Colgan Institute News

September 2011
The information contained in this Newsletter was prepared from medical and scientic sources which are referenced and are believed to be accurate and reliable. The information herein should not be used to treat or to prevent any medical condition unless it is used with the full knowledge, compliance and agreement of your personal physician or other licensed health care professional. Readers are strongly advised to seek the advice of their personal health care professional(s) before proceeding with any changes in any health care program.

Whey Protein Concentrate Benets A Selection of the Latest Science Dr. Michael Colgan
Whey Protein Concentrate Increases Protein Synthesis and Nitrogen Balance in Human Subjects, Increases Fat Loss, and Confers Cardiovascular Benets Without Adverse Effects.
Increased protein consumption has become popular among individuals, especially athletes, trying to increase or maintain lean muscle mass and lose body fat. Whey protein concentrate (WPC) in liquid form has become the most used protein supplement because it is shown to be rapidly and easily digestible without adverse side effects. Clinical studies show that approximately 30 g of WPC as a liquid meal produces a large rise in postprandial plasma amino acid levels in approximately 90 minutes, which returns to baseline within 5 hours. The rise in amino acid levels reliably increases protein synthesis and nitrogen balance. (1,2) Recently, it has been reported that intake of WPC above 1.5 g/kg/day helps to decrease body fat, increase lean body mass, and maintain nitrogen balance (3-14). WPC intake as high as 2.8 g/kg/day (3.5 times the current Recommended Daily Allowance) is reported to have no adverse effects on renal or other organ function. There is considerable evidence that protein intakes above the current RDA may be benecial during weight loss. Early evidence in support of higher protein intakes was derived from studies using very low calorie diets. This research found that increasing dietary protein to levels of 1.5 g protein per kilogram of ideal body weight reduced loss of lean tissue during rapid weight loss. Other researchers have found that there is a metabolic advantage with a high protein- low carbohydrate diet associated with increased thermogenesis, and that WPC has a higher satiety value, thus reducing net food intake (4-14). Increased dietary protein as WPC, contributes to a mix of metabolic outcomes benecial to
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fat loss and retention of lean muscle mass. Recent research shows that WPC consumption also confers positive cardiovascular benets, including improved insulin function, improved lipid proles, and reduced levels of C-reactive protein (CRP), the main inammatory marker of heart disease.(9,10,15,16)
1. Boirie Y, Dangin M, Gachon P, Vasson MP, Maubois JL, Beaufrere B. Slow and fast dietary proteins differently modulate postprandial protein accretion. Proc Natl Acad Sci. 1997;94:1493014935. doi: 10.1073/pnas.94.26.14930 2. Dangin M, Boirie Y, Garcia-Rodenas C, Fauquant J, Callier P, Ballevre O, Beaufrere B. The digestion rate of protein is an independent regulating factor of postprandial protein retention. Am J Physiol Endocrinol Metab. 2001;280:E340E348. 3. Layman D. Protein quantity and quality at levels above the RDA improves adult weight loss. J Am Coll Nutr. 2004;23:631S636S 4. Halton TL, Hu FB. The effects of a high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr. 2004;23:373385. 5. Ruan-Henares JA, Delgado-Andrade C, Jimenez-Perez S. Assessing nutritional quality of milk-based sport supplements as determined by furosine. Food Chemistry. 2007;101:573578. doi: 10.1016/j.foodchem.2006.02.016. 6. Sindayikengera S, Wen-shui X. Nutritional evaluation of caseins and whey proteins and their hydrolysates from Protamex. J Zhejiang Uni. 2006;7:9098. doi: 10.1631/jzus.2006.B0090. 7. Bilsborough S, Mann N. A review of issues of dietary protein intake in humans. Int J Sport Nutr Exerc Metab. 2006;16:129152. 8. Johnston CS, Tjonn SL, Swan PD. High-protein, low-fat diets are effective for weight loss and favorably alter biomarkers in healthy adults. J Nutr. 2004;134:58691. 9. Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Speizer FE, et al. Dietary protein and risk of ischemic heart disease in women. Am J Clin Nutr. 1999;70:221227. 10. Pins JJ, Keenan JM. Effects of whey peptides on cardiovascular disease risk factors. J Clin Hypertens. 2006;8:77582. doi: 10.1111/j.1524-6175.2006.05667. 11. Bistran BR, Winterer J, Blackburn GL, Young V, Sherman M: Effect of a protein-sparing diet and brief fast on nitrogen metabolism in mildly obese subjects. , J Lab Clin Med, 1997;89:1030 1035, . 12. Feinman RD, Fine EJ: Thermodynamics and metabolic advantage of weight loss diets. Metab Syn Relat Dis 2003;1:209 219. 13. Hill JH, Blundell JE: macronutrients and satiety: The effects of a high-protein or high-carbohydrate meal on subjective motivation to eat and food preferences. Nutr Behav 1986;3:133144. 14. Anderson GH, Moore SE: Dietary proteins in the regulation of food intake and body weight in humans. J Nutr, 2004;134 :974S 979S,. 15. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J: Increased dietary protein modies glucose and insulin homeostasis in adult women during weight loss. J Nutr 2003;133 :405 410. 16. Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD: A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid proles during weight loss in adult women. J Nutr. 2003;133 :411 417.

