Supplementation

How I Solved My Sleep Problems Forever

How I Solved My Sleep Problems Forever

By Ryback Reeves

The life of a pro wrestler is unlike anything else in the world. Living in airplanes, hotel rooms, arenas, rental cars and learning to live Groundhog Day over and over, 5 days a week, and sometimes for weeks at a time without a day off. Let’s not forget learning to live daily with nonstop pain and tightness from wrecking your body relentlessly, and living off coffee to stay awake on days you get very little rest. With this lifestyle the most important thing to keep going is to get enough sleep and be able to recover, and it’s often the one thing that gets neglected the most.

I remember it started so innocently, I would simply pop a Benadryl to wind down towards the end of the evening after performing in front of thousands and being watched by millions across the globe on TV, and then driving 3-5 hours to the next town, usually having a cup or 2 of coffee to ensure I didn’t fall asleep at the wheel. I would pop a Benadryl when I was about 15 minutes away from the hotel so it would start working by the time I got in and situated. This worked beautifully for a while, but I always noticed I felt groggy in the morning despite how well I slept. I then started needing 2 Benadryls to get to sleep, which led to stacking NyQuil with Benadryl, and eventually on nights when I was extra wired I would drink 1-2 beers with the Benadryl and NyQuil just to get my system to start winding down. I would say this is still harmless compared to the stories I’ve heard of wrestlers in the past, but you can see a trend here where it all kept adding up and then waking up after taking all this stuff was just brutal. Feeling foggy and taking hours and large amounts of caffeine to fully feel awake just didn’t sit well with me, as I’ve always tried to be as healthy as possible, despite some of these bad habits.

Cue my desire to create a sleep formula, much like I did along the way with my other supplements. As the owner of Feed Me More Nutrition, my story is a bit different from that of other supplement companies, as my brand is an extension of me and my disdain for the supplement companies selling for profit only. I started making my own formulas in my mid 20s for myself, because I could see what it was all about and I felt that if we could sell to do good then it would be a good form of capitalism. I truly believe that this mindset would solve a lot of the world's problems if it were implemented across the board, but that’s another blog for another time.

I started researching natural sleep ingredients that were proven to work and, much like I figured with my other formulas along the way, the one thing I found was that nearly all companies and sleep products would give you one ingredient at the proper dosage, but the “blend” or supporting ingredients just never were enough to do the job. I also was obsessed with recovery and found that ZMA Zinc Magnesium Aspartate was fantastic at helping with this, and would actually make a great sleep product with other key powerful ingredients. So I began my quest for the perfect sleep aid that would give me deep natural sleep with no morning hangover feeling by formulating individual ingredients at the research proven dosages. I eventually found after a year of trial and error that the following combination of ingredients gave me exactly what I wanted!




I would take the ingredients about an hour before bed, and they would give me a very natural "I need to lie down and go to sleep (thus the name GTS) feeling"; then I would wake up feeling amazing, with no morning hangover or fogginess. This was huge for me and got me off the Benadryl and NyQuil; I did not even need any alcohol prior to going to bed to relax. Eventually, when I created Feed Me More Nutrition the one thing I was a little hesitant on was the capsule count on some of our formulas, as we use more ingredients and the correct dosages, so nothing is a 1-capsule miracle. In order to create supplements that work, we have to use a lot more ingredients that work synergistically together to give the desired result. I knew deep down though that if I could give people a product that actually works and solves their problems the capsule count wouldn’t be an issue, and that theory has proven to be true for me. Also, many of our customers only need half the dosage to be put to sleep, so essentially they’re getting a 2-month supply in that situation; but, as for myself, I need the full dosage and it works beautifully time and time again! If you would like to learn more about our GTS Go To Sleep High-Powered Sleep Aid, you can click below and read further on the ingredients we use and see if it’s something that might benefit you. We also offer a Money Back Policy, because I want people to be satisfied with our products. I just ask you please give it a fair chance, and I think you won’t regret it. I also want to mention our product costs are 3-5X cheaper than those of other companies; I don’t charge the price we probably should for our products, because the one thing I always hated as a customer was having to pay a lot more for quality. Quite frankly, I’m happy with my margins and don’t need to be greedy in a sector that is supposed to be about helping people. So don’t be alarmed at our lower prices, that is a belief of mine and my quest for a "capitalism for good" for all. Thanks for reading and let me know what you think after trying it!

Sucralose in Supplements: The hidden “filler” that threatens your health?

Sucralose in Supplements: The hidden “filler” that threatens your health?

[Original Article]

By Dr. Dwayne N. Jackson, PhD
Does the supplement company you support use artificial chemical sweeteners? It’s easy to tell, you can look at the label, or just evaluate taste. Be honest, does your favorite preworkout, intraworkout, or postworkout supplements taste like sweet candy? Although flavor is one easy way to decide your favorite brand, I want to enlighten you on a big supplement formulation secret. Large doses of artificial sweeteners like sucralose and ACE-K are being pumped into supplements simply because these cheap and make flavoring easier—but, most of all, they make great hidden fillers and increase profit margins. If you use a sucralose sweetened supplement, serving for serving, you sacrifice a proportion of your active ingredients for cheap sweetener. Even more importantly, by ingesting the large amounts of sucralose found in chemically sweetened supplements, you are detracting from your gains in performance and health.

