Eat Tumeric (Curry) for a Healthy Brain

There were two articles from the National Institute for the Clinical Application of Behavioral Medicine (NICABM) over the last two months on the benefits of tumeric (curcumin, or curry) for a healthy brain. I have been preaching the benefits of curcumin for a while now, for its actions as a COX-2 inhibitor (reduces inflammation and pain), anti-cancer benefits (has been found to cause apoptosis in some forms of cancer), for cholesterol and glucose control, and most recently there have been several studies of curcumin for preventing Alzheimer's Disease and other neurodegenerative diseases.

Improve Your Brain Health: Eat Curry

February 28, 2012 By Ruth 

I have to admit, I didn’t grow up eating curry. It just wasn’t a mainstay in the New England diet, and my parents still aren’t much into trying new foods.

And while this follows the whole “you can’t teach old dogs new tricks” thinking, anyone who doesn’t at least try curry, or more importantly, turmeric, is possibly missing out on some pretty spectacular health benefits.

Turmeric is a spice used in various dishes in many Asian and Middle Eastern countries. The reason that turmeric is so important is the derived chemical, curcumin. Curcumin has been implicated in numerous studies as a booster of brain health.

In a recent study in the journal PLoS ONE, investigators led by Ina Caesar from Linköping University in Sweden looked at how curcumin affected transgenic fruit flies which developed Alzheimer’s Disease (AD) symptoms.

(If you’re wondering why we would care about fruit fly studies, fruit flies are increasingly used for research into neurodegenerative diseases like AD.)

The flies that received the curcumin lived up to 75% longer and maintained their mobility longer than the sick flies that did not receive the substance.

However, it should be noted that there was no decrease of amyloid in the brain or eyes (that’s the plaque normally associated with Alzheimer’s Disease).

So while curcumin didn’t dissolve amyloid plaque, the researchers still found that it reduced neurodegeneration.

Diet is just one way of influencing neuroplasticity – or the brain’s ability to rewire itself.
Would you like to learn more about the possibilities of neuroplasticity?

We are offering a Free Report featuring Norman Doidge, MD, where he talks about:

• How to use the brain’s potential to change to achieve better patient outcomes


• A closer look at how neuroplasticity is changing real peoples’ lives – a case study


• How to rewire the brain to bring healing to patients with depression, PTSD, and chronic pain


• The paradox of plasticity – what every practitioner needs to know about the “dark side” of neuroplasticity

You can find more right here.

What are your favorite health promoting strategies for the brain? Please leave a comment below.

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Turmeric for a Healthy Brain: Part II

March 28, 2012 By Ruth 

Have you had your turmeric yet this week?

In a recent post, I talked about the neuroplastic possibilities of curcumin (a brain-boosting chemical in turmeric) for slowing the progression of Alzheimer’s Disease.

Did that convince you to start eating it? If not, consider this my second attempt.

Slowing the progression of Alzheimer’s Disease isn’t the only benefit from eating turmeric.

We were curious and so did a PubMed search. We came across so many other important studies on curcumin that we had to share some of them with you.

Let’s start with some more brain benefits.

A randomized, controlled study published in the journal PLoS ONE looked at the neurogenetic potential of prolonged curcumin use.

Neurogenesis is the process by which neurons are created in the brain, including in the hippocampus (one of the centers of neural learning).

Researchers led by Z. Zhao out of the Key Laboratory of Brain Functional Genomics, Shanghai, China looked at performance and brain growth in rats after 6 and 12 weeks on a curcumin-fortified diet.

(I hope those sweet rats got something tasty.)

The result?

Curcumin enhanced memory (both spatial and non-spatial), as well as hippocampal cell growth compared to rats in the control group.

But in addition to brain health, curcumin has been linked to:

• The slowing of prostate tumor growth (S. A. Shah et al. Cancer Research, 2012)

• Prevention and treatment of tendinitis (C. Buhrmann et al. Journal of Biological Chemistry, 2011)

• Increasing the effectiveness of drugs used to fight colon, neck and head cancers (I. Aroch et al. Therapeutic Advances in Gastroenterology, 2010 and W. M. Abuzeid et al. Archives of Otolaryngology – Head and Neck Surgery, 2011)

Want to find out what else is good for the brain?