Whey Protein Concentrate reduces Airway Congestion in a Guinea Pig Model of Asthma
Abstract Allergen-induced asthmatic reactions are accompanied by oxidative stress. A diet based on undenatured whey protein concentrate is proven to increase levels of the major endogenous antioxidant glutathione. This new research investigated whether undenatured whey protein concentrate can alleviate allergen-induced lung contractions. Guinea pigs were fed water or a whey drink twice daily for 17 days. On day 1 the animals were sensitized to the allergen ovalbumin. On Day 20, lungs were isolated and perfused with buffer containing ovalbumin. Airway contractions were assessed, and mediators and indicators for oxida988 North End Road, Saltspring Island, BC, Canada V8K 1L7 Ph: 250-537-2069. Website: www.colganinstitute.com Colgan Institute, 2010

tive stress were measured in the lung efuent. Glutathione levels were measured in the liver. Oxidative stress and airway contraction increased upon ovalbumin challenge in ovalbumin-sensitised groups. Thiobarbituric acid-reactive substances (TBARS), potent indicators of stress, also increased. The undenatured whey protein concentrate diet signicantly enhanced glutathione levels in the liver, and signicantly reduced the ovalbumininduced airway contraction by 45 %. This study shows for the rst time that, during an asthmatic response, there is acute oxidative stress in the respiratory tract. The researchers concluded: The undenatured whey protein concentrate diet profoundly reduces allergen-induced airway constrictions, which opens new avenues for dietary management of allergic diseases.(3)
Kloek j, et al. A whey-based glutathione-enhancing diet decreases allergen-induced airway contraction in a guineapig model of asthma. Br J Nutr. 2011 May;105(10):1465-70.

Whey Protein Concentrate Reverses Weight Loss Caused by Cancer Treatment

Cancer chemotherapy and radiotherapy work partly be inducing massive oxidative stress into the tumors. This stress, however is systemic, and also causes widespread muscle loss, partly because of depletion of the endogenous antioxidant glutathione, the main protector of cell integrity. Because of their ease of use as drinks, milk proteins are fed to patients to combat these side effects. In a double-blind trial a whey protein concentrate, which is rich in cysteine, the main precursor of glutathione, was compared with casein, a protein supplement low in cysteine that is widely used in hospitals. Sixty-six patients with stage IIIB-IV lung cancer who were rapidly losing muscle, were randomly assigned to whey protein concentrate or casein for six months. The patients treated with the cysteine-rich whey protein concentrate showed a mean increase of 2.5% body weight, whereas casein-treated patients lost 2.6% (p = 0.049). The whey protein concentrate patients also showed greater strength (measured by hand grip), a better quality of life, and a higher survival rate.(1)
Tozer RG, et al. Cysteine-rich protein reverses weight loss in lung cancer patients receiving chemotherapy or radiotherapy. Antioxid Redox Signal. 2008 Feb;10(2):395-402.