 

If you haveIIIf IIIIISucrolose in your supplements? Supplement companies are slowly damaging your health to protect their bottom line. TheTtttttis a synthetic organochlorine sweetener (OC) that is a common ingredient in the world's food supply. Sucralose interacts with chemosensors in the alimentary tract that play a role in sweet taste sensation and hormone secretion. In rats, sucralose ingestion was shown to increase the expression of the efflux transporter P-glycoprotein (P-gp) and two cytochrome P-450 (CYP) isozymes in the intestine. P-gp and CYP are key components of the presystemic detoxification system involved in first-pass drug metabolism. The effect of sucralose on first-pass drug metabolism in humans, however, has not yet been determined. In rats, sucralose alters the microbial composition in the gastrointestinal tract (GIT), with relatively greater reduction in beneficial bacteria. Although early studies asserted that sucralose passes through the GIT unchanged, subsequent analysis suggested that some of the ingested sweetener is metabolized in the GIT, as indicated by multiple peaks found in thin-layer radiochromatographic profiles of methanolic fecal extracts after oral sucralose administration. The identity and safety profile of these putative sucralose metabolites are not known at this time. Sucralose and one of its hydrolysis products were found to be mutagenic at elevated concentrations in several testing methods. Cooking with sucralose at high temperatures was reported to generate chloropropanols, a potentially toxic class of compounds. Both human and rodent studies demonstrated that sucralose may alter glucose, insulin, and glucagon-like peptide 1 (GLP-1) levels. Taken together, these findings indicate that sucralose is not a biologically inert compound.Sucralose is a synthetic organochlorine sweetener (OC) that is a common ingredient in the world's food supply. Sucralose interacts with chemosensors in the alimentary tract that play a role in sweet taste sensation and hormone secretion. In rats, sucralose ingestion was shown to increase the expression of the efflux transporter P-glycoprotein (P-gp) and two cytochrome P-450 (CYP) isozymes in the intestine. P-gp and CYP are key components of the presystemic detoxification system involved in first-pass drug metabolism. The effect of sucralose on first-pass drug metabolism in humans, however, has not yet been determined. In rats, sucralose alters the microbial composition in the gastrointestinal tract (GIT), with relatively greater reduction in beneficial bacteria. Although early studies asserted that sucralose passes through the GIT unchanged, subsequent analysis suggested that some of the ingested sweetener is metabolized in the GIT, as indicated by multiple peaks found in thin-layer radiochromatographic profiles of methanolic fecal extracts after oral sucralose administration. The identity and safety profile of these putative sucralose metabolites are not known at this time. Sucralose and one of its hydrolysis products were found to be mutagenic at elevated concentrations in several testing methods. Cooking with sucralose at high temperatures was reported to generate chloropropanols, a potentially toxic class of compounds. Both human and rodent studies demonstrated that sucralose may alter glucose, insulin, and glucagon-like peptide 1 (GLP-1) levels. Taken together, these findings indicate that sucralose is not a biologically inert compound. been led to believe that sucralose is a healthy calorie free sweetener, you are not alone--- after all, sucralose is made from sugar and has no calories. Sucralose is produced from sucrose (table sugar) by chemically replacing its hydrogen-oxygen groups for chlorine atom.

 


Seems harmless, right? This chemical processing of sugar increases its sweetness 600x and eliminates its caloric load, which has misled the public to equate sucralose use with health. However, we now know that although sucralose is calorie free and very sweet, it actions in your body are far from “healthy”. Sucralose is considered a synthetic organochlorine sweetener (OC), which has become a major ingredient in the world's food chain. Sucralose interacts with chemosensors in the digestive tract that play a role in sweet taste sensation and hormone secretion. Early studies claimed that sucralose passes through the gastrointestinal tract unaltered---suggesting that it is not metabolized. It was these past studies that led us to believe sucralose was harmless and healthy. However, contrary to early reports, recent science illustrates that about 15% of ingested sucralose is digested and metabolized, producing different compounds in the body which impact can health. So, the more sucralose you take in, the greater the potential impact these sucralose metabolites. In the grand scheme, although a diet soda here and there may not show up on your health charts, chronic ingestion of large amounts of chemical sweeteners, like sucralose, will likely have a negative impact on your overall health down the road.

 


In recent years, the unnecessary addition of large amounts of sucralose and artificial sweeteners in fitness supplements has become epidemic. That’s right, under the guise of health and taste, chemical sweeteners are being added to most products simply as “tasty hidden fillers”. In a review published in The Journal of Toxicology and Environmental Health, several health concerns of sucralose were raised:

  1. Sucralose and one of its metabolic by-products were found to increase genetic mutations at elevated concentrations in several testing methods. You want to avoid mutagenic compounds, as they are initiators to diseases like cancer.
  2. Cooking with sucralose was reported produce compounds called chloropropanols, a potentially toxic class of compounds that are also linked to cancers and other alterations in biological processes.
  3. Sucralose has been shown to negatively impact gut flora and gut health by decreasing the number of healthy bacteria. Sucralose also modifies glucose handling through initiating insulin spikes and affecting glucagon-like peptide 1 (GLP-1) levels. This can be a major issue for those who engage in intermittent fasting for fat management or in overweight individuals who are insulin insensitive or glucose intolerant.


Taken together, the above summary of findings indicate that sucralose is not the biologically inert compound we once thought it was.
Why are most supplement companies still using chemical sweeteners? Well, simply because chemical sweeteners are much cheaper and easier to flavor products with than the organic healthy alternatives like Stevia. Here’s the skinny:
FORMULATOR’S COST (per kilogram) FOR COMMON SWEETNERS IN FOUND YOUR SUPPLEMENTS ACE-K: $4.80 ASPARTAME: $6.20 ATP LAB’s Organic GMO Free Stevia: $200.00
That’s right! It costs 3000% to 4000% percent more to sweeten your products with healthy stevia! So, no wonder companies who still use chemical sweeteners tout the largest scoops and greatest taste.
At ATP LAB we use only organic non-GMO stevia in our products and since it’s so much more expensive than unhealthy chemical alternatives, we obviously use only what’s needed for taste. So, when comparing our products to others---gram for gram, you get less filler and more active ingredient. In the end, with ATP LAB supplements you get what you pay for---efficacious nutraceuticals, without detriment to your health.

