Tuesday, December 23, 2008

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.

Wednesday, December 17, 2008

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.

Monday, December 15, 2008

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.

Thursday, December 11, 2008

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.


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.

Wednesday, December 10, 2008

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.

Monday, December 8, 2008

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.

Friday, December 5, 2008

Which came first, the high glucose or the depression?

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

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

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

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

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

Which has me wondering a few things.

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

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

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

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

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

Wednesday, December 3, 2008

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

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

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

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

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

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

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

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

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

Monday, December 1, 2008

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!

Friday, November 28, 2008

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

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

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

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

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

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

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

Wednesday, November 26, 2008

Zinc KO's Prozac in the fight against depression

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

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

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

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

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

Monday, November 24, 2008

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.

Friday, November 21, 2008

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.

Wednesday, November 19, 2008

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

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

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

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

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

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

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

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

Monday, November 17, 2008

Pregnant women and psychotropic medications really don't mix

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

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

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

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

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

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

Friday, November 14, 2008

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.

Wednesday, November 12, 2008

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

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.

Tuesday, November 11, 2008

Smoking reduces serum levels of lamotrigine.

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.

Monday, November 10, 2008

Television, epilepsy, and children

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.

Friday, November 7, 2008

Your brain loves lipoic acid!

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.

Wednesday, November 5, 2008

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

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

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

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

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

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

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

Monday, November 3, 2008

Aging brains and medicine

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.

Friday, October 31, 2008

Sneak peek at new drug booklet

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"...

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.

Thursday, October 30, 2008

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

Wednesday, October 29, 2008

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

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.

Tuesday, October 28, 2008

New booklet: This Is Your Brain On Psych Drugs

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!

Monday, October 27, 2008

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

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.

Friday, October 24, 2008

A Chinese herb with antidepressant activity

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.

Thursday, October 23, 2008

My new alternative to medication

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!

Tuesday, October 21, 2008

Mental health and the presidency

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.


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.

Monday, October 20, 2008

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

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.

Friday, October 17, 2008

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

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.