Whey Protein Concentrate Reduces Rheumatoid Arthritis

At any time your intestines house about 100 billion bacteria. Mostly they are rendered harmless by your immune system. Some of the more aggressive of these bacteria are now linked with development of rheumatoid arthritis. Undenatured whey protein concentrate contains natural antibodies against a wide array of pathogenic intestinal bacteria.
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In this new research 18 patients with rheumatoid arthritis, whose disease activity was out of control by medications due to drug resistance, complications and/or risk factors, were treated for 3 months with a daily drink of whey protein concentrate containing high levels of natural milk antibodies. Eighteen matched rheumatoid arthritis patients, were used as controls. The patients receiving whey protein concentrate showed signicant reductions in arthritis symptoms and signicant improvement in intestinal disorders. This disease reducing effect of the whey protein concentrate disappeared upon cessation of treatment, but reappeared again upon reintroduction of it. The researchers concluded that whey protein concentrate deserves more attention as a potential adjunct in the treatment of rheumatoid arthritis.
Katayama K, et al. Supplemental treatment of rheumatoid arthritis with natural milk antibodies against enteromicrobes and their toxins: results of an open-labelled pilot study. Nutr J. 2011 Jan 6;10:2.

Use of a nutritional cleansing regimen by triathletes in training for the Olympic distance triathlon. Colgan M, Colgan L.A
Urban and suburban environments, in the US and Canada expose the population to multiple toxic chemicals (xenobiotics) in the air, food water, at the workplace, and in the home. Almost all pharmaceutical drugs are also zenobiotics. Xenobiotics accumulate in human body fat and other tissues impair bodily function and promote disease.(1-6) Because of their greater use of oxygen (up to 12 times that of sedentary people), and their greater ingestion of food and water (up to 3 times that of sedentary people), endurance athletes absorb larger amounts of these xenobiotics. Some 70-80% of endurance athletes also use pharmaceutical xenobiotics regularly, primarily for the reduction of pain and inammation caused by their training.(7) Half a century after the thalidomide disaster, (a harmless pharmaceutical given to pregnant women to reduce morning sickness) the public remains generally unaware that xenobiotics cause a wide range of damage, of which the anatomic malformations of thalidomide provide only an obvious example. Current research shows that common environmental chemicals cause numerous dysfunctions in brain function and physical performance. The ubiquitous toxin formaldehyde is now implicated in increasing incidence of various cancers, including adenocarcinomas and brain cancers.(2) Elevated body burdens of lead affect one million children in the United States (3), and prenatal exposure of mothers to even low levels of lead result in lifelong reductions of intellectual function and disorders of behavior (4,5). Organic mercury compounds are also potent neurotoxins (6,7).We rst detected lead and mercury pollution in the sweat of triathletes living and training on the sea coast north of San Diego, California in 1985. In order to counteract the likely higher body burden of these and other xenobiotics in athletes, the Colgan Institute advises a particular nutritional regimen, including regular nutritional cleansing. We are especially concerned with preventing toxic effects on the athletes brain; because all physical performance is neuro988 North End Road, Saltspring Island, BC, Canada V8K 1L7 Ph: 250-537-2069. Website: www.colganinstitute.com Colgan Institute, 2010

muscular, and even a slight neural decit can dramatically affect motor control. The body removes xenobiotics by deactivation and secretion, mostly through the liver. Hepatic enzymes are responsible for oxidation, reduction, hydrolysis and/or hydration of the xenobiotic, followed by conjugating the active secondary metabolite with glutathione or glucuronic acid, followed mostly by excretion in bile or urine, with some excretion in breath and sweat.
1. Colborn T, Voom Saal FS, Soto AM. Developmental effects of endocrine-disrupting chemicals in wildlife and humans. Environ Health Perspect 101:378384 (1993). . 2. National Toxicology Program. Final Report on Carcinogens Background Document for Formaldehyde. Rep Carcinog Backgr Doc. 2010 Jan;(10-5981):i-512. 3. Centers for Disease Control and Prevention. Screening Young Children for Lead Poisoning: Guidance for State and Local Public Health Ofcials. Atlanta, GA:Centers for Disease Control and Prevention,1997. 4. Needleman HL, Schell A, Bellinger D, Leviton A, AlIred EN. The long-term effects of exposure to low doses of lead in childhood: an 11-year follow-up report. N EngI J Med 1990;322:83-88. 5. Needleman HL, Riess JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA 1996;275:363-369. 6. Burbacher TM, Rodier PM, Weiss B. Methylmercury developmental neurotoxicity: a comparison of effects in humans and animals. Neurotoxicol Teratol 1990;3:191-202 (). 7. Watanabe C, Satoh H. Evolution of our understanding of methylmercury as a health threat. Environ Health Perspect 1996;104(suppl 2):367-379. 8. Colgan M. The Anti-Inammatory Athlete. Vancouver: Science Books, 2011.