We have invited nine neuroscience experts to be a part of the New Brain Science 2012 series.

We’ll discuss not just new findings in neuroscience, but even more importantly, how to apply these findings for peak brain health.

It’s free to listen at the time of initial broadcast, you just have to sign up.


What have you recommended to your patients in order to change their brains? Please leave a comment below. And if you’ve got a recipe that includes turmeric, let us all know here.

PLoS ONE - Creatine Protects against Excitoxicity in an In Vitro Model of Neurodegeneration

Creatine . . . it's not just for bodybuilders anymore. I have periodically reported on the various health benefits of creatine over the years, including virus suppression (herpes), memory enhancement, and neurocognitive benefits. This new research supports another aspect of its cognitive benefits - it can suppress some of the excititory activity that leads to neurodegeneration.

As an aside, one of the authors is named Just Genius - how cool is that?!

Creatine Protects against Excitoxicity in an In Vitro Model of Neurodegeneration

Just Genius¹, Johanna Geiger¹, Andreas Bender², Hans-Jürgen Möller¹, Thomas Klopstock², Dan Rujescu^1*

1 Department of Psychiatry, Ludwig-Maximilians-University, Munich, Germany, 2 Department of Neurology, Ludwig-Maximilians-University, Munich, Germany

Abstract

Creatine has been shown to be neuroprotective in aging, neurodegenerative conditions and brain injury. As a common molecular background, oxidative stress and disturbed cellular energy homeostasis are key aspects in these conditions. Moreover, in a recent report we could demonstrate a life-enhancing and health-promoting potential of creatine in rodents, mainly due to its neuroprotective action. In order to investigate the underlying pharmacology mediating these mainly neuroprotective properties of creatine, cultured primary embryonal hippocampal and cortical cells were challenged with glutamate or H₂O₂. In good agreement with our in vivo data, creatine mediated a direct effect on the bioenergetic balance, leading to an enhanced cellular energy charge, thereby acting as a neuroprotectant. Moreover, creatine effectively antagonized the H₂O₂-induced ATP depletion and the excitotoxic response towards glutamate, while not directly acting as an antioxidant. Additionally, creatine mediated a direct inhibitory action on the NMDA receptor-mediated calcium response, which initiates the excitotoxic cascade. Even excessive concentrations of creatine had no neurotoxic effects, so that high-dose creatine supplementation as a health-promoting agent in specific pathological situations or as a primary prophylactic compound in risk populations seems feasible. In conclusion, we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function, along with reduced glutamate spillover, oxidative stress and subsequent excitotoxicity.

Citation: Genius J, Geiger J, Bender A, Möller H-J, Klopstock T, et al. (2012). Creatine Protects against Excitoxicity in an In Vitro Model of Neurodegeneration. PLoS ONE, 7(2): e30554. doi:10.1371/journal.pone.0030554

Here is the introduction to the article:

Introduction

The protective potential of creatine (1-methyl-guanidino acetic acid) has been extensively assessed in various models of neurodegeneration, including in vivo models of oxidative stress [1], [2].

Aging, neurodegenerative diseases like Alzheimer's disease, Huntington's disease and amyotrophic lateral sclerosis, and potentially also neuropsychiatric disorders like schizophrenia share some bioenergetic core features, specifically the contribution of oxidative stress caused by a progressive dysfunction of the respiratory chain along with mitochondrial DNA damage [3]–[5]. Thus, as a potential antioxidative agent and buffer of intracellular energy stores, creatine - specifically in a preventive approach - may also become an interesting new agent to increase life span and to delay the progression of the disorders mentioned above.

