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 www.republicbroadcasting.org. 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!

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 monika@afterthediet.com.

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
http://www.foodnavigator.com/news/ng.asp?n=84424-aspartame-sweetener

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

http://www.foodnavigator.com/news/ng.asp?n=84424-aspartame-sweetener

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.

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,

http://www.parkinson.org/,

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!

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 (http://www.ncbi.nlm.nih.gov/sites/entrez)and 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.

Rischke R, Krieglstein J. Effects of vinpocetine on local cerebral blood flow and glucose utilization seven days after forebrain ischemia in the rat. Pharmacology. 1990;41(3):153-60.

Rischke R, Krieglstein J. Protective effect of vinpocetine against brain damage caused by ischemia. Jpn J Pharmacol. 1991 Jul;56(3):349-56.

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.

Seyahi A, Atalar AC, Ergin HK. Tumoral calcinosis: Clinical and biochemical aspects of a patient treated with vinpocetine. Eur J Intern Med. 2006 Oct;17(6):436-8.

Sitges M, Nekrassov V. Vinpocetine prevents 4-aminopyridine-induced changes in the EEG, the auditory brainstem responses and hearing. Clin Neurophysiol. 2004 Dec;115(12):2711-7.

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.

Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database Syst Rev. 2003;(1):CD003119.

Szilágyi G, Nagy Z, Balkay L, Boros I, Emri M, Lehel S, Márián T, Molnár T, Szakáll S, Trón L, Bereczki D, Csiba L, Fekete I, Kerényi L, Galuska L, Varga J, Bönöczk P, Vas A, Gulyás B. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J Neurol Sci. 2005 Mar 15;229-230:275-84. Epub 2005 Jan 8.

Tohgi H, Sasaki K, Chiba K, Nozaki Y. Effect of vinpocetine on oxygen release of hemoglobin and erythrocyte organic polyphosphate concentrations in patients with vascular dementia of the Binswanger type. Arzneimittelforschung. 1990 Jun;40(6):640-3.

Trejo F, Nekrassov V, Sitges M. Characterization of vinpocetine effects on DA and DOPAC release in striatal isolated nerve endings. Brain Res. 2001 Aug 3;909(1-2):59-67.

Truss MC, Stief CG, Uckert S, Becker AJ, Schultheiss D, Machtens S, Jonas U. Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor vinpocetine in the treatment of urge incontinence and low compliance bladder. World J Urol. 2000 Dec;18(6):439-43.

Truss MC, Stief CG, Uckert S, Becker AJ, Wefer J, Schultheiss D, Jonas U. Phosphodiesterase 1 inhibition in the treatment of lower urinary tract dysfunction: from bench to bedside. World J Urol. 2001 Nov;19(5):344-50.

Vas A, Gulyás B, Szabó Z, Bönöczk P, Csiba L, Kiss B, Kárpáti E, Pánczél G, Nagy Z. Clinical and non-clinical investigations using positron emission tomography, near infrared spectroscopy and transcranial Doppler methods on the neuroprotective drug vinpocetine: a summary of evidences. J Neurol Sci. 2002 Nov 15;203-204:259-62.

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 (http://www.ncahf.org/articles/s-z/wheatgrass.html), 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.

Photo courtesy of www.healthyjuicer.com