Googled Out
Feeling Googled out? The ctional Sherlock Holmes told Dr Watson repeatedly that he had to be careful what he studied because the brain has limits on what memory can hold. Here is a quote from Study in Scarlet. I consider that a mans brain originally is like a little empty attic, and you have to stock it with such furniture as you choose. A fool takes in all the lumber of every sort that he comes across, so that the knowledge which might be useful to him gets crowded out, or at best is jumbled up with a lot of other things so that he has a difculty in laying his hands upon it. Now the skilful workman is very careful indeed as to what he takes into his brain-attic. He will have nothing but the tools which may help him do his work, but of these he has a large assortment, and all in the most perfect order. It is a mistake to think that that little room has elastic walls and can distend to any extent. Depend upon it there comes a time when for every addition of knowledge you forget something that you knew before. It is of the highest importance, therefore, not to have useless facts elbowing out the useful ones. New research coming out in Nature, September 2011, led by Betsy Sparrow from Columbia University, New York, supports Holmes. It shows that writer Sir Arthur Conan Doyle, was not merely enriching the eccentricity of his famous detective. Easy access to encyclopedic knowledge on line, at the click of a mouse, produces information overload. Research now conrms that it is reducing our ability to remember. Read too much on any subject and you may remember nothing about it, not even that you ever read about it.
Lewis S. Googled brains? Nature Reviews Neuroscience 12, 490 (September 2011) doi:10.1038/nrn3091. 988 North End Road, Saltspring Island, BC, Canada V8K 1L7 Ph: 250-537-2069. Website: www.colganinstitute.com Colgan Institute, 2010

Telomeres: Brief Summary of the Latest Research Michael Colgan

As the diagram shows, inside the nucleus of the cell, at the terminal ends of each chromosome, are specialized DNA structures called telomeres. Their main function is to maintain stability of the genome. Telomeres consist of non-coding double-stranded tandem DNA sequences with the nucleotide repeats TTAGGG that extend for 9,00015,000 bases in humans and end in a 50300 nucleotide single guanine strand overhang.

Because DNA polymerase cannot fully replicate the terminal end of the DNA strand, telomeres lose 30150 bases with each cell division. Eventually, telomeres reach a critical short length and can no longer form fully protective nucleotide caps on the ends of the chromosomes. This impairment activates a pathway called p53, resulting in cellular senescence. On average, cells reach this Hayick limit after about 50 doublings.
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Telomere shortening is not the only factor that dictates cell death. The presence of the enzyme telomerase itself is another critical factor. Telomerase not only functions to maintain telomere length but also preserves healthy cell function and long-term immune function. When telomerase is active, it effectively moves back the hands of the so-called aging clock. Active telomerase enables even very short telomeres to be functional. Massive research is currently trying to activate the telomerase gene reliably and safely in adults. Women for example, have a lower rate of age-dependent telomere loss likely due to the stimulating properties of estrogen on telomerase. Studies in vitro show that estrogen rapidly up-regulates telomerase gene expression and activity.

Oxidative Damage Shortens Telomeres the Worst

Owing to their high content of guanine, telomeres are highly sensitive to damage by oxidative stress. Telomere loss by oxidative DNA damage is greater than by the end-replication problem. Conversely, addition of antioxidants decelerates telomere shortening in cultured cells and prolongs telomerase activity. Systemic oxidative stress in hypertensive men from the Framingham Heart Study is linked to shorter telomeres. A higher level of oxidized LDL (low-density lipoprotein) is also linked with shorter telomere length and increased stiffness of the carotid artery.

Inammation Shortens Telomeres

The chronic inammation that occurs with usual aging also produces telomere attrition. Increased production of certain inammatory cytokines also reduces telomerase activity and telomere length. My new book, The Anti-Inammatory Athlete, contains the program to inhibit chronic inammation. Psychological and life stresses are also signicantly linked with higher levels of inammation and oxidative stress, lower telomerase activity and shorter leucocyte telomere lengths. Numerous in vitro studies also demonstrate that oxidative stress and inammation both reduce telomerase activity and shorten telomere length. Physical exercise is linked with longer telomeres in adults another indication of its anti-aging benets. Compared with untrained individuals, both young and middle-aged athletes show a profound up-regulation of telomerase activity and telomere proteins as well as down-regulation of apoptotic (cell death) proteins.

