Wednesday, April 30, 2008

Can a pill really cure stress?

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

"Are you from Phoenix or DC?"

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

"What was the conference about?"

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

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

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

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

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

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

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

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

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

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

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

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

Monday, April 28, 2008

There's something fishy about depression treatment...

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

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

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

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

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

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

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

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

Friday, April 25, 2008

Another gift from the rain forest

Here's an article I found interesting. When I review medication research a huge percentage of the off-label uses of medications are in the area of chronic pain. Catuama is a medication that appears to help with inflammatory-based pain. Unfortunately, it didn't seem to help with neuropathic pain. (That's the kind of pain diabetics get after having the disease for awhile.)

A Pub Med search found only 7 articles, and the ones I felt strong enough to share were one suggesting that Catuama also has a mild antidepressant effect and one suggesting that it may help with ventricular fibrillation.

A very huge disclaimer here...I did not see anything about interactions with other medications and I did not see anything about toxicity. That doesn't mean these are not potential risks, it mostly means research is so new this may not yet be published. So please don't mix this med with your heart medications and please don't just stop taking medications because you read this post. If you'd like to try Catuama it's a good idea to coordinate this with the person who is managing any prescription medications you may be taking.

I couldn't find a decent photo to show you what it looks like. The most I can gather is that it comes from Brazil. But if the information helps some of you...then I wanted to share it.

Have a great weekend!

Quintão NL, Ferreira J, Beirith A, Campos MM, Calixto JB. Evaluation of the effects of the herbal product Catuama in inflammatory and neuropathic models of nociception in rats. Phytomedicine. 2008 Apr;15(4):245-52.

Campos MM, Fernandes ES, Ferreira J, Bortolanza LB, Santos AR, Calixto JB.Pharmacological and neurochemical evidence for antidepressant-like effects of the herbal product Catuama. Pharmacol Biochem Behav. 2004 Aug;78(4):757-64.

Pontieri V, Neto AS, de França Camargo AF, Koike MK, Velasco IT.The herbal drug Catuama reverts and prevents ventricular fibrillation in the isolated rabbit heart. J Electrocardiol. 2007 Nov-Dec;40(6):534.e1-8. Epub 2007 Sep 24.

Wednesday, April 23, 2008

Watch out comes Lipton!

Who thought such a simple item you may already have in your cupboard could be so beneficial? I'm talking about tea!

I think if you're interested enough in health and the brain to even be reading this blog, you know that green tea has many health benefits. It's a great antioxidant, and it improves the brain's blood flow, making it easier for waste products to be flushed away from where they can do damage.

Scientists took green tea one step further in the following experiment. Mice were divided into three groups, each group receiving one of the following treatments: green tea, an antidepressant (in this case, desipramine/Norpramin), or an anti-anxiety medication (in this study, diazepam/Valium). Both low and high doses of green tea reduced depression-like behaviors within 30 minutes of administration.

Depression can slow thought processes and therefore problem solving, so these mice were put in a maze and timed for their performance. Higher doses of green tea reduced the time it took to complete the task.

One potential downside to the higher doses of green tea was that the higher doses also had somewhat of a sedative effect and reduced muscle strength and activity. The mice also were less responsive to exposures to a painful stimulus, in this case, heat.

The moral of the story appears to be that moderate doses of green tea might not be a bad thing. I'd recommend the decaffeinated version--and there are lots of great ones out there.

A green tea tip for all of you: Did you know you can cook with green tea? One of my company's sponsors, Organic Bistro, has a frozen dinner with green tea vegetables ( So if you don't like to drink tea, you can sneak in some of its benefits by combining it with foods you DO enjoy.

Since it's Earth Day week, I'll slip in a little plug for thinking "outside the brain" and looking for organic brands of green tea. Here's a nice website with some options...

Sattayasai J, Tiamkao S, Puapairoj P. Biphasic effects of Morus alba leaves green tea extract on mice in chronic forced swimming model. Phytother Res. 2008 Apr;22(4):487-92.

Tuesday, April 22, 2008

HMO's and Insurance Companies...Who's In YOUR Wallet?

First of's great to be back! I was traveling, and while it's kind of fun to say I saw both the Atlantic and Pacific oceans in the period of a week, I do like my base camp and I really missed reading research. I'm looking forward to getting back into my daily groove.

Last week, I read an article in the New York Times about insurance companies, and how they are starting to ask consumers to absorb the cost of medications by asking that these medications be paid for not by flat copayment, but proportionate to the cost of the medication.

