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The Remarkable Properties of Curcumin

  [ 8 votes ]   [ 1 Comment ]
By Excerpts from Longvida and intro by Karen Lee Richards • www.ProHealth.com • May 23, 2014


The Remarkable Properties of Curcumin
Nearly 700 studies from all around the world confirm the remarkable properties of the ancient spice curcumin. It is showing amazing potential for support of the body's defenses against a wide variety of illnesses including Alzheimer's, cancer, arthritis, diabetes and multiple sclerosis to name a few.

Curcumin is the primary component of turmeric (Curcuma longa L.) and is what gives the spice its rich yellow color. Native to southern India and Indonesia, turmeric is the star ingredient in curry and is widely used in Indian cuisine.

In addition to its uses as a condiment, food coloring and textile dye, turmeric has been employed in Ayurvedic medicine for more than 4,000 years, utilized for everything from cuts and sores to gastrointestinal pain, rheumatism and liver disorders.

Uncovering the Secrets of Curcumin

About 50 years ago researchers began noticing that many diseases prevalent in Western culture, like Alzheimer's and multiple sclerosis, were rare in India. Their search to figure out why led them to curcumin. Turmeric - and thereby curcumin - is a staple in every Indian household. Not only do they ingest lots of it in their diet, but they also put it on their bandages to support wound healing(1) and take it orally for many illnesses. In fact, it is so much a part of their culture that brides and grooms apply turmeric and milk to their skin prior to their wedding so they will look more beautiful.

So Western scientists began taking a closer look at curcumin, trying to discover how it works and in what ways it might be used to help various health problems. The result has been more than 2,800 research papers published about the effects of curcumin.

However with all the amazing things curcumin intake is attributed to, there is one key problem - it is very difficult for the human body to absorb. That is why it does not matter how much curcumin you take, but rather how much your body can absorb.

So, in the late 90's a group of neuroscientists at UCLA began researching how they could make curcumin more bioavailable. Through much trial and error they were able to develop a material they named Longvida. This breakthrough material they created was soluble, permeable and stable, meaning it possessed all of the qualities needed to be bioavailable in the human body.

So What Makes Longvida® Unique?

  1. More than a dozen research studies and clinical trials in independent labs have been completed on Longvida.
  2. One small, single daily dose of Longvida offered significant health benefits in just 30 days.
  3. Published chronic-dosing safety studies on Longvida support a strong safety profile.
  4. Longvida is 65 times more bioavailable than regular curcumin.
  5. Longvida offers therapeutic levels of free (not deactivated/metabolized) curcumin.
  6. Curcumin from Longvida passes the blood-brain barrier.
  7. Longvida contains no metabolic inhibitors, volatile oils, or crude, unpurified ingredients.


Cutting-edge SLCP™ Technology

Longvida SLCP SLCP (Solid-Lipid Curcumin Particle) technology is responsible for the 'magic' of Longvida®. Longvida® is a finely-tuned matrix of ingredients brought together in a gentle multi-step process.

The end product is precisely set in a way that preserves and protects the curcumin from the harsh environment of the stomach, dissolves it at the point of absorption in the GI tract, and helps the free form of curcumin cross into the bloodstream and target tissues.*

SLCP is the ideal absorption-promoting system, based on real, live research data that was repeated over and over using validated analytical methodologies. Yet all the ingredients are generally recognized as safe (GRAS) food additives, and Longvida® is free of harsh solvents or volatile oils.

Longvida® and Healthy Brain Aging

In a 30 day, randomized placebo-controlled trial, low-dose Longvida (400 mg) in healthy, middle-aged (40-60 year old) people led to sigfigicant improvements versus placebo in the following markers related to cognitive health and healthy brain aging:
  • Amyloid-beta 1-42
  • Triglycerides
  • Catalase
  • sICAM
  • Nitric oxide
  • Total antioxidant capacity
  • Salivary amylase
No adverse events in either group were reported.

"I think what was interesting about this study is that we saw a number of effects, not just one thing," said Dr. Robert DiSilvestro, Ph.D, Professor at Ohio State and collaborator on the study. "The kinds of effects we saw for the intervention could conceivably help people of different ages and health status."

Amyloid-beta, Curcumin and Cognitive Function

Circulating levels of amyloid-beta are strongly associated with normal levels of brain deposits, healthy brain aging and cognitive function. Amyloid and other deposits begin to accumulate in the brain more than 20 years before signs of cognitive loss are shown. A decrease in plasma amyloid in healthy individuals may represent a clearance of amyloid from the brain and excretion from the body.

