and weight gain

2008-07-04T10:27:00.001-07:00

For anyone looking for a list of antidepressants and weight gain, I have a summary chart on my website: http://afterthediet.com/antidepressant_medications.htm

This listing is an excerpt from my CD, Nutritional Implications of Psychotropic Medications, a collection of fact sheets on the neuroendocrine and nutritional considerations of 59 different medications and over the counter supplements used for brain and nervous system conditions. Antidepressants are just one category.

I'll keep the link on the blog for anyone wanting it in the future.

Happy Fourth!

Zzzzzzzzzzap that snoring!

2008-07-02T09:42:00.000-07:00

,
Snoring is one of those things we do that we tend to laugh at, but which is important not to ignore. Snoring not only impairs the sleep of the person who does it, but that of the poor loved one who tries to sleep in the same bed with a snorer.

Today's post is devoted to snorers, and their loved ones...especially my loved ones who have patiently tolerated my snoring. I promise...I'm working on it! :)

(Since I am a guilty party, I wanted a photo of a couple in which the woman was the snorer, but there appears to be a clipart gender bias when it comes to this issue. Trust me, women snore too, and when we do it ain't a dainty thang!)

One of the primary reasons people snore is because they have obstructive sleep apnea (OSA). This is a condition in which, due to certain sleep postures, the airway is obstructed during the night, cutting off oxygen supply. At multiple intervals during the night, air supply is completely cut off...snoring is the result of trying to breathe through an impaired airway. One of the more common cures for this type of snoring is a CPAP (continuous positive airway pressure) machine, fashioned after the oxygen masks used by fighter pilots. It works, but honestly, sleep docs, it's really not the most amorous solution if you're working on behalf of both people affected by this problem.

Often times the culprit in OSA is excess weight. Obesity can force new and different sleeping positions that challenge healthy breathing during sleep. People who don't sleep well can easily fall into a habit of living on caffeine and sugar for energy during the day, which can worsen the cycle of poor sleep and weight problems. Before you know it...you're backed into a corner!

My programs all stress the importance of good sleep hygiene, in other words, making sure that most of what you do in the evenings is about signaling to your brain that sleep is coming...and then quieting your environment in order to promote that actually happening. Even little things such as changing into casual clothing, sitting in a reading chair, having a cup of chamomile tea, avoiding violent television shows and movies, minimizing alcohol intake, and avoiding intense exercise...can all help promote healthy sleep.

A very important issue to keep in mind is that with OSA, part of the problem is oxidative stress. In other words, little things you're doing that stress the brain promote degeneration of the cells in the brain that help to regulate breathing. It's not all about your weight or your habits.

Nutritionally, eating more fruits and vegetables and fewer simple carbohydrates (sweets and refined breads/pastas) can be very good anti-oxidative strategies. So can increasing your intake of omega-3 fatty acids and decreasing your intake of omega-6 fatty acids.

Recently, some researchers reported that the sleep aid melatonin may also be helpful.

What they found in rats that had been exposed to hypoxic conditions was that indices of inflammation started to show up. Brain cells started to die. And the brain, ironically, started making less of the enzymes needed to make antioxidants. When melatonin was provided, cell death was completely prevented, there were fewer inflammatory markers to measure, and antioxidant production increased.

There are two important things this study tells us. (1) When our sleep is impaired, and we're not producing enough of our own melatonin, we have potentially created an environment that gradually kills brain cells. As annoying as snoring is, the problem is about a whole lot more and it needs to be addressed. (2) Melatonin supplements can help correct the imbalance that caused the problem.

Just a footnote, I've had many clients tell me they started taking melatonin and when it didn't help them sleep...they stopped. The authors in this study did not seem to care whether or not melatonin produced sleepy rats. They focused on and reported cellular changes. These can occur whether or not you feel sleepy the first few times you try melatonin. If snoring is an issue for you, consider trying melatonin and being consistent with its use, whether or not it's immediately improving your sleep quality.

Hung MW, Tipoe GL, Poon AM, Reiter RJ, Fung ML. Protective effect of melatonin against hippocampal injury of rats with intermittent hypoxia. J Pineal Res. 2008 Mar;44(2):214-21.