 

 


    References: Schiffman SS, Rother KI. Sucralose, a synthetic organochlorine sweetener: overview of biological issues. J Toxicol Environ Health B Crit Rev. 2013;16(7):399-451. Abou-Donia M. B., Menzel D. B. Chick microsomal oxidases. Isolation, properties, and stimulation by embryonic exposure to 1,1,1-trichloro-2,2-bis(p chlorophenyl)ethane. Biochemistry. 1968a;7:3788–3794.  [PubMed] Abou-Donia M. B., Menzel D. B. The metabolism in vivo of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) in the chick by embryonic injection and dietary ingestion. Biochem. Pharmacol. 1968b;17:2143–2161.  [PubMed] Abou-Donia M. B., El-Masry E. M., Abdel-Rahman A. A., McLendon R. E., Schiffman S. S. Splenda alters gut microflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ. Health A. 2008;71:1415–1429.  [PubMed] Abu-Qare A. W., Elmasry E., Abou-Donia M. B. A role for P-glycoprotein in environmental toxicology. J. Toxicol. Environ. Health B. 2003;6:279–288.  [PubMed] Adachi Y., Suzuki H., Sugiyama Y. Comparative studies on in vitro methods for evaluating in vivofunction of MDR1 P-glycoprotein. Pharm. Res. 2001;18:1660–1668.  [PubMed] Adas F., Berthou F., Picart D., Lozac'h P., Beaugé F., Amet Y. Involvement of cytochrome P450 2E1 in the (ω-1)-hydroxylation of oleic acid in human and rat liver microsomes. J. Lipid Res. 1998;39:1210–1219.  [PubMed] Aiba T., Takehara Y., Okuno M., Hashimoto Y. Poor correlation between intestinal and hepatic metabolic rates of CYP3A4 substrates in rats. Pharm. Res. 2003;20:745–748.  [PubMed] Albert M. J., Mathan V. I., Baker S. J. Vitamin B12 synthesis by human small intestinal bacteria. Nature. 1980;283:781–782.  [PubMed] Anderson E. S. The problem and implications of chloramphenicol resistance in the typhoid bacillus. J. Hyg. (Lond). 1975;74:289–299. [PMC free article]  [PubMed] Anderson G. H., Catherine N. L., Woodend D. M., Wolever T. M. Inverse association between the effect of carbohydrates on blood glucose and subsequent short-term food intake in young men. Am. J. Clin. Nutr. 2002;76:1023–1030.  [PubMed] Anderson M., Opawale F., Rao M., Delmarre D., Anyarambhatla G. Excipients for oral liquid formulations. In: Katdare A., Chaubal M. V., editors. Excipient development for pharmaceutical biotechnology, and drug delivery systems. New York, NY: Informa Healthcare USA; 2006. pp. 155–180. Anway M. D., Cupp A. S., Uzumcu M., Skinner M. K. Epigenetic transgenerational actions of endocrine disruptors. Science. 2005;308:1466–1469.  [PubMed] Aronson K. J., Miller A. B., Woolcott C. G., Sterns E. E., McCready D. R., Lickley L. A., Fish E. B., Hiraki G. Y., Holloway C., Ross T., Hanna W. M., SenGupta S. K., Weber J. P. Breast adipose tissue concentrations of polychlorinated biphenyls and other organochlorines and breast cancer risk. Cancer Epidemiol. Biomarkers Prev. 2000;9:55–63.  [PubMed] Backman J. T., Olkkola K. T., Neuvonen P. J. Rifampin drastically reduces plasma concentrations and effects of oral midazolam. Clin. Pharmacol. Ther. 1996;59:7–13.  [PubMed] Bae W., Mehra R. K., Mulchandani A., Chen W. Genetic engineering of Escherichia coli for enhanced uptake and bioaccumulation of mercury. Appl. Environ Microbiol. 2001;67:5335–5338.[PMC free article]  [PubMed] Bain L. J., LeBlanc G.A. Interaction of structurally diverse pesticides with the human MDR1 gene product P-glycoprotein. Toxicol. Appl. Pharmacol. 1996;141:288–298.  [PubMed] Baird I. M., Shephard N. W., Merritt R. J., Hildick-Smith G. Repeated dose study of sucralose tolerance in human subjects. Food Chem. Toxicol. 2000;38(suppl. 2):S123–S129.  [PubMed] Bannach G., Almeida R. R., Lacerda L. G., Schnitzler E., Ionashiro M. Thermal stability and thermal decomposition of sucralose. Ecl. Quím. São Paulo. 2009;34:21–26. Bapiro T. E., Egnell A. C., Hasler J. A., Masimirembwa C. M. Application of higher throughput screening (HTS) inhibition assays to evaluate the interaction of antiparasitic drugs with cytochrome P450s. Drug Metab. Dispos. 2001;29:30–35.  [PubMed] Barndt R. L., Jackson G. Stability of sucralose in baked goods. Food Technol. 1990;44(Jan):62–66. Bauer S., Störmer E., Johne A., Krüger H., Budde K., Neumayer H. H., Roots I., Mai I. Alterations in cyclosporin A pharmacokinetics and metabolism during treatment with St John's wort in renal transplant patients. Br. J. Clin. Pharmacol. 2003;55:203–211. [PMC free article]  [PubMed] Bauer T. M. The role of gut bacteria in drug metabolism. In: Blum H. E., Bode C., Bode J. C., Sartor R. B., editors. Gut and the liver. Hingham, MA: Kluwer Academic; 1998. pp. 177–184. Baumhäkel M., Kasel D., Rao-Schymanski R. A., Böcker R., Beckurts K. T., Zaigler M., Barthold D., Fuhr U. Screening for inhibitory effects of antineoplastic agents on CYP3A4 in human microsomes. Int. J. Clin. Pharmacol. Ther. 2001;39:517–528.  [PubMed] Baune B., Flinois J. P., Furlan V., Gimenez F., Taburet A. M., Becquemont L., Farinotti R. Halofantrine metabolism in microsomes in man: Major role of CYP 3A4 and CYP 3A5. J. Pharm. Pharmacol. 1999;51:419–426.  [PubMed] Becquemont L., Mouajjah S., Escaffre O., Beaune P., Funck-Brentano C., Jaillon P. Cytochrome P-450 3A4 and 2C8 are involved in zopiclone metabolism. Drug Metab. Dispos. 1999;27:1068–1073.[PubMed] Benet L. Z., Izumi T., Zhang Y., Silverman J. A., Wacher V. J. Intestinal MDR transport proteins and P-450 enzymes as barriers to oral drug delivery. J. Control Release. 1999;62:25–31.  [PubMed] Benet L. Z. The drug transportermetabolism alliance: Uncovering and defining the interplay. Mol. Pharm. 