In 30 days, a significant 8% decrease in plasma amyloid-beta was observed in the treatment group, versus no significant change in the placebo group.

Stress and Cognitive Function

Salivary amylase is an established marker for physiological and emotional stress. The impact of stress on healthy aging and cognition is well known (Chida 2008, Kivimaki 2006). Stress and anxiety are also correlated with increased amyloid-beta (Ray 2011).

80mg curcumin from 400mg Longvida significantly reduced salivary amylase, a key marker for physiological stress, in just 30 days.

Lipid Metabolism, Triglycerides and Cognition

Typically, interventions for a short duration as performed in this study in healthy individuals does not significantly impact blood lipids or triglycerides. Plasma triglyceride levels are strongly correlated with plasma amyloid-beta levels in human populations (Fujiwara 2003). Triglyceride levels are also related to healthy brain aging and Alzheimer's disease (Razay 2007). Elevated plasma triglycerides precede amyloid-beta deposits in Alzheimer's disease models, suggesting that reduction of triglycerides correlated to a decrease in amyloid-beta and supports healthy brain aging.(Burgess 2006).

30-day dosing of Longvida led to a significant 14% reduction in plasma triglycerides (p<0.05) vs placebo.

Antioxidant Defenses, Catalase and Cognitive Function

Catalase is an antioxidant enzyme that binds with high affinity to amyloid-beta (Milton 1999). Catalase is also responsible for eliminating peroxide radicals, which increase the toxicity of beta-amyloid (Behl 1994). Further, reduced levels of circulating plasma catalase in humans are associated with cognitive impairment, beta-amyloid plaque formation, and Alzheimer's disease (Torres 2011 ).

30-day dosing of Longvida led to a significant increase in plasma catalase (p<0.05) vs placebo.

Cell Adhesion Molecule SlCam-1 and Cognition

Elevated levels of sICAM -1 are associated with elevated levels of amyloid deposits (Esmaillzadeh 2008). sICAM-1 is strongly associated with dysfunctional endothelial and vascular function. Elevated plasma levels of sICAM-1 have been observed as a possible risk factor for Alzheimer's and cerebrovascular diseases (Frohman 1991, Nielsen 2007).

30 days dosing of Longvida led to a 14% reduction in sICAM-1 (p<0.05) vs placebo.

Summary

Longvida was developed by neuroscientists using a Pharma-Type Research Approach (PTRA). This methodology has been used to answer essential scientific questions to substantiate the efficacy and safety of Longvida.

Just 80mg of curcumin from Longvida supports a number of markers of healthy brain aging in placebo-controlled research. The key message: it is not about how much is consumed, it is about how much is absorbed.