Some help for skin problems

2008-06-30T07:29:00.001-07:00

About a week ago I was visiting an addictions treatment center and something that really struck me was the severity of skin issues I saw in many of the residents. Part of that may be due to poor nutrition, part to stress, and part as a result of drug use itself.

In any case, there's a great website I found with information on healthy skin care that I thought would be of interest to some of you reading this blog. I'll post the information as a permanent link, but if you are interested now, the name is http://www.highonhealth.org.

Cigarettes and coffee for breakfast...why it's so easy to get stuck in that rut

2008-06-27T10:22:00.000-07:00

My teaching assistant today comes from Star Wars. He is here with me, because I have lost track of the number of times, when trying to do a serious presentation about neurotransmitters, I have said, "R2D2" when I meant to say "DRD2". I will have to check the Universal Diagnostic and Statistical Manual to see if I meet the criteria for Intergalactical Dyslexia...

What R2D2 and I would like to tell you about his almost-namesake today, the DRD2 receptor, is that this subset of dopamine receptors is sensitive to how we eat. DRD2 is responsible for impulse control. People who have a disturbed DRD2 system are more prone to problems such as shoplifting, gambling, alcohol addiction, nicotine addiction, and binge eating. They also seem to have more intensive carbohydrate cravings.

Scientists recently reported that this receptor is especially sensitive to food restriction. That is, people who restrict their food intake seem to be more sensitive to the reinforcing effects (the effects that make you feel good and want to use) of several addictive substances, including opiates, nicotine, and psychostimulants.

(That is why R2D2 is a little wired today; he was running late and drank his coffee but skipped breakfast to be sure we got this posted.)

This particular study suggests that the same effect can be provoked when restricting food and using dopamine-promoting medications such as pramipexole (Mirapex). For anyone taking medications for Parkinson's disease or restless legs syndrome, this could be important information to discuss with a nutritionist.

One of the enhanced responses with food restriction is locomotion. And that makes me think of people who abuse some of these chemicals. They stimulate themselves, which suppresses their appetite, which enhances their stimulation and increases their physical activity. On an ongoing basis, (and people who abuse drugs tend to not only use them just once) that can create a calorie deficit which reinforces the positive effects of the drug use. And that can reinforce staying addicted.

Even if you're not using illicit drugs, maybe not eating and living on cigarettes and coffee is kind an offbeat, roundabout way to jumpstart the dopamine system into motion. I have had many, many clients who tell me they feel addicted to sugar, and when they simply don't eat it they feel better. Maybe this is one of the reasons for that relationship.

Just a little fun fact on this Friday that will hopefully give you something to think about.

R2D2 and I are now going to eat breakfast.

Collins GT, Calinski DM, Newman AH, Grundt P, Woods JH. Food restriction alters N'-propyl-4,5,6,7-tetrahydrobenzothiazole-2,6-diamine dihydrochloride (pramipexole)-induced yawning, hypothermia, and locomotor activity in rats: evidence for sensitization of dopamine D2 receptor-mediated effects. J Pharmacol Exp Ther. 2008 May;325(2):691-7.

Great video on why we need omega-3 fats

2008-06-25T16:45:00.001-07:00

http://www.youtube.com/watch?v=eIgNpsbvcVM

I'll let Susan take credit for today's lesson. :)

When you play with antipsychotics, you play with fire.

2008-06-23T07:28:00.000-07:00

Antipsychotic medications have worked wonders to enhance the lives of many people. However, in recent years, antipsychotics have also been used for an increasing number of off-label uses and in progressively younger populations than they ever were before. Before handing these medications out like they are candy, it's important to evaluate the risks associated with using these medications. A recent study suggested that we should be much more careful about choosing our treatment populations than we have been to date.