Nice. First we're convinced that we absolutely need all these drugs, and that we can get them for cheap, then once we're dependent on them...we're thrown under the financial bus.

Right now, the medications that are being sold under this new proportionate plan are not any of the medications that I focus on with this blog. However...since several of the medications you readers are on, are some of the most popular medications out there, I suspect it won't be long before these insurance companies start to see dollar signs in terms of the quantity of people they can expect to help finance this venture. Categories of medications like antidepressants...and insulin sensitizers and statins, which are commonly prescribed when the antidepressants start to mess with hormone balance.

That's the bad news.

The GOOD news is, I finally felt vindicated for having sat through this scenario for the last 25 years, wishing people would see what I have always seen...that when you take responsibility for your own health, and don't depend on people who make money off of you to help you, you have a good chance of getting better results. Think about it. Why would a drug company spend millions and millions of dollars to develop a product that you eventually wouldn't need once you started using it?

My goal, ever since I started what I do, is to put myself out of business. I started learning to play golf last year and it has been very frustrating to have to put it aside to attend to the demands of my growing business. I have a children's story I'd like to publish. And there are a couple of screenplays roaming around in my head that I'd love to get into theaters.

But the drug and insurance industries don't have that goal. Their goal, as is the goal of most corporations, is to increase market share and return on investment. Which means you can (1) increase the dosages of medications you sell to already existing customers, (2) find new customers for your medications by either creating new diagnoses or finding off-label uses for your already developed products, and/or (3) increase the price you charge for the product. Hmmmmm...nowhere in there do I see "helping the patient feel better".

Of course, I'm not naive. I know some medications are entirely necessary and even life-saving. But I also see so many conditions that could drastically improve with a few judicious lifestyle choices.

Last week I listened to the husband of a friend tell me what it was like to go through an in-vitro fertilization (IVF) procedure with his wife. He was near tears as he spoke about the trauma, the callousness of the providers, the emotional stress...the expense, and the feeling of failure as a human being when the entire investment of time, emotions and money did not produce the desired result.

He drove me to the bus stop, and I headed to the airport. As I was standing in line to board my plane, a colleague phoned me. She'd gone through my professional training and had been using my protocol on women with infertility. And she told me, that with just a few nutritional tweaks, these women were getting pregnant! Not only that, their depression was responding with equal profundity. Even the women who'd failed with the same IVF procedure as my other friend and who had given up on ever having children, were seeing results.

There's something very wrong with a system that promotes a $20,000 emotional and financial (mis)adventure over a $12 bottle of Costco fish oil...but we as consumers need to shift our expectations for help from those who stand to make money off of our misfortunes and invest in choices, behaviors, and financial purchases that are empowering and affirming. You'll never get a company making money off of you to change how they do things if it means less money. But we can certainly get their attention if, collectively, we start to say "no" to some of their answers to our problems and "yes" to options that make more sense.

You bet the power of where you pull out your wallet is tremendous. And when groups of thousands of wallets get together...well, that's the vision I have that will finally get these screenplays out of my head!

Eating well. Physical activity. Adequate sleep. Less stress. It's that simple. It's incredible what prioritizing these four areas can do to your overall health. Not to mention your budget.

Tuesday, April 15, 2008

Some kinder, gentler options for epilepsy

Epilepsy is one of those disorders that I think we just assume is medical, and that medication and complex neurological procedures are the only options for treatment. This is where I have to disagree! A lot of epilepsy is metabolic and nutritional, and it's exciting to see colleagues researching some of these kindler, gentler options.

This particular study focused on children with mental retardation, a demographic where epilepsy is very common.

The bad news is, only 20% of these children were even given metabolic testing.

The good news is, twenty-eight percent of those children chosen in the study, who had been given metabolic testing, were shown to have some kind of metabolic abnormality. That percentage jumped to 75% when the seizures were originating from multiple locations! In 22% of the children studied, a carnitine deficiency was identified, and that was linked to their medication--valproic acid or Depakote. Carnitine is an easy to find, very practical supplement to use in situations such as this.

The researchers concluded that a systematic evaluation of mentally retardation would help to identify those who have a metabolic (and potentially treatable) component to their seizure disorder.

The good news is...if they can get the word out to other practitioners, the other 80% of those kids can also have the world of nutritional therapies opened up to them as treatment options.