2009;6:1631–1643. [PMC free article]  [PubMed] Bennett C., Dordick J. S., Hacking A. J., Cheetham P. S. J. Biocatalytic synthesis of disaccharide high-intensity sweetener sucralose via a tetrachlororaffinose intermediate. Biotechnol. Bioeng. 1992;39:211–217.  [PubMed] Beringer P. M., Slaughter R. L. Transporters and their impact on drug disposition. Ann. Pharmacother. 2005;39:1097–1108.  [PubMed] Berson A., Descatoire V., Sutton A., Fau D., Maulny B., Vadrot N., Feldmann G., Berthon B., Tordjmann T., Pessayre D. Toxicity of alpidem, a peripheral benzodiazepine receptor ligand, but not zolpidem, in rat hepatocytes: Role of mitochondrial permeability transition and metabolic activation. J. Pharmacol. Exp. Ther. 2001;299:793–800.  [PubMed] Berthou F., Dreano Y., Belloc C., Kangas L., Gautier J. C., Beaune P. Involvement of cytochrome P450 3A enzyme family in the major metabolic pathways of toremifene in human liver microsomes. Biochem. Pharmacol. 1994;47:1883–1895.  [PubMed] Bertilsson L., Höjer B., Tybring G., Osterloh J., Rane A. Autoinduction of carbamazepine metabolism in children examined by a stable isotope technique. Clin. Pharmacol. Ther. 1980;27:83–88.  [PubMed] Bertilsson L., Tomson T., Tybring G. Pharmacokinetics: Time-dependent changes—Autoinduction of carbamazepine epoxidation. J. Clin. Pharmacol. 1986;26:459–462.  [PubMed] Biles R. W., Piper C. E. Mutagenicity of chloropropanol in a genetic screening battery. Fundam. Appl. Toxicol. 1983;3:27–33.  [PubMed] Birnbaum L. S. When environmental chemicals act like uncontrolled medicine. Trends Endocrinol. Metab. 2013;24:321–323.  [PubMed] Björkholm B., Bok C. M., Lundin A., Rafter J., Hibberd M. L., Pettersson S. Intestinal microbiota regulate xenobiotic metabolism in the liver. PLoS One. 2009;4:e6958. [PMC free article]  [PubMed] Blaser M. J., Falkow S. What are the consequences of the disappearing human microbiota? Nat. Rev. Microbiol. 2009;7:887–894.  [PubMed] Bogaards J. J., van Ommen B., Wolf C. R., van Bladeren P. J. Human cytochrome P450 enzyme selectivities in the oxidation of chlorinated benzenes. Toxicol. Appl. Pharmacol. 1995;132:44–52.[PubMed] Bonnet U. Moclobemide: Therapeutic use and clinical studies. CNS Drug Rev. 2003;9:97–140.[PubMed] Booth D. A.  Psychology of nutrition. London, UK: Taylor & Francis; 1994. pp. 56–57. Borchers A. T., Selmi C., Meyers F. J., Keen C. L., Gershwin M. E. Probiotics and immunity. J. Gastroenterol. 2009;44:26–46.  [PubMed] Bort R., Macé K., Boobis A., Gómez-Lechón M. J., Pfeifer A., Castell J. Hepatic metabolism of diclofenac: Role of human CYP in the minor oxidative pathways. Biochem. Pharmacol. 1999;58:787–796.  [PubMed] Bort R., Ponsoda X., Carrasco E., Gómez-Lechón M. J., Castell J. V. Metabolism of aceclofenac in humans. Drug Metab. Dispos. 1996;24:834–841.  [PubMed] Boulton D. W., DeVane C. L., Liston H. L., Markowitz J. S. In vitro P-glycoprotein affinity for atypical and conventional antipsychotics. Life Sci. 2002;71:163–169.  [PubMed] Brannan M. D., Affrime M. B., Radwanski E., Cayen M. N., Banfield C. Effects of various cytochrome P450 inhibitors on the metabolism of loratadine. Clin. Pharmacol. Ther. 1995;57:193. (OII-A-4). Brown A. W., Bohan Brown M. M., Onken K. L., Beitz D. C. Short-term consumption of sucralose, a nonnutritive sweetener, is similar to water with regard to select markers of hunger signaling and short-term glucose homeostasis in women. Nutr. Res. 2011;31:882–888.  [PubMed] Brown R. J., Rother K. I. Nonnutritive sweeteners and their role in the gastrointestinal tract. J. Clin. Endocrinol. Metab. 2012;97:2597–2605. [PMC free article]  [PubMed] Brown R. J., Walter M., Rother K. I. Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care. 2009;32:2184–2186. [PMC free article]  [PubMed] Brown R. J., Walter M., Rother K. I. Effects of diet soda on gut hormones in youths with diabetes. Diabetes Care. 2012;35:959–964. [PMC free article]  [PubMed] Brownlee K. A.  Statistical theory and methodology in science and engineering. New York, NY: John Wiley & Sons; 1960. Brusick D., Borzelleca J. F., Gallo M., Williams G., Kille J., Hayes A. W., Pi-Sunyer F. X., Williams C., Burks W. Expert panel report on a study of Splenda in male rats. Regul. Toxicol. Pharmacol. 2009;55:6–12.  [PubMed] Bruyère A., Declevès X., Bouzom F., Proust L., Martinet M., Walther B., Parmentier Y. Development of an optimized procedure for the preparation of rat intestinal microsomes: Comparison of hepatic and intestinal microsomal cytochrome P450 enzyme activities in two rat strains. Xenobiotica. 2009;39:22–32.  [PubMed] Burdge G. C., Hanson M. A., Slater-Jefferies J. L., Lillycrop K. A. Epigenetic regulation of transcription: A mechanism for inducing variations in phenotype (fetal programming) by differences in nutrition during early life? Br. J. Nutr. 2007;97:1036–1046. [PMC free article]  [PubMed] Cabrini L., Landi L., Stefanelli C., Barzanti V., Sechi A.M. Extraction of lipids and lipophilic antioxidants from fish tissues: A comparison among different methods. Comp. Biochem. Physiol. Part B. 1992;101:383–386.  [PubMed] Calafat A. M., Ye X., Wong L. Y., Reidy J. A., Needham L. L. Urinary concentrations of triclosan in the U.S. population: 2003–2004. Environ. Health Perspect. 2008;116:303–307. [PMC free article][PubMed] Chadwick R. W., Cooper R. L., Chang J., Rehnberg G. L., McElroy W. K. Possible antiestrogenic activity of lindane in female rats. J. Biochem. Toxicol. 1988;3:147–158.  [PubMed] Chang T. K., Yu L., Maurel P., Waxman D. J. Enhanced cyclophosphamide and ifosfamide activation in primary human hepatocyte cultures: Response to cytochrome P-450 inducers and autoinduction by oxazaphosphorines. Cancer Res. 1997;57:1946–1954.  [PubMed] Chen C., Hanson E., Watson J. W., Lee J. S. P-glycoprotein limits the brain penetration of nonsedating but not sedating H1-antagonists. Drug Metab. Dispos. 2003a;31:312–318.  [PubMed] Chen C., Staudinger J. L., Klaassen C. D. Nuclear receptor, pregname X receptor, is required for induction of UDP-glucuronosyltranferases in mouse liver by pregnenolone-16 alpha-carbonitrile. Drug Metab. Dispos. 2003b;31:908–915.  [PubMed] Chen J., Raymond K. Roles of rifampicin in drug-drug interactions: Underlying molecular mechanisms involving the nuclear pregnane X receptor. Ann. Clin. Microbiol. Antimicrob. 2006;5:3.[PMC free article]  [PubMed] Chen Y., Tang Y., Guo C., Wang J., Boral D., Nie D. Nuclear receptors in the multidrug resistance through the regulation of drug-metabolizing enzymes and drug transporters. Biochem. Pharmacol. 2012;83:1112–1126. [PMC free article]  [PubMed] Cho I., Blaser M. J. The human microbiome: At the interface of health and disease. Nat. Rev. Genet. 2012;13:260–270. [PMC free article]  [PubMed] Cho W. S., Han B. S., Lee H., Kim C., Nam K. T., Park K., Choi M., Kim S. J., Kim S. H., Jeong J., Jang D. D. Subchronic toxicity study of 3-monochloropropane-1,2-diol administered by drinking water to B6C3F1 mice. Food Chem. Toxicol. 2008;46:1666–1673.  [PubMed] Chonan O., Takahashi R., Watanuki M. Role of activity of gastrointestinal microflora in absorption of calcium and magnesium in rats fed ß1–4 linked galactooligosaccharides. Biosci. Biotechnol. Biochem. 2001;65:1872–1875.  [PubMed] Choo E. F., Leake B., Wandel C., Imamura H., Wood A. J., Wilkinson G. R., Kim R. B. Pharmacological inhibition of P-glycoprotein transport enhances the distribution of HIV-1 protease inhibitors into brain and testes. Drug Metab. Dispos. 2000;28:655–660.  [PubMed] Cizza G., Rother K. I. Beyond fast food and slow motion: Weighty contributors to the obesity epidemic. J. Endocrinol. Invest. 2012;35:236–242. [PMC free article]  [PubMed] Claus S. P., Tsang T. M., Wang Y., Cloarec O., Skordi E., Martin F. P., Rezzi S., Ross A., Kochhar S., Holmes E., Nicholson J. K. Systemic multicompartmental effects of the gut microbiome on mouse metabolic phenotypes. Mol. Syst. Biol. 2008;4:219. [PMC free article]  [PubMed] Clement B., Demesmaeker M. Formation of guanoxabenz from guanabenz in human liver. A new metabolic marker for CYP1A2. Drug Metab. Dispos. 1997;25:1266–1271.  [PubMed] Clemente J. C., Ursell L. K., Parfrey L. W., Knight R. The impact of the gut microbiota on human health: An integrative view. Cell. 2012;148:1258–1270. [PMC free article]  [PubMed] Colditz G. A., Willett W. C., Stampfer M. J., London S. J., Segal M. R., Speizer F. E. Patterns of weight change and their relation to diet in a cohort of healthy women. Am. J. Clin. Nutr. 1990;51:1100–1105.  [PubMed] Coleman S., Linderman R., Hodgson E., Rose R. L. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Environ. Health Perspect. 2000;108:1151–1157. [PMC free article]  [PubMed] Corkey B. E. Banting lecture 2011: Hyperinsulinemia: Cause or consequence? Diabetes. 2012;61:4–13.[PMC free article]  [PubMed] Coumoul X., Diry M., Barouki R. PXR-dependent induction of human CYP3A4 gene expression by organochlorine pesticides. Biochem. Pharmacol. 2002;64:1513–1519.  [PubMed] Crabbe E., Nolasco-Hipolito C., Kobayashi G., Sonomoto K., Ishizaki A. Biodiesel production from crude palm oil and evaluation of butanol extraction and fuel properties. Process Biochem. 2001;37:65–71. Cummings J. H., Macfarlane G. T. The control and consequences of bacterial fermentation in the human colon. J. Appl. Bacteriol. 1991;70:443–459.  [PubMed] Cummings J. H., Macfarlane G. T. Role of intestinal bacteria in nutrient metabolism. J. Parenter. Enteral. Nutr. 1997;21:357–365.  [PubMed] Custodio J. M., Wu C. Y., Benet L. Z. Predicting drug disposition, absorption/elimination/transporter interplay and the role of food on drug absorption. Adv. Drug Deliv. Rev. 2008;60:717–733.[PMC free article]  [PubMed] Dantzig A. H., Shepard R. L., Law K. L., Tabas L., Pratt S., Gillespie J. S., Binkley S. N., Kuhfeld M. T., Starling J. J., Wrighton S. A. Selectivity of the multidrug resistance modulator, LY335979, for P-glycoprotein and effect on cytochrome P-450 activities. J. Pharmacol. Exp. Ther. 1999;290:854–862.[PubMed] Davies E. Sweets for my sweet. Chem. World. 2010;7:46–49. Decherf S., Demeneix B. A. The obesogen hypothesis: A shift of focus from the periphery to the hypothalamus. J. Toxicol. Environ. Health B. 2011;14:423–448.  [PubMed] Deichmann W. B., MacDonald W. E., Cubit D. A., Beasley A. G. Effects of starvation in rats with elevated DDT and dieldrin tissue levels. Int. Arch. Arbeitsmed. 1972;29:233–252.  [PubMed] Dekant W., Assmann M., Urban G. The role of cytochrome P450 2E1 in the species-dependent biotransformation of 1,2-dichloro-1,1,2-trifluoroethane in rats and mice. Toxicol. Appl. Pharmacol. 1995;135:200–207.  [PubMed] de Ruyter J. C., Olthof M. R., Seidell J. C., Katan M. B. A trial of sugar-free or sugar-sweetened beverages and body weight in children. N. Engl. J Med. 2012;367:1397–1406.  [PubMed] Desta Z., Soukhova N., Mahal S. K., Flockhart D. A. Interaction of cisapride with the human cytochrome P450 system: Metabolism and inhibition studies. Drug Metab. Dispos. 2000;28:789–800.  [PubMed] Desta Z., Wu C. M., Morocho A. M., Flockhart D. A. The gastroprokinetic and antiemetic drug metoclopramide is a substrate and inhibitor of cytochrome P450 2D6. Drug Metab. Dispos. 2002;30:336–343.  [PubMed] Dhingra R., Sullivan L., Jacques P. F., Wang T. J., Fox C. S., Meigs J. B., D'Agostino R. B., Gaziano J. M., Vasan R. S. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation. 2007;116:480–488.[