In neuronal cells, aerobic glycolysis is the primary source for ATP synthesis [6]. As stores of glucose, glycogen and O₂ are limited in the brain, the availability of the creatine kinase/phosphocreatine (CK/PCr) system may operate as an important alternative energy source in tissues or subcellular compartments with high and fluctuating energy demands, e.g. in neurons [7]. Based on substrate level phosphorylation of adenine with CK/PCr this system is capable of rapidly restoring ATP levels within certain limits, determined by the tissue concentrations of creatine/CPK itself and the enzymatic system required for phosphorylation and phosphate group transfer. ATP is required to maintain the function of energy-demanding Na⁺/K⁺-ATPase and Ca²⁺-ATPase, thus preserving the membrane potential [8]. Considering that high relative CK activity could be demonstrated in the brain [9], it has been concluded that this enzyme serves as a key factor in the CNS energy metabolism. In support of this notion, a direct correlation between CK flux and brain activity has been provided by in vivo ³¹P nuclear magnetic resonance transfer determinations [10], [11]. The brain-specific isoform of the CK (CK-BB) in concert with a mitochondrial isoform (uMT-CK) and the required substrates (creatine/PCr) regulate intracellular ATP levels [12]. Via formation of an CK “energy shuttle”, CK activity has moreover been discussed to be directly implicated in neurotransmitter release, maintainance of membrane potentials and restoration of ion gradients over the membrane after depolarization [12]–[14].

Primarily, creatine is synthesized in a two step mechanism via AGAT (arginine: glycine amidinotransferase) in the kidney and pancreas [15]. The resultant guanidinoacetate is then shuttled to the liver, where it is subsequently methylated by GAMT (guanidinoacetate methyltransferase to result in creatine which ultimately is actively exported to tissues where it is energetically required. Loss of GAMT activity results in a well-defined creatine deficiency syndrome, which is characterized by developmental delay, neurological dysfunction and mental retardation [16]. In Huntington's disease, a further neurodegenerative condition, brain-type creatine kinase expression is reduced, which might contribute to damage in specifically energy-demanding tissues such as the brain and the cochlea, where intact energy shuttling processes are crucial [17]. The endogenous de novo creatine synthetic activity in the brain is rather low. It is interesting to note, that GAMT was identified to act as a novel target for p53, which serves as a further mechanism for metabolic stress adaptation [18]. Under normal conditions dietary intake constitutes about 50% of the total creatine content of the organism. Moreover, the blood-brain barrier permits passage of systemically supplemented creatine to the brain [19], which ultimately reaches the neuronal cytoplasm via a specific sodium and chloride dependent transmembrane transporter (CRT) working against a concentration gradient [20]. We thus speculate, that a specific diet should serve as an efficient strategy to enhance brain tissue creatine concentrations and establish an “energy buffer”.

In a previous report, we demonstrated that creatine supplementation in mice could increase healthy life span. Beyond a moderately increased life span, the most favourable effects of creatine related to neurobehavioral performance, most markedly in memory tests [21]. In an attempt to gain a better understanding of these neuroprotective properties on the cellular level, we conducted a study on a hippocampal cell culture model.

Read the whole article.

Dietary Patterns and Alzheimer's Disease Risk

JAMA's Archives of Neurology published an article last week that looked at dietary patterns in older adults and the incidence of Alzheimer's Disease - "Food Combination and Alzheimer Disease Risk: A Protective Diet."

Reference:

Gu, Y. Nieves, J.W., Stern, Y. Luchsinger, J.A. & Scarmeas, N. (2010). Food Combination and Alzheimer Disease Risk: A Protective Diet. Archives of Neurology.;67(6):699-706. Published online April 12, 2010 (doi:10.1001/archneurol.2010.84).

This was a large group, long-term study, which marks it as useful for looking at which facotrs in the diet might help prevent AD. This is the key finding:

In this prospective study, we identified a DP that explained variation of AD-related nutrients and was strongly protective against the development of AD, even after controlling for multiple covariates. This DP reflected a diet rich in -3 PUFA, -6 PUFA, vitamin E, and folate, but with lower SFA and vitamin B₁₂. Furthermore, dietary habits of subjects adhering more to this DP were characterized as high intake of salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, and dark and green leafy vegetables and low intake of high-fat dairy, red meat, organ meat, and butter.