Parikh S, Cohen BH, Gupta A, Lachhwani DK, Wyllie E, Kotagal P. Metabolic testing in the pediatric epilepsy unit. Pediatr Neurol. 2008 Mar;38(3):191-5.

Monday, April 14, 2008

Nuts about nuts

Hello everyone,

I'm doing a bit of cross-posting between my two blogs today, since this topic is important for both areas of interest. I'm waist deep in drug research so you'll be getting more of that information as the month progresses (and as my tax paperwork is officially en route).


Happy Monday to all of you!

Sorry for the silence, I was in Boston for a sports nutrition conference, promoting the Nordic Naturals line of fish oils. I've been sidelined from my half marathon training with a cranky knee, and it was so nice to get off of the elliptical trainer, get outside, and walk along the Charles River to and from my hotel and the conference!

Something I was very happy to see, throughout the conference, was the emphasis on nuts in general as a healthy food. I've been frustrated for a long, long time that the walnut people seemed to be the only nut commodity board with media contacts. Not that I don't like walnuts, but there's nothing wrong with other nuts as well.

I did an analysis for an article a few years ago, in which I compared the ratios of beneficial fats (omega-3's and monounsaturated) to potentially detrimental fats (omega-6's and polyunsaturated). And when they were all lined up in terms of most beneficial to least beneficial...walnuts actually turned up at the bottom of the list. Macadamias came out on top!

I use that analysis in my trainings, and dietitians will always immediately say, "But macadamias are so high in fat." Precisely. But it's the kind of fat that keeps us healthy. Lucky for very favorite way to have nuts is macadamia nuts roasted in coffee, the way they fix them in Hawaii.

Anyway...(I tend to get distracted in this blog, don't I?)... of the presentations showed data for macadamias, pecans, and pistachios, suggesting that they, too, are good foods to include in an anti-inflammatory (aka pro-mental health) diet. Nuts, in addition to good fats, have a variety of antioxidants that can delay and prevent aging and help fight stress. I even learned that the green part of pistachios contains lutein, which makes them good for eye health. Who knew a food so fun to eat would also be so helpful to my health?

Of course, there's a limit to how many nuts can be healthy, and fat has calories, no matter where it comes from. But if you're reaching for a handful of pistachios instead of a bag of Fritos, it's nice to know you're also reaching for better health.

So this week...go nuts!

Wednesday, April 9, 2008

More conversation about aspartame

Thank you to the many people who found this blog through my post on aspartame! It's rewarding to know that my voracious appetite for research was useful to a few people in Internet-land.

If aspartame is an area of interest to you, please consider tuning in to The American Awakening with Michael Herzog, this coming Tuesday (April 15, 2008), where we will be expanding on the discussion. You can learn more about his program at He's calling me to establish the phone connection just after noon Pacific/Arizona time, so I assume it won't be long after that when we begin to chat.

I will qualify, I am a scientist with an interest in the brain, so my area of knowledge in this area is research studies regarding food, medication, and supplements affecting brain function. That's what I am most qualified to speak about and what I will focus on when chatting with Michael.

Hope to see you there!

Tuesday, April 8, 2008

Omega 3's and epilepsy

When I was a nutrition intern, waaaay back when, one of the special diets we had to learn about was the ketogenic diet. Epilepsy researchers were looking for a way to control seizures without medication, since so many medications have side effects worse than the problem they are designed to treat. The ketogenic diet, developed at Johns Hopkins University, is a high fat diet designed to do just that. The reason it never took off, and that you never see "The Epilepsy Diet Miracle" on the shelf at Borders, is because this diet is extremely unpalatable and impossible to follow. (Think butterballs!) It is also not nutritionally complete.

However, despite the downside, scientists were encouraged by the early success of this diet and have persisted at improving on the original model.

What seems to be coming out of this persistent research, is that it's not so much the AMOUNT of fat, but the TYPE of fat, that matters. And if your diet is high in omega-3 fatty acids (especially those that come from fish), you can better control seizures.

These omega-3's seem to raise the seizure threshold in neurons, meaning they "chill out" neurons and make it harder for them to become excited or overstimulated. Mice with a genetic ability to synthesize high levels of DHA, (which we typically get when we eat fish), have significantly less seizure activity than mice who don't have this ability.

The Atkins Diet is a moderate version of the ketogenic diet. I have often wondered if people who say they feel better on this diet are not describing the weight loss, but rather are trying to describe how it feels to finally have their brains finally relax!