What is Ginseng? Benefits and Uses for this Ancient Herb

What is Ginseng? Benefits and Uses for this Ancient Herb

[Original Article}

 

What’s in a name? Rénshēn or “Jen Sheng"—Chinese for “man root”—were the names originally given to ginseng due to its resemblance of a stick figure person with legs. Not ironically, the root also has many known health benefits on the human body. Old cultures thought the closer the root was to resembling a human form, the more potent it would be once consumed.

 

Anatomical similarities aside, ginseng is one powerful herb. In fact, Swedish botanist Carl Linnaeus later gave it the name Panax—greek for “cure all.” While it may not be a panacea for everything that ails you, ginseng has some pretty potent health-boosting effects.

A Remedy With a History

Before Linnaeus and the western world became aware of ginseng, it already had a long history of use in traditional Chinese medicine. Records dating back to 100 A.D describe the use of ginseng in China, particularly the mountains of Manchuria—where it was often reserved for use only by royalty. The fleshy roots may have also been used for food.1 Before the advent of modern healthcare, the strength-giving properties and regenerative powers of ginseng endeared many cultures to this powerful herbal medicine.

Ancient cultures believed in the medicinal properties of ginseng to treat a cornucopia of diseases and ailments. The Chinese Canon of Medicine even shows reverence to ginseng, stating that, “ginseng strengthens the soul, brightens the eye, opens the heart, expels evil, benefits understanding and if taken for prolonged periods of time will invigorate the body and prolongs one’s life.”1

The belief in ginseng to treat and cure medical conditions was so profound that it was soon being sold for more than its weight in gold.

Chinese emperors began to hoard the stuff, and an industry for this ancient nootropic was born—along with a black market.

Now, ginseng and ginseng supplements are a worldwide sensation. Since its “discovery” in North America in 1716 and now into modern day, ginseng has become popularized and revered by the United States and throughout the western world for many of the same qualities it was loved for in ancient times. Ginseng is marketed in over 35 countries, with yearly sales exceeding $2 billion dollars. A 2002 survey indicated that 4% - 5% of men and women 45 - 64 years old living in the United States have used ginseng.2 It’s popular, and for a good reason.

Types of Ginseng

Due to its high levels of ginsenosides—ginsenosides are the main biologically-active constituents of ginseng (more on these later)—Panax ginseng is the main type of ginseng used for supplementing and in research studies. The Panax variety can include both American ginseng (Panax quinquefolius) and Asian ginseng (Panax notoginseng) or Korean ginseng (Panax ginseng).

In addition to these types, ginseng can come in other forms including Siberian ginseng (eleutherococcus senticosus), Indian ginseng (withania somnifera a.k.a ashwagandha), and Brazilian ginseng (pfaffia paniculata).

Unless stated otherwise, any studies and benefits discussed refer to the Panax varieties of American ginseng and Asian ginseng.

