Diet and Parkinson's disease

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

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.

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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.

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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.

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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.

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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.

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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.

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