There are important benefits to reducing seizure activity. (1) When neurons are relaxed, they are less metabolically active, which means they are using less energy. Since the brain prefers glucose for energy, this often means that relaxing the brain reduces carbohydrate cravings. I've seen this over and over again in clients who start to incorporate more omega-3 fatty acids into their diet. (2) Metabolic activity is oxidative activity, and oxidation is a degenerative process. I'm not saying the goal here is to be brain dead so you can live longer...but it certainly is worth considering ways to use your brain cells judiciously and not waste them on unfocused, unproductive activity.

Taha AY, Huot PS, Reza-López S, Prayitno NR, Kang JX, Burnham WM, Ma DW. Seizure resistance in fat-1 transgenic mice endogenously synthesizing high levels of omega-3 polyunsaturated fatty acids. J Neurochem. 2008 Apr;105(2):380-8. Epub 2007 Nov 25.

Voskuyl RA, Vreugdenhil M, Kang JX, Leaf A. Anticonvulsant effect of polyunsaturated fatty acids in rats, using the cortical stimulation model. Eur J Pharmacol. 1998 Jan 12;341(2-3):145-52.

Are you interested in nutrition for recovery from addiction?

I'm working on a new resource, and would love to keep you in the loop. Please contact me privately about being placed on the mailing list I will use to announce this endeavor. My e-mail address is

Monday, April 7, 2008

Aspartame and the brain

As Americans, we assume and insist that our food be safe. We'll take spinach off the market the minute there's even a hint of e Coli. We're paranoid about mad cow disease. But when it comes to our beloved sugar? We'll go around and around and around about the safety of aspartame until we're blue in the face. We just don't want to admit that maybe we should not be insisting and expecting that we get to be healthy and have our sweeteners (and fake sweeteners) too.

Twelve years ago I wrote the American Dietetic Association's first book ever on eating disorders. Back then, I found a peer-reviewed reference on aspartame, suggesting that it had a particular ability to have a negative effect on individuals with a history of depression. In the years since, I've shared that reference with clients, challenged them to clear their systems of aspartame for 6 weeks, then go back and try a little bit of it to see how they feel. I've yet to have a single person come back to report they'd gotten back on it once they'd cleared their systems.

The problem is, aspartame was not intended to be consumed in large quantities by a population of people who insisted on being in denial about what it means to have insatiable cravings for a refined compound with no nutritional value. And while it started out in soft drinks, it eventually showed up in yogurts, and protein powders, and anything food manufacturers could think of to make a buck off of our addiction. As aspartame gradually crept into the food supply, and accumulated in larger and larger amounts in our bodies...we lost the ability to even remember how we felt when we were completely off the stuff. Which is why I love the power of my "washout experiment".

Now, it seems, there is more information suggesting that aspartame may not be so great for the brain. This new study is not even cited yet in Pub Med as I write this. I don't normally do this in this blog, but I am pasting the entire release for anyone who would like to evaluate the information for themselves.

A few years ago there was an aspartame e-mail circulating the Internet that quickly became regarded as urban legend. It illustrated the importance of doing your homework before speaking out about anything. The person who circulated this piece used a fake name, and did not take the time to gather data and citations. So most scientists dismissed the warning. I'd already seen the aspartame/depression study at this time. I was perturbed at the well-intended person who was more engaged in stirring up controversy than in helping people, because, having read that there may be some REAL dangers with aspartame, I knew that when those were eventually elucidated, it was going to be even harder to convince hard scientists that these dangers existed because they'd immediately think of the earlier "aspartame urban legend" and associate any other warnings with this irresponsible piece of Internet writing.

Which is why I'm giving you my source. Whether or not you use artifical sweeteners is your choice. But remember, as you've seen before in this blog, in medicine and science, there is no such thing as a perfect choice. Every food, every supplement, every treatment, you choose to try, has its benefits as well as its risks. Perhaps the best way for you to decide for yourself, is to try my washout challenge. What matters is not what a panel of experts says about aspartame in general, but how aspartame makes you feel. Only you know this, and the only person who gets to decide whether or not you should use it...should be you.

Below the review is the reference for the old study I mention as well.

Review raises questions over aspartame and brain health
By staff reporter

03-Apr-2008 - Excessive intake of aspartame may inhibit the ability of
enzymes in the brain to function normally, suggests a new review that
could fan the flames of controversy over the sweetener.

The review, by scientists from the University of Pretoria and the University of Limpopo and published recently in the European Journal of Clinical Nutrition, indicated that high consumption of the sweetener may lead to neurodegeneration.