Ginseng Pharmacology

Although referred to as “alternative medicine,” the heroic health effects of ginseng aren’t due to ancient spiritual healing powers.

Instead, we know certain molecular actors are to thank for the benefits of ginseng. Of these, tetracyclic triterpenoid saponins—also known as ginsenosides—are the main active ingredient proposed to explain why ginseng is such a powerful herbal medicine.

What are ginsenosides? Molecularly speaking, they’re steroid-like ring structures with sugars attached to them at various carbon side chains. Over 40 different ginsenosides have been identified and isolated from ginseng root. This large group of active molecules are responsible for the antioxidant, anti-cancer, and anti-inflammatory effects of ginseng.2

Ginsenosides work their molecular magic by acting through signal transduction pathways in the body. Several important processes modulated by ginsenosides include antioxidant signaling, steroid hormones, vascular regulation through the molecule nitric oxide (NO), and neuronal signaling through NMDA and GABA, two super-important neurotransmitters.3

By binding to certain receptors, ginsenosides act as “ligands”—molecular keys that fit into the receptor keyhole and help exert a biological function.

The main receptor targets for ginsenosides seem to be glucocorticoid receptors (GR) and androgen (sex-steroid) receptors.2 Each of these are vitally important in our ability to respond to stress, modulate hormones, and properly grow, recover, and maintain our health.

Protect and Defend

Might the protective effects of ginsenosides be due to the fact that their primary purpose is to defend their host, the ginseng root? Just like a mighty cactus produces spines to prevent certain critters from nibbling it do death, the ginseng root produces ginsenosides as a protective strategy against nature.

Ginsenosides are known to be anti-microbial, anti-fungal, and antifeedant—their bitter taste is a reason that some insects and animals steer clear of eating ginseng. When we consume these compounds, they may impart many of the same host-protective effects for our body.

 

Health Benefits of Ginseng

With such a long and ancient medical history, ginseng’s use as an herbal supplement has been studied in nearly every medical condition imaginable. No, you can’t get an herbal medicine prescription from your healthcare provider, however, this powerful plant has been shown in clinical trials to benefit many diseases and is available in a variety of herbal supplement forms.

Ginseng and Cardiovascular Disease

One area where the medical potential of ginseng has been vastly explored is within the cardiovascular system.

Specifically, the ginsenosides have powerful anti-inflammatory effects that can prevent oxidative stress and damage to the heart, blood vessels, and circulation. The vascular system may benefit from ginseng, since ginsenosides also increase a protective molecule known as nitric oxide (NO) in the circulation—helping to maintain blood vessel function and blood pressure.4

Indeed, ginseng might help lower blood pressure, but results of clinical trials seem to vary widely on this outcome. A meta-analysis of studies on ginseng supplementation found there was a minor but favorable trend for improved blood pressure for the group consuming ginseng herbal supplements, but the beneficial effect was only seen in individuals with cardiovascular and other types of disease, suggesting that healthy individuals with normal blood pressure may not benefit.5

Nevertheless, ginseng might act on other aspects of the cardiovascular system.

Some benefits of ginseng might partially be due to the fact that it leads to the production and release of nitric oxide (NO), which we need to help dilate our blood vessels.

Studies in patients with reduced coronary blood flow and hypertension have shown that ginseng improves blood circulation (by the anti-clotting mechanism targeted by blood thinners) and lowered arterial stiffness. The wide-ranging actions of ginseng on the cardiovascular system make it apparently beneficial for certain diseases.4

To reduce cardiovascular risk factors like blood pressure, blood vessel dysfunction, and overall heart health, ginseng supplementation seems to have some evidence in those who might be at an increased risk. The good news is, no trials show an adverse effect of supplementation—so it can’t hurt to try.

Depression and Anxiety

Physical, mental, or emotional stress takes a toll on the body. It can lead to a variety of negative health effects, many of which can include changes in mood and outlook on life. In a “fight or flight” world, ginseng may provide some much needed stress relief.

Ginseng may have the potential to boost mood, regulate levels of anxiety, and reduce symptoms of depression.6 It does this through effects on the brain which are known to include neurogenesis (the sprouting of neurons), synaptogenesis (growth of new synapses), neuron growth, and neurotransmitter activity—all of which “protect” the central nervous system.

How you respond to stressful situations (think, road rage) may be improved with ginseng.

In one study, rats were given ginseng and then put in a plus-sized maze (a stressful situation for a small rat) showed fewer anxiety-like behaviors. The anxiety-reducing effects of both types of ginseng used in the study were actually similar to the antidepressant drug Diazepam.7 In mice, red ginseng supplementation for seven days alleviated the psychological fatigue in animals induced by this stressful situation. Ginseng has also been shown to reduce levels of the stress hormone corticosterone.8

Depression can often be associated with stress-like symptoms. In the few studies available, ginseng treatment had been shown to exert antidepressant-like effects in animal models of depression and may improve measures of quality of life and depressive symptoms in postmenopausal women.6 Further research is needed to clarify the extent to which ginseng might be useful as an antidepressant.

Anti-Cancer Properties

Protective effects of ginseng on cancer have been also explored since the root’s discovery in the ancient world. It’s now known that compounds of ginseng can act on several signal pathways involved in the cell cycle, and prevent the unwanted growth and proliferation of cells—a hallmark of cancer development.

Observational studies suggest a benefit (i.e. lower risk) for cancer. It has been shown that ginseng consumption is associated with a 16% lower cancer risk in individuals compared those who don’t consume ginseng,9 and several other studies have shown a relationship between a higher ginseng intake and a reduced risk for cancer.10

The chemoprotective effects are shown to be present for different cancer types, including lung cancer, gastric cancer, liver cancer, and colorectal cancer. So far, most experimental studies have only been conducted in isolated cell cultures or animals, and human trials on ginseng and anti-cancer have yet to be done. For now, all we have are associations, but the data shows that ginseng may have some anti-cancerous properties for people munching it down on the regular.