We previously reported that higher adherence to the MeDi was associated with reduced risk of AD in this WHICAP population.^5-6 However, this multiethnic population may not strictly consume foods typical of the ones consumed in Mediterranean countries. Hence, one goal of the present study was to see whether there are "naturally existing" DPs in our population that may also be associated with AD risk. Interestingly, the identified protective DP 2 was very similar to the MeDi,^5-7,47 and they are correlated with each other (Pearson r = 0.35; P < .001). Nevertheless, from another point of view, this means only about 12% of DP 2's variance was shared by the MeDi, indicating that despite some overlap, important new information was obtained in the current study. For example, rather than treating each food group equally in MeDi, the factor loadings of food–DP 2 help to identify the relative importance of each food group, thus providing more specific information.

So, as far as individual nutrients: omega-3 fats, omega-6 fats, vitamin E, and folate are good, but with lower SFA and vitamin B_12. In terms of actual foods: high intake of salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, and dark and green leafy vegetables are good, along with low intake of high-fat dairy, red meat, organ meat, and butter. (See what I did there - green means go, red means stop.)

As they note, this is similar to, but not identical with, the Mediterranean Diet, which these researchers have also looked at:

Scarmeas N, Stern Y, Tang MX, Mayeux R, Luchsinger JA. Mediterranean diet and risk for Alzheimer's disease. Ann Neurol. 2006;59(6):912-921. FULL TEXT | WEB OF SCIENCE | PUBMED Scarmeas N, Stern Y, Mayeux R, Manly JJ, Schupf N, Luchsinger JA. Mediterranean diet and mild cognitive impairment. Arch Neurol. 2009;66(2):216-225. FREE FULL TEXT Scarmeas N, Luchsinger JA, Mayeux R, Stern Y. Mediterranean diet and Alzheimer disease mortality. Neurology. 2007;69(11):1084-1093. FREE FULL TEXT

Good to know - although I have been promoting foods such as these for several years as part of a healthy diet for body and brain.

Tags: Alzheimer Disease, nutrition, food, Health, dietary patterns, JAMA, Archives of Neurology, Food Combination and Alzheimer Disease Risk, A Protective Diet, omega-3 fats, omega-6 fats, vitamin E, folate, salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, dark and green leafy vegetables

William B. Grant - Brain Food and Vitamin D

Excellent article from Frontiers in Neuroscience - vitamin D is much more crucial than people ever thought.

Brain Food and Vitamin D

By William B. Grant

An ecological study found total fat intake, along with total energy supply, highly correlated with Alzheimer's disease (AD) prevalence – with fish and cereals inversely correlated (Grant, 1997). These findings initiated the AD-dietary hypothesis, which continues to gain support. For example, a recent study in Poland found that the AD dietary pattern was characterized by a high intake of processed meat, butter, high-fat dairy products, eggs, and refined sugar, while the control pattern was characterized by a high intake of grains and vegetables (Gustaw-Rothenberg, 2009). An additional contributing factor to AD is the genetic risk based on apolipoprotein ε4 (ApoE4), which increases both cholesterol and insulin production (and weight in conjunction with a high-energy diet). ApoE4 is an important consideration for African Americans.

The 1997 study noted that because AD patients' brains have elevated concentrations of aluminum and transition metal ions, along with a reduced concentration of calcium, the dietary findings were consistent with a lower pH level in the digestive tract. The "metals hypothesis", i.e., metal-catalyzed hydroxyl radicals damage neurons, has gained considerable support (Bush and Tanzi, 2008). Although dealing with the aftermath of a long-term unhealthy diet by using chelation therapy or drugs might be indicated, eating with brain and general health in mind seems a more reasonable and practical measure.

Vitamin D is the current wonder compound, gaining increasing recognition for reducing the risk of many chronic and infectious diseases and mortality rates. Recently, interest has also extended to studying vitamin D's benefits for the brain. Several recent observational studies reported an inverse correlation between prevalence of cognitive impairment and serum 25-hydroxyvitamin D [25(OH)D] levels, such as one in the UK (Llewellyn et al., 2009). In this study, a serum 25(OH)D level in the lowest quartile (3–12 ng/ml) was correlated with an odds ratio of cognitive impairment of 2.3 (95% confidence interval, 1.4–3.8) compared with those in the fourth quartile (26–68 ng/ml) after adjustment for confounding factors.