Other Curcumin References:
  1. Aggarwal BB, Bhatt ID, Ichikawa H, Ahn KS, Sethi G, Sandur SK, et al. Turmeric: the genus Curcuma. Taylor and Francis Group; 2006. p. 297–368.
  2. Aggarwal S, Ichikawa H, Takada Y, Sandur SK, Shishodia S, Aggarwal BB. Mol Pharmacol 2006;69:195–206. Baum L. et al. Letter in Journal of Clinical Psychopharmacology Volume 28, Number 1, February 2008 pp110-112.
  3. Began G, Sudharshan E, Appu Rao AG. Lipids 1998;33:1223–8.
  4. Bundy R, Walker AF, Middleton RW, Booth J. J Altern Complement Med 2004;10:1015–8.
  5. Cheng AL, Hsu CH, Lin JK, et al. Antican Res. 2001;21:2895-2900.
  6. Cho JW, Lee KS, Kim CW. Int J Mol Med 2007;19:469–74.
  7. Conteas CN, Panossian AM, Tran TT, Singh HM. Dig Dis Sci. 2008 Dec 3.
  8. Cruz-Correa M, Shoskes DA, Sanchez P, Zhao R, Hylind LM, Wexner SD, et al. Clin Gastroenterol Hepatol 2006;4:1035–8
  9. Deodhar SD, Sethi R, Srimal RC. Indian J Med Res 1980;71:632–4.
  10. Dhillon N, Aggarwal BB, Newman RA, Wolff RA, Kunnumakkara AB, Abbruzzese JL, Ng CS, Badmaev V, Kurzrock R. Clin Can Res. 2008 Jul 15;14(14):4491-9.
  11. Ganguli M, Chandra V, Kamboh MI, Johnston JM, Dodge HH, Thelma BK, Juyal RC, Pandav R, Belle SH, DeKosky ST. Arch Neurol. 2000 Jun;57(6):824-30.
  12. Garcea G, Berry DP, Jones DJ, Singh R, Dennison AR, Farmer PB, et al. Can Epidemiol Biomarkers Prev 2005;14:120–5.
  13. Goel A, Kunnumakkara AB, Aggarwal BB. Biochem Pharmacol. 2008 Feb 15;75(4):787-809. Epub 2007 Aug 19.
  14. Hanai H, Iida T, Takeuchi K, Watanabe F, Maruyama Y, Andoh A, et al. Clin Gastroenterol Hepatol 2006;4:1502–6
  15. Holt PR, Katz S, Kirshoff R. Dig Dis Sci 2005;50:2191–3.
  16. Lal B, Kapoor AK, Agrawal PK, Asthana OP, Srimal RC. Phytother Res. 2000;14:443-447.
  17. Lal B, Kapoor AK, Asthana OP, Agrawal PK, Prasad R, Kumar P, et al. Phytother Res 1999;13:318–22.
  18. Lao CD, Ruffin MT, Normolle D, Heath DD, Murray SI, Bailey JM, et al. BMC Complement Altern Med 2006;6:10.
  19. Ng TP, Chiam PC, Lee T, Chua HC, Lim L, Kua EH. Am J Epidemiol 2006;164:898–906.
  20. Ono et al. J Neurosci Res. 2004 Mar 15;75(6):742-50.
  21. Satoskar RR, Shah SJ, Shenoy SG. Int J Clin Pharmacol Ther Toxicol 1986;24:651–4.
  22. Sharma RA, McLelland HR, Hill KA, Ireson CR, Euden SA, Manson MM, et al. Clin Can Res 2001;7:1894–900.
  23. Shishodia S, Singh T, Chaturvedi MM. Adv Exp Med Biol 2007;595:127–48.
  24. Shoskes D, Lapierre C, Cruz-Correa M, Muruve N, Rosario R, Fromkin B, et al. Transplantation 2005;80:1556–9
  25. Skrzypczak-Jankun E, Zhou K, McCabe NP, Selman SH, Jankun J. Int J Mol Med 2003;12:17–24.
  26. Soni KB, Kuttan R. Indian J Physiol Pharmacol 1992;36:273–5.
  27. Yang F, Lim GP, Begum AN, Ubeda OJ, Simmons MR, Ambegaokar SS, et al. J Biol Chem 2005;280:5892–901.


Please Discuss This Article:   Post a Comment 

A Powerful Lesson
Posted by: me/cfs
May 26, 2014
While curcumin is remarkable, and a great deal of research has verified its health benefits, its potent properties can cause interactions with other medications or supplements used in ME/CFS or fibromyalgia.

I tried using a curcumin supplement four years ago. Initially, I was experiencing some positive benefit. But as I slowly increased the amount I was taking over a two month period, I suddenly experienced headaches and an intense burning pain in my spine that made the next two weeks the worst of my life (pain that was easily worse than a compound fracture I had previously experienced). After three visits to the ER, they finally did some blood tests on the third visit. I was immediately admitted to the hospital with elevated liver enzymes and dangerously low potassium levels. While I explained my suspicion of the curcumin causing some type of interaction, the thought was dismissed.

After being released from the hospital, I went back to read the information labels on the medications that I was on at the time, as well as the label on the curcumin. While an internet search revealed nothing, a search of Pubmed literature revealed an article explaining the effects of curcumin on the serotonin and dopamine systems (http://www.ncbi.nlm.nih.gov/pubmed/18766332). In effect, the curcumin acts by inhibiting the monoamine oxidase enzyme in the body. Drugs (or in this case a supplement) that do so are known as MAO inhibitors, and are a class of antidepressant.

This was significant in that I was being prescribed hydrocodone at the time. The drug interaction label for hydrocodone states "The use of MAO inhibitors or tricyclic antidepressants with hydrocodone preparations may increase the effect of either the antidepressant or hydrocodone." In other words, there is potential for an unpredictable interaction between the two.
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