Some Nutrients Preserve Telomeres

Increased dietary intake of omega-3 fatty acids is linked with longer survival in patients with coronary heart disease. Farzaneh-Far and colleagues showed recently over 5 years, that individuals in the lowest quartile of DHA+EPA (docosahexaenoic acid+eicosapentaenoic acid) intake had the fastest telomere shortening. Individuals in the highest quartile had the slowest telomere shortening. Each standard deviation increase in DHA+EPA levels, yielded a 32% reduction in the risk of telomere shortening. Resveratrol has also been shown to increase telomerase activity.

Telomerase and Degenerative Disease

Stem cells regenerate the body. They maintain tissue homoeostasis by replenishing senescent or apoptotic cells and repairing damage that occurs throughout life. Telomeres and telomerase are main components of the stem cell ignition mechanism, providing a new way to restrain disease and delay aging. Through activity of telomerase, stem cells are able to continue to divide past the Hayick limit. One in three U.S. adults suffers from hypertension. Both animal and human studies indicate that telomere
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dysfunction and hypertension are causally linked. Atherosclerosis is an aging-related systemic disease with early origins. Cell senescence induced by telomere shortening contributes to the development of atherosclerosis. The pioneer clinical study, conducted by Samani et al., in 2001, showed that leucocyte telomere length was 303 bases shorter in patients with coronary artery disease than that in age-matched controls. That is equivalent to 8.6 years of aging. Type 2 diabetes is another aging-related epidemic in the US. It is caused by a combination of peripheral insulin resistance and pancreatic cell dysfunction. Recent evidence indicates that Type 2 diabetes is also caused by impaired cell regeneration because of telomere attrition. The obesity and insulin resistance epidemics in the US are also associated with reduced leucocyte telomere length. Recent research shows, a direct causal link between impaired telomerase activity and insulin resistance and glucose intolerance. Alzheimers the major manifestation of dementia, is an aging-associated progressive neurodegenerative disorder that begins decades before it shows. Alzheimers patients have signicantly shorter leucocyte telomere length than age-matched controls. Parkinsons is another common neurodegenerative disorder characterized by a progressive degeneration of dopaminergic neurons. Inammation and oxidative stress which both shorten telomeres, are also linked to the aetiology of Parkinsons. Precise analyses of Swedish twins demonstrate that telomere length at advanced age is a biomarker that predicts survival. The elderly Danish twin cohort study shows similar results. The co-twin with the shorter telomeres died rst, another indication that telomere length is not only a biomarker of aging, but also a determinant of lifespan.
A review of most of the above research has just been published in, Zhu H. et al. Clin Sci (Lond). 2011;120(Pt 10):427440.