Aspartame is made up of phenylalanine (50 per cent), aspartic acid (40 per cent) and methanol (10 per cent). It is commonly used in food products for the diet or low calorie market, including soft drinks and chewing gums. It was approved for use in foods in the US and EU member states in the early 1980s.

The sweetener has caused much controversy amid suspicions on whether it is entirely safe, with studies linking the ingredient and cancer in rats.

It has also previously been found that aspartame consumption can cause neurological and behavioural disturbances in sensitive individuals. Symptoms that have been reported include headaches, insomnia and seizures.

Despite strong concerns being raised from some quarters over the sweetener, both the European Food Safety Authority (EFSA) and the US Food and Drug Administration (FDA) have not changed their guidelines regarding the safety of the ingredient or intake advice.

The new review also challenges finding published last year in the journal Critical Reviews in Toxicology (Informa Healthcase) that considered over 500 studies, articles and reports conducted over the last 25 years - including work that was not published, but that was submitted to government bodies as part of the regulatory approvals process.

The earlier review concluded: "The weight of existing evidence is that aspartame is safe at current levels of consumption… No credible evidence was found that aspartame is carcinogenic, neurotoxic, or has any other adverse effect on health when consumed even at quantities many times the established ADI [acceptable daily intake] levels."

New review

Writing in the European Journal of Clinical Nutrition, a Nature journal, the scientists behind the new review state: "The aim of this study was to discuss the direct and indirect cellular effects of aspartame on the brain, and we propose that excessive aspartame ingestion might be involved in the pathogenesis of certain mental disorders, and also in compromised learning and emotional functioning."

The researchers found a number of direct and indirect changes that occur in the brain as a result of high consumption levels of aspartame, leading to neurodegeneration.

They found aspartame can disturb the metabolism of amino acids, protein structure and metabolism, the integrity of nucleic acids, neuronal function and endocrine balances. It also may change the brain concentrations of catecholamines, which include norepinephrine, epinephrine and dopamine.

Additionally, they said the breakdown of aspartame causes nerves to fire excessively, which can indirectly lead to a high rate of neuron depolarisation.

The researchers added: "The energy systems for certain required enzyme reactions become compromised, thus indirectly leading to the inability of enzymes to function optimally.

"The ATP stores [adenosine triphosphate] in the cells are depleted, indicating that low concentrations of glucose are present in the cells, and this in turn will indirectly decrease the synthesis of acetylcholine, glutamate and GABA (gamma-aminobutyric acid)."

Furthermore, the functioning of glutamate as an excitatory neurotransmitter is inhibited as a result of the intracellular calcium uptake being altered, and mitochondria are damaged, which the researchers said could lead to apoptosis (cell death) of cells and also a decreased rate of oxidative metabolism.

As a result of their study, the researchers said more testing is required to further determine the health effects on aspartame and bring an end to the controversy.

Source: European Journal of Clinical Nutrition
2008, doi: 10.1038/sj.ejcn.1602866
"Direct and indirect cellular effects of aspartame on the brain"
Authors: P. Humphries, E. Pretorius, H. Naude

Biol Psychiatry. 1993 Jul 1-15;34(1-2):13-7. Links
Adverse reactions to aspartame: double-blind challenge in patients from a vulnerable population.Walton RG, Hudak R, Green-Waite RJ.
Department of Psychiatry, Northeastern Ohio Universities College of Medicine, Youngstown.

This study was designed to ascertain whether individuals with mood disorders are particularly vulnerable to adverse effects of aspartame. Although the protocol required the recruitment of 40 patients with unipolar depression and a similar number of individuals without a psychiatric history, the project was halted by the Institutional Review Board after a total of 13 individuals had completed the study because of the severity of reactions within the group of patients with a history of depression. In a crossover design, subjects received aspartame 30 mg/kg/day or placebo for 7 days. Despite the small n, there was a significant difference between aspartame and placebo in number and severity of symptoms for patients with a history of depression, whereas for individuals without such a history there was not. We conclude that individuals with mood disorders are particularly sensitive to this artificial sweetener and its use in this population should be discouraged.

Sunday, April 6, 2008

New contributor--and great info to come on Parkinson's disease!