Because cognitive impairment is often a precursor of dementia, it is reasonable to expect that low serum 25(OH)D levels would also be a risk factor for dementia (Grant, 2009). Other diseases that seem to precede dementia, and for which risk increases with lower serum 25(OH)D levels, include cardiovascular disease, diabetes, and tooth loss from either dental caries or periodontal disease (Grant, 2009).

On the basis of cross-sectional and observational studies, and randomized controlled trials of non-neurological diseases, serum 25(OH)D levels of 40–60 ng/ml are considered optimal. For each 1000 International Units (IU)/day of vitamin D production or oral intake, serum 25(OH)D levels increase by 6–10 ng/ml. Because mean population serum 25(OH)D levels range from 16 to 30 ng/ml, 2000–4000 IU/day of vitamin D from UV-B irradiance and/or oral intake would be indicated.

Thus, there appear to be two good ways to reduce the risk of cognitive impairment and dementia: diet modification and increased vitamin D.

Acknowledgments

I receive funding from the UV Foundation (McLean, VA), the Vitamin D Society (Canada), the Sunlight Research Forum (Veldhoven), and Bio-Tech-Pharmacal (Fayetteville, AR).

References

Bush, A. I., and Tanzi, R. E. (2008). Therapeutics for Alzheimer's disease based on the metal hypothesis. Neurotherapeutics 5, 421-432.

Grant, W. B. (1997). Dietary links to Alzheimer's disease. Alz. Dis. Rev. 2, 42-55. (http://www.sunarc.org/JAD97.pdf)

Grant, W. B. (2009). Does vitamin D reduce the risk of dementia? J. Alzheimer's Dis. 17, 151-159.

Gustaw-Rothenberg, K. (2009). Dietary patterns associated with Alzheimer's disease: population based study. Int. J. Environ. Res. Public Health 6, 1335-1340.

Llewellyn, D. J., Langa, K. M., and Lang, I. A. (2009). Serum 25-hydroxyvitamin D concentration and cognitive impairment. J. Geriatr. Psychiatry Neurol. 22, 188-195.

Biography

William B. Grant obtained a Ph.D. in Physics, University of California, Berkeley, in 1971. His professional career was devoted to developing and using laser systems for the remote sensing of atmospheric constituents such as aerosols and ozone, including 15 years with the NASA Langley Research Center. In Virginia, he performed an ecological study of the effects of acid rain on eastern hardwood forests, which led to his seminal paper on diet and Alzheimer's disease. He turned his attention to the health benefits of vitamin D in 2000, moved to San Francisco, and founded SUNARC in 2004.
wbgrant@infionline.net

Tags: William B. Grant, Brain Food and Vitamin D, Frontiers in Neuroscience, nutrition, Alzheimer Disease, brain, Psychology, Vitamin D, 25-hydroxyvitamin D

Archives of Neurology - Food Combination and Alzheimer Disease Risk

The Archives of Neurology has released an excellent article ahead of its publication date: Food Combination and Alzheimer Disease Risk.

Here are the basic details of the study and the outcome:

Objective To assess the association between food combination and Alzheimer disease (AD) risk. Because foods are not consumed in isolation, dietary pattern (DP) analysis of food combination, taking into account the interactions among food components, may offer methodological advantages.

Design Prospective cohort study.

Setting Northern Manhattan, New York, New York.

Patients or Other Participants Two thousand one hundred forty-eight community-based elderly subjects (aged 65 years) without dementia in New York provided dietary information and were prospectively evaluated with the same standardized neurological and neuropsychological measures approximately every 1.5 years. Using reduced rank regression, we calculated DPs based on their ability to explain variation in 7 potentially AD-related nutrients: saturated fatty acids, monounsaturated fatty acids, -3 polyunsaturated fatty acids, -6 polyunsaturated fatty acids, vitamin E, vitamin B₁₂, and folate. The associations of reduced rank regression–derived DPs with AD risk were then examined using a Cox proportional hazards model.