Telomere Length and Cancer

I have recently received a ton of questions about the relationship between telomerase, telomere length, and cancer. From a great deal of research, it is correct that many cancers grow by expressing telomerase, and by increasing telomere length. The contrary assumption, that expressing telomerase to maintain telomeres may cause cancer, is dead wrong. I have studied this science since the 1970s. I rst wrote for the public about the HE-LA strain of immortal cancer cells in 1982.(1) Henrietta Lacks was a cancer patient who died in 1951 and bequeathed some of her cells for cancer research. Her cells proved to be immortal and live on today in laboratories worldwide. HE-LA are so persistent in expressing telomerase and increasing telomere length, that they are used as a standard to measure all other attempts to express telomerase in normal cells. Thus far, (August 2011) no non-toxic chemical or chemical combination has increased telomerase expression by more than about 10% of the expression found reliably in HE-LA. Nevertheless, some folk still fear that there is a danger of causing cancer by deliberately expressing telomerase to maintain telomere length. Quite the contrary. There is extensive evidence from basic research, animal studies, and genome-wide association studies, indicating that short telomeres are the worst problem. Short telomeres cause chromosomal instability, fail to protect the DNA code, and promote both cancer growth and premature aging.(2-7)
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Some folk persist that this research is not prospective. That is, in order to be sure that maintaining telomeres does not cause cancer, you have to do a controlled trial with human subjects. This trial has to follow a population-based random sample of human subjects, measuring their telomeres over a long period, and comparing the length of telomeres of those who develop cancer with those who remain cancer free. The appropriate trial was begun in 1995, in the town of Bruneck, Italy by a multi-university collaboration. Researchers precisely measured the telomere length of 787 subjects who tested free of cancer, and followed them for 10 years. The initial results were published in the Journal of the American Medical Association on 7 July 2010. The full paper is available free for download.(8) Here is a brief summary of the ndings. Over 10 years, 92 subjects developed cancer. Short telomere length at baseline was strongly linked with cancer development, independent of standard cancer risk factors. Compared with subjects with the longest telomere length (top 30%), the group with the shortest telomere length (bottom 30%) had 3.1 times the risk of developing cancer, and up to 10 times the risk of dying of cancer. Aggressive cancers with a high fatality rate (lung cancer, bladder cancer, kidney cancer, and brain cancer) were especially linked to short telomere length. This prospective trial conrms the prior evidence that, as telomere expert Bill Andrews says, Bad things happen when telomeres get short. All our cells replace themselves from stem cells. As telomere expert and head of the Spanish Cancer Institute, Maria Blasco wrote in 2010, During the last years it has become evident that telomeres and telomerase are main components of the stem cell ignition mechanism, providing a way to restrain cancer and delay aging.(9) Nuff said.
1. Colgan M. Your Personal Vitamin Prole. New York: William Morrow, 1982. 2. Artandi SE, Chang S, Lee SL, et al. Telomere dysfunction promotes non-reciprocal translocations and epithelial cancers in mice. Nature. 2000;406(6796): 641-645. 3. Rudolph KL, Chang S, Lee HW, et al. Longevity, stress response, and cancer in aging telomerasedecient mice. Cell. 1999;96(5):701-712. 4. Rudolph KL, Millard M, Bosenberg MW, DePinho RA. Telomere dysfunction and evolution of intestinal carcinoma in mice and humans. Nat Genet. 2001; 28(2):155-159. 5. Chin K, de Solorzano CO, Knowles D, et al. In situ analyses of genome instability in breast cancer. Nat Genet. 2004;36(9):984-988. 6. Rafnar T, Sulem P, Stacey SN, et al. Sequence variants at the TERT-CLPTM1L locus associate with many cancer types. Nat Genet. 2009;41(2):221-227. 7. Calado RT, Young NS. Telomere diseases. N Engl J Med. 2009;361(24):2353-2365. 8. http://jama.ama-assn.org/content/304/1/69.full.pdf+html 9. Flores I, Blasco M. The role of telomeres and telomerase in stem cell aging. FEBS Lett, 2010;584(17):3826-3830.

Induced Neurogenesis Improves Cognition Michael Colgan Ph D

Adult neurogenesis involves neural circuit plasticity that results in the generation of new neurons in the dentate gyrus of the hippocampus throughout life. These new neurons can total up to 10% of the whole granule cell population of the granular layer of the dentate gyrus and are critical for learning and memory. How many you get depends on the health of your brain.
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Research has shown that four interventions that benet cognition, learning programs, environmental enrichment, improved brain nutrition, and specic exercise programs, increase levels of adult hippocampal neurogenesis. Together, these properties of adult neurogenesis indicate that these interventions are now being harnessed to improve normal levels of hippocampal function. Substantial studies show that adultborn neurons are necessary for maintaining learning and memory, But, until now, there was no controlled evidence that an increase in adult hippocampal neurogenesis is sufcient to improve cognition. Sahav and colleagues at the Department of Neuroscience at Columbia University have just reported in Nature (28 April 2011) that inducible expansion of the population of new neurons, through enhancing their survival, improves performance in a specic cognitive task in which two similar contexts need to be distinguished. Mice with increased adult hippocampal neurogenesis show signicantly improvement in differentiating between overlapping contextual representations, which is indicative of enhanced pattern separation. This task is used as an animal model of enhanced cognition in humans. When combined with an intervention of voluntary exercise, stimulation of adult hippocampal neurogenesis, also produced a signicant enhancement of exploratory behaviour. This task is also used as an animal model of enhanced cognition in humans Twelve new patents have been issued in the US in 2011for compounds that may improve cognition in both healthy human adults and in people with mild cognitive impairment. This breakthrough science is the start of brain formulae that, will be used in the near future to make smart people smarter, and to make their brains last longer. The best investment you will ever make is in the future health of your brain. Nah. Spent the money on a great new PorscheIf only I could remember where I parked it?
Sahay A, Scobie KN, Hill AS, OCarroll CM, Kheirbek MA, Burghardt NS, Fenton AA, Dranovsky A, Hen R. Increasing adult hippocampal neurogenesis is sufcient to improve pattern separation. Nature. 2011 Apr 28;472(7344):466-70.

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Colgan Institute, 2010