I'm really excited to announce, I will soon have a co-contributer to this blog! My partner in crime will be Kathrynne Holden, a registered dietitian who specializes in diet for Parkinson's disease. She has authored numerous publications on the topic and she has spoken at many conferences as well. Kathrynne is THE "go to" person in this area, and has agreed to share her expertise regarding medications and nutrition aspects of this diagnosis.

If Parkinson's disease is a special interest of yours, you can see more of Kathrynne at the National Parkinson Foundation website,,

where Kathrynne moderates a listserve and answers personal questions. Once you get to the website, click "Ask the Parkinson Dietitian", follow the instructions, then post your question.

A warm and excited welcome to Kathrynne!

Friday, April 4, 2008

V is for brain Viagra....REALLY?

Since I spent the last post questioning the validity of an herbal supplement, I wanted to balance my blog by sharing another herb with some evidence-based potential.

One of my friends is very into nutrition...and his questions for me challenge me to keep up-to-date and be cutting edge. One day he wrote to ask if I'd ever heard of an herb called "vinpocetine." He'd heard it was like Viagra for the brain, in that it increased brain blood flow and circulation of vital nutrients, while making it easier for the brain to remove toxic waste products.

I rolled my eyes as I read his email, thinking I'd heard it all. But, curious, I went to PubMed. Sure enough, there were 23 pages of titles about vinpocetine and the hopeful actions it seemed to have on the brain and nervous system; the first one was published way back in 1979!

If you happen to be reading this, Michael, I greatly appreciate your voracious curiosity and your generosity in sharing things you learn with me. You get credit for this "find" and I want to thank you for giving me a great opportunity to help a lot of people who may benefit from this information. :)

Vinpocetine, also known as Caviton, is a derivative of a plant in the periwinkle family. In the brain, some of the effects of vinpocetine appear to be:
(1) protecting the brain against ischemic cell damage (the kind of damage that occurs when there is insufficient oxygen). Improved glucose utilization and blood flow in damaged areas has been shown when vinpocetine was administered even a week or two after the ischemic damage occurred;
(2) acting as a vasodilator (as my friend suggested, improves blood flow), which has been shown to be beneficial in treating vascular dementia and stroke;
(3) reducing seizure activity and potentially helping to manage epilepsy;
(4) improving the flexibility of red blood cells, making it easier for them to move through constricted spaces and therefore improving blood flow;
(5) preventing death to neurons that have been overstimulated by excitatory substances such as glutamate;
(6) protecting cells from the damage created by amyloid beta peptides, making it a potential treatment for Alzheimer's disease;
(7) improving the function of norepinephrine, a neurotransmitter important to memory function;
(8) enhancing the neuroprotective activity of other compounds such as adenosine;
(9) improving the uptake of glucose through the blood-brain barrier (glucose is the brain's primary energy source);
(10)acting as an antioxidant, protecting neurons from stress-related damage; and
(11) protecting astrocytes, another type of brain cell that supports the blood-brain barrier, nourishes other brain cells, and repairs brain tissue.

Vinpocetine appears to be particularly effective in the hippocampus, the brain's factual memory center. Learning and memory have actually been shown to improve in individuals who have been given vinpocetine.

Vinpocetine may also promote health outside of the brain and nervous system. It has been shown to lessen menopausal symptoms, prevent the development of gastric lesions created on exposure to substances such as alcohol, and help with urinary incontinence. It reduces gallbladder motility and, potentially, gallstone formation. It has been used to treat tumoral calcinosis, (calcium-based masses). And it shows potential in controlling pain.

One small nutritional note: vinpocetine appears to be better absorbed when taken after a meal than it does when taken on an empty stomach.

Many of the articles about vinpocetine are in Russian, Chinese, and Hungarian. On the chance that anyone reading this may wish to read some of the references, I only cited studies written in English. But if you go to Pub Med ( key in "vinpocetine", you can see for yourself just how much this herb has been studied.

I will note, there are also studies refuting the effectiveness of vinpocetine, but the results seem to vary depending on study design. My guess is that, just like with medications, different people will respond to different treatments in a variety of ways. The one thing I DID like about what I found, was that there were no studies suggesting any dangers to using vinpocetine. If it can't hurt...and it might help...why not try it?

Abdel Salam OM. Vinpocetine and piracetam exert antinociceptive effect in visceral pain model in mice. Pharmacol Rep. 2006 Sep-Oct;58(5):680-91.

Araki T, Kogure K, Nishioka K. Comparative neuroprotective effects of pentobarbital, vinpocetine, flunarizine and ifenprodil on ischemic neuronal damage in the gerbil hippocampus. Res Exp Med (Berl). 1990;190(1):19-23.

