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

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!

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

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!

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!

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

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

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?

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
expectations and actual results could differ materially. There are a
number of factors that could cause actual events to differ materially
from those indicated by such forward-looking statements. These factors
include, but are not limited to, substantial competition; uncertainties
of patent protection and litigation; uncertainties of government or
third party payer reimbursement; reliance on sole source suppliers;
limited sales and marketing efforts and dependence upon third parties;
risks related to the development of innovative products; and risks
related to failure to obtain FDA clearances or approvals and
noncompliance with FDA regulations. As with any pharmaceutical under
development, there are significant risks in the development, regulatory
approval and commercialization of new products. There are no guarantees
that future clinical studies discussed in this press release will be
completed or successful or that any product will receive regulatory
approval for any indication or prove to be commercially successful.
VIVUS does not undertake an obligation to update or revise any
forward-looking statement. Investors should read the risk factors set
forth in VIVUS' Form 10-K for the year ended December 31, 2007 and
periodic reports filed with the Securities and Exchange Commission.

Safely using eicosapentaenoic acid (fish oil) for schizophrenia

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

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?

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!

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

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

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

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

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?

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

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

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

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.