Before I get to the meat of the study, I'd like to preface this post with an explanation of the study design. The authors of this study are concerned about safety risks in young children and pregnant women when they are given antipsychotic medications. However, they had to develop a research model that did not place young children and pregnant women at risk in the process of looking into this issue. So...rather than give antipsychotics to these two populations, they chose to administer a battery of antipsychotics to a group of roundworms. Roundworms were chosen because they are an accepted research model for investigating matters related to brain and nervous system development. That is definitely a limitation of the study, as most people I know would not say they have much in common with this guy...but that's one of the tough things about studying medications and their risks...how to investigate those risks without causing more damage.

Anyway...when the roundworms were given three of these medications, clozapine (Clozaril), fluphenazine (Prolixin), and haloperidol (Haldol), there was less development of neurons in general and axons (a specific anatomical feature of a neuron) in neurons devoted to mechanosensory function (that's touching and registering what you're touching). Neurons that were produced also tended to not migrate to the location where they would be expected to migrate, meaning there might have been neurons there, but they were, so to speak, all dressed up with no place to go.

In some neurons, axons grew past their functional anatomical size. And some had abnormal anatomical features.

Other antipsychotics produced similar results, although not to as significant a degree. The drugs mentioned included: risperidone (Risperdal), aripiprazole (Abilify), quetiapine (Seroquel), trifluoperazine (Stelazine) and olanzapine (Zyprexa).

I'm not going to pontificate about the ethical dilemma encountered when treating a pregnant woman with schizophrenia. The choices made in those situations involve complex risk/benefit considerations that are the responsibility of the patient and her physician.

However, I will say that responsible use of these medications in women of childbearing age is imperative. Forty-nine percent of all pregnancies ending in childbirth in 1994 were unintended, and 48% of all women aged 15-44 in 1994 had had at least one unintended pregnancy at some point in their life. It happens, and it happens a lot.

So if you're a physician and you're handing out prescriptions for antipsychotics for off-label uses to women of childbearing age...no matter how much judgment, education, evaluation, etc. you think you're providing, you really are playing with fire.

Donohoe DR, Weeks K, Aamodt EJ, Dwyer DS. Antipsychotic drugs alter neuronal development including ALM neuroblast migration and PLM axonal outgrowth in Caenorhabditis elegans. Int J Dev Neurosci. 2008 May-Jun;26(3-4):371-80.

http://www.guttmacher.org/pubs/journals/3002498.html

Who is the real addict?

2008-06-22T15:59:00.000-07:00

Friday I participated in a meeting at a chemical dependency treatment center. This is a place where people have been medicating their problems with stimulants and who are learning to use communication, conflict resolution, and coping skills to ride through life's challenges so that life does not defeat them. One of the biggest problems in this population is stimulant use, in the form of methamphetamine.

The message this and other treatment centers are working hard to encourage...is that when you listen to your body, it will tell you if you need to sleep, eat, address a conflict, or participate in a relaxing activity to help ride through situations that cannot be immediately addressed. When you push through feelings and ignore what they're telling you, you can push yourself to a point so low that it becomes tempting to use chemicals to pull out of the situation.

Today, I was reviewing research and ran across an abstract that completely contradicts this point of view. This article discusses the "potential" for treating CFS with neurostimulants, such as bupropion (Wellbutrin), dextroamphetamine (Dexedrine), and methylphenidate (Ritalin, Concerta).

No wonder treatment centers abound. The drug industry is advocating throwing stimulants at problems that very well may best respond to intensive self-care. I'm not trying to say that chronic fatigue is not a genuine problem. I just wonder where the logic is in trying to blast a person out of a fatigued state that may be telling us something very important about the person's overall health, their lifestyle choices, and the way they deal with stress.

It's no wonder our many public service attempts at reducing illicit drug use fall on deaf ears. The message seems to be that if you can figure out a way to present your problem to the doctor in a way that fits with an "official" medical problem, you can legally buy a way out of your problem. If you're less savvy, or don't have access to a doctor who is open to such creative thinking, you can still get the job done. It just might land you in jail at some point down the road.

An addict is an addict, whether legally managed or scoring treatment off the street.

Valdizán Usón JR, Idiazábal Alecha MA. Diagnostic and treatment challenges of chronic fatigue syndrome: role of immediate-release methylphenidate. Expert Rev Neurother. 2008 Jun;8(6):917-27.