Bereczki D, Fekete I. Vinpocetine for acute ischaemic stroke. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD000480.

Bönöczk P, Gulyás B, Adam-Vizi V, Nemes A, Kárpáti E, Kiss B, Kapás M, Szántay C, Koncz I, Zelles T, Vas A. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Brain Res Bull. 2000 Oct;53(3):245-54.

Bönöczk P, Panczel G, Nagy Z. Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study. Eur J Ultrasound. 2002 Jun;15(1-2):85-91.

Erdö SL, Cai NS, Wolff JR, Kiss B. Vinpocetin protects against excitotoxic cell death in primary cultures of rat cerebral cortex. Eur J Pharmacol. 1990 Oct 23;187(3):551-3.

Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol. 2001 Jan;8(1):81-5.

Gaál L, Molnár P. Effect of vinpocetine on noradrenergic neurons in rat locus coeruleus. Eur J Pharmacol. 1990 Oct 23;187(3):537-9.

Gabryel B, Adamek M, Pudełko A, Małecki A, Trzeciak HI. Piracetam and vinpocetine exert cytoprotective activity and prevent apoptosis of astrocytes in vitro in hypoxia and reoxygenation. Neurotoxicology. 2002 May;23(1):19-31.

Hadjiev D. Asymptomatic ischemic cerebrovascular disorders and neuroprotection with vinpocetine.Ideggyogy Sz. 2003 May 20;56(5-6):166-72.

Hayakawa M. Comparative efficacy of vinpocetine, pentoxifylline and nicergoline on red blood cell deformability. Arzneimittelforschung. 1992 Feb;42(2):108-10.

Hayakawa M. Effect of vinpocetine on red blood cell deformability in vivo measured by a new centrifugation method. Arzneimittelforschung. 1992 Mar;42(3):281-3.

Hayakawa M. Effect of vinpocetine on red blood cell deformability in stroke patients. Arzneimittelforschung. 1992 Apr;42(4):425-7.

Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol. 1991 Spring;6(1):31-43.

Horvath B, Marton Z, Halmosi R, Alexy T, Szapary L, Vekasi J, Biro Z, Habon T, Kesmarky G, Toth K. In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine. Clin Neuropharmacol. 2002 Jan-Feb;25(1):37-42.

Ishihara K, Katsuki H, Sugimura M, Satoh M. Idebenone and vinpocetine augment long-term potentiation in hippocampal slices in the guinea pig. Neuropharmacology. 1989 Jun;28(6):569-73.

Kaneda T, Watanabe A, Shimizu K, Urakawa N, Nakajyo S. Effects of various selective phosphodiesterase inhibitors on carbachol-induced contraction and cyclic nucleotide contents in the guinea pig gall bladder. J Vet Med Sci. 2005 Jul;67(7):659-65.

Kemény V, Molnár S, Andrejkovics M, Makai A, Csiba L. Acute and chronic effects of vinpocetine on cerebral hemodynamics and neuropsychological performance in multi-infarct patients. J Clin Pharmacol. 2005 Sep;45(9):1048-54.

Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive dysfunction. Altern Med Rev. 1999 Jun;4(3):144-61.

Kiss E. Adjuvant effect of cavinton in the treatment of climacteric symptoms. Ther Hung. 1990;38(4):170-3.

Krieglstein J. Vinpocetine increases the neuroprotective effect of adenosine in vitro. Eur J Pharmacol. 1991 Nov 19;205(1):7-10.

Lakics V, Sebestyén MG, Erdö SL. Vinpocetine is a highly potent neuroprotectant against veratridine-induced cell death in primary cultures of rat cerebral cortex. Neurosci Lett. 1995 Feb 9;185(2):127-30.

Lakics V, Sebestyén MG, Erdö SL. Cerebral effects of a single dose of intravenous vinpocetine in chronic stroke patients: a PET study.Szakáll S, Boros I, Balkay L, Emri M, Fekete I, Kerényi L, Lehel S, Márián T, Molnár T, Varga J, Galuska L, Trón L, Bereczki D, Csiba L, Gulyás B. J Neuroimaging. 1998 Oct;8(4):197-204.

Lindaman BA, Hinkhouse MM, Conklin JL, Cullen JJ. The effect of phosphodiesterase inhibition on gallbladder motility in vitro. J Surg Res. 2002 Jun 15;105(2):102-8.