Main Outcome Measure Incident AD risk.

Results Two hundred fifty-three subjects developed AD during a follow-up of 3.9 years. We identified a DP strongly associated with lower AD risk: compared with subjects in the lowest tertile of adherence to this pattern, the AD hazard ratio (95% confidence interval) for subjects in the highest DP tertile was 0.62 (0.43-0.89) after multivariable adjustment (P for trend = .01). This DP was characterized by higher intakes of salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, and dark and green leafy vegetables and a lower intake of high-fat dairy products, red meat, organ meat, and butter.

Conclusion Simultaneous consideration of previous knowledge regarding potentially AD-related nutrients and multiple food groups can aid in identifying food combinations that are associated with AD risk.

Published online: April 12, 2010 (doi:10.1001/archneurol.2010.84)

This study offers further confirmation that the traditional Western diet is deadly, and that eating closer to nature is better for our bodies and our brains.

Specifically, eating a diet high salad dressing (olive oil or sometimes safflower oil), nuts, fish, tomatoes, poultry, cruciferous vegetables (broccoli, cauliflower, Brussels sprouts, kale, cabbage, and bok choy, among others), fruits, and dark and green leafy vegetables offers protection against illness, including Alzheimer's Disease.

These are all part of the typical Mediterranean diet. This diet is rich in omega-3 & omega-6 polyunsaturated fatty acids (PUFA), vitamin E, and folate. It is also lower saturated fatty acids (SFA) and vitamin B12. The B12 finding is interesting, but this single nutrient is not an indicator for increased AD risk, as the authors point out. Rather, "source foods of vitamin B12 like meat and dairy products may also contain a high level of SFA, which is a potential AD risk factor."

On the other hand, a diet high in high-fat dairy products, red meat, organ meat, and butter increases the risk of AD significantly. This diet is much higher in saturated fats,

The authors point out in the discussion that looking at a single nutrient is unlikely to generate meaningful results - with which I am in total agreement. Far too many studies try to isolate a single nutrient and then proclaim that it does nothing to increase health or decrease disease. But that is not how we eat - we eat foods that contain a variety of nutrients, which more than likely work together to create disease or prevent disease.

For example, the healthiest diet in this group included omega-3 fats (which are known to reduce the risk of heart disease and stroke while helping to reduce symptoms of hypertension, depression, attention deficit hyperactivity disorder (ADHD), joint pain and other rheumatoid problems) and cruciferous vegetables (which are known to contain anti-cancer chemicals), as well as nuts (I recommend walnuts, almonds and seeds such as pumpkin seeds and sunflower seeds), fish (salmon is best, but other fish are low in SFAs), and fruit (low sugar fruits such as apples, dark berries, and melons are best) - all of which contain healthy nutrients.

No one of these foods by itself is likely to offer overwhelming health benefits, but the combination of foods is a powerful diet-based way to increase health and longevity.

The final paragraph of the discussion sums up this study quite well:

In conclusion, we identified a DP that was strongly protective against the development of AD. The results of the current study indicate that higher consumption of certain foods (salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, dark and green leafy vegetables) and lower of others (high-fat dairy, red meat, organ meat, and butter) may be associated with a decreased risk of developing AD via a more favorable profile of nutrients (ie, lower ingestion of SFA and higher ingestion of PUFA, vitamin E, and folate). Our findings provide support for further exploration of food combination–based dietary behavior for the prevention of this important public health problem.

Reference:

Food Combination and Alzheimer Disease Risk

A Protective Diet

Yian Gu, PhD; Jeri W. Nieves, PhD; Yaakov Stern, PhD; Jose A. Luchsinger, MD, MPH; Nikolaos Scarmeas, MD, MS

Arch Neurol. 2010;67(6):(doi:10.1001/archneurol.2010.84).

Tags: Alzheimer's Disease, Health, nutrition, brain, Archives of Neurology, Food Combination, Alzheimer Disease Risk, dietary patterns, salad dressing, nuts, fish, tomatoes, poultry, cruciferous vegetables, fruits, dark and green leafy vegetables, omega-3 fats, omega-6 fats