Lohmann A, Dingler E, Sommer W, Schaffler K, Wober W, Schmidt W. Bioavailability of vinpocetine and interference of the time of application with food intake. Arzneimittelforschung. 1992 Jul;42(7):914-7.

McDaniel MA, Maier SF, Einstein GO. "Brain-specific" nutrients: a memory cure? Nutrition. 2003 Nov-Dec;19(11-12):957-75. Comment in: Nutrition. 2003 Nov-Dec;19(11-12):955-6.

Molnár P, Erdö SL. Vinpocetine is as potent as phenytoin to block voltage-gated Na+ channels in rat cortical neurons. Eur J Pharmacol. 1995 Feb 6;273(3):303-6.

Nosálová V, Machová J, Babulová A. Protective action of vinpocetine against experimentally induced gastric damage in rats. Arzneimittelforschung. 1993 Sep;43(9):981-5.

Pereira C, Agostinho P, Oliveira CR. Vinpocetine attenuates the metabolic dysfunction induced by amyloid beta-peptides in PC12 cells. Free Radic Res. 2000 Nov;33(5):497-506. Erratum in: Free Radic Res 2001 Oct;35(4):following 446.

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Santos MS, Duarte AI, Moreira PI, Oliveira CR. Synaptosomal response to oxidative stress: effect of vinpocetine. Free Radic Res. 2000 Jan;32(1):57-66.

Sauer D, Rischke R, Beck T, Rossberg C, Mennel HD, Bielenberg GW, Krieglstein J. Vinpocetine prevents ischemic cell damage in rat hippocampus. Life Sci. 1988;43(21):1733-9.

Schmidt J. Comparative studies on the anticonvulsant effectiveness of nootropic drugs in kindled rats. Biomed Biochim Acta. 1990;49(5):413-9.

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Sitges M, Chiu LM, Guarneros A, Nekrassov V. Effects of carbamazepine, phenytoin, lamotrigine, oxcarbazepine, topiramate and vinpocetine on Na+ channel-mediated release of [3H]glutamate in hippocampal nerve endings. Neuropharmacology. 2007 Feb;52(2):598-605. Epub 2006 Oct 30.

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Wednesday, April 2, 2008

What's the deal with wheatgrass?

Many of my work connections (as well as personal friends) are people working in the addictions recovery field. Part of the challenge of being in recovery is developing comfort with emotions-all of them--comfortable and uncomfortable. Even if you're off the hard stuff, it can still be tempting to want to manage moods with external tools. So it's very common for people in recovery to look to nutritional supplements as mood regulators, rather than to learn to ride through the natural ups and downs of daily life.

It can be a slippery slope, because some supplements actually CAN help you to feel better. That's why I talk about fish oil so much--it has been proven in many research studies to actually help regenerate neurons and to improve aspects of all Axis I (psychiatric) diagnoses in measurable ways. I do make other recommendations as well, but only when I've been able to find peer-reviewed literature in the National Library of Medicine (PubMed) database that supports those claims.

Which brings me to the supplement in the title, wheatgrass. Most people who know about wheatgrass either own cats, or shop at health food stores. Wheatgrass got its comical five minutes of fame recently on The Apprentice, when one of the Backstreet Boys requested it in his dressing room, and Trace Adkins, the country singer who was managing this performance, had absolutely no idea where, in all of Manhattan, to find it. (I was throwing things at my TV, yelling..."DUDE! WHOLE FOODS!!!).

Back to my point.

This Backstreet Boy wanted a shot of wheatgrass juice before going on stage, because he felt it gave him an energy boost and helped him perform better. And that's what most people will tell you about it. In all of my training and all of my hours in PubMed, I've never, ever seen any research to back up or support wheatgrass as an evidence-based energy booster.

This morning on a professional listserve, a colleague posted a position statement on wheatgrass, published by the National Council on Health Fraud. You can follow this link for the entire report (, but in general, the author suggests that while feeling better on wheatgrass is a common report, this enhanced feeling is not evidence-based and is more likely due to one of the following:
--natural changes in the symptoms people experience
--the placebo effect mentioned above
--wishful thinking on the part of the desperate
--lying by people who have a financial interest
--something else that the patient is doing--especially if they are using
psychoactive drugs, such as herbal uppers or downers.

My cats love wheatgrass, but my observation is that not long after they eat it...they throw up hair balls. I don't know about you...but that's not anything I hope to achieve personally in my quest for better health.

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