Immune Boost

To stay at your best, avoiding sickness should be a priority. Just consuming vitamin C is probably not your best bet. Ginseng, on the other hand, has shown to have potent effects on boosting the immune system. In particular, our innate immunity—the ability to recognize foreign “invaders” and prevent and eliminate infections—may benefit from ginseng supplementation.

Consuming ginseng has been shown to fortify defense systems by boosting the activity of macrophages, molecules that engulf harmful bacteria present in our cells.

Subjects consuming 100mg of ginseng extract for eight weeks also showed enhanced death of infectious agents in the body, indicating an enhanced ability to fend of certain vicious viruses. In an aging population with reduced immunity, ginseng saponin extract enhanced the function of immune cells called lymphocytes,11 suggesting they had an enhanced ability to respond to bacterial stress.

Along with enhancing the death of “bad” cells, ginseng may also reduce the amount of inflammation present in the body, whether chronic or due to an invading bacteria. Ginseng has been shown to lower the amount of pro-inflammatory cytokines like TNF-alpha, IL-1B, IL-6, IFN-y, IL-12, and IL-18.12 Many of these inflammatory markers are associated with autoimmune diseases.

Whether by enhancing the ability to fend off viruses or boosting our ability to clear them out, ginseng could keep your defense systems robust and keep you out of the doctor's office.

Let’s Talk Sex (Hormones)

Now that we have your attention, let’s look at one of the most historic uses of ginseng.

It’s supposed to act as an aphrodisiac, stimulating “sexual appetite” in anyone consuming it.

 

Numerous placebo-controlled studies support a beneficial effect of ginseng supplementation on male ED. Supplemented in doses of 900mg (for eight weeks) and 1,000mg (for 12 weeks) three times per day, ginseng was shown to improve symptoms of ED in over 60% of those in the treatment group. Results of several other studies indicate that ginseng supplementation also improves various markers of sexual function in men with ED,13 enhances sexual drive,14 and even boosts sperm count and motility.

Ginsenosides are mainly responsible for these improvements by increasing amount of neurotransmitters such as dopamine and GABA, and enhanced nitric oxide (NO) levels in blood vessels, allowing enhanced flow of blood to body parts where it's needed.

Women aren’t excluded from the aphrodisiac-like qualities of ginseng. Post-menopausal women ingesting ginseng capsules (1,000mg) experienced improved sexual function scores and higher arousal levels compared to a placebo group, with no adverse effects reported.15 Another trial in premenopausal women indicated that Korean red ginseng supplementation for eight weeks improved sexual drive and satisfaction however, this was not different than the placebo group, who also increased their function.16

Why the boost? Ginseng appears to have effects on sex-steroid hormone receptors like the estrogen receptor and the androgen receptor. By maintaining healthy levels of receptors and receptor signaling, ginseng can prevent the decline in sex hormones that occur with aging and disease.17

Brain Food

Ginseng might be your next go-to for enhancing cognitive health and performance; it has even been shown to be neuroprotective.

Mice given ginseng compounds showed improvements in learning and memory,18 and just one 500mg dose of a ginseng-containing supplement enhanced long term potentiation (LTP)—a strengthening of synapses related to memory formation.19

Further evidence of brain benefits have been shown in studies where ginseng supplementation improved cognitive performance, reduced mental fatigue, and improved working memory and reaction time.20,21,22,23 Combining ginseng with other cognitive enhancers like caffeine and L-theanine might even have benefits above and beyond ginseng alone.

Through its various anti-inflammatory, antioxidant, and neuroprotective qualities, ginseng may be beneficial as an adjunct therapeutic in various neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and multiple sclerosis.24 Protecting the squishy ball of neurons in our head might be one of the most important and promising benefits of ginseng.

Mental and Physical Performance

We’ve got the health-boosting properties of ginseng down, and there are many. On top of the disease-fighting benefits of this herb, ginseng may also be able to enhance your physical performance, make the most of your exercise routine or training plan, and help you reach your health and fitness goals. At the same time, ginseng can enhance cognitive function, potentially giving you that much needed boost at weekly pub trivia.

Get Fit

There have been very few randomized trials to evaluate the ability of ginseng to improve physical performance and other measures of fitness. In general, a small effect for reducing fatigue had been shown when ginseng was investigated compared to placebo treatments.25

One study noted improved muscular strength and aerobic work or endurance capacity after ginseng supplementation.

Participants given a ginseng extract of 300mg/day for eight weeks improved their aerobic capacity by over 12% as well as their anaerobic capacity, anaerobic power, and leg strength (just as much as exercise training).26 A 30-day regimen of supplementation with 1,350mg/day of Panax notoginseng (PNG) increased time to exhaustion and lowered VO2 and blood pressure during steady state exercise,27 suggesting endurance performance was improved. Pretty remarkable findings for a plant.

Cognitive Performance

Effects on the muscle between your ears have also been promising for ginseng. Studies using ginseng extract supplementation have shown positive improvements in cognitive performance parameters like vitality, alertness, concentration, visual-motor coordination, mental accuracy, reaction times, even better math skills.28,29 Sign me up!

Ginseng’s effect on the brain might be responsible for these improvements—it can improve neuron activity, increase nerve growth factors, enhance levels of neurotransmitters, and enhanced brain blood flow.

Ginseng appears to help everything balance out in the cranium, allowing the brain to receive the nutrients needed for proper function, and clear the mind for thinking and performance.

How to Take Ginseng

Depending on your taste and preferred method, there are many ways to supplement with ginseng. Common forms of consumption include ginseng tea (made from ginseng root), ginseng powder (made from the herb and leaves), ginseng-containing drinks, ginseng seeds, and the most commonly used form, ginseng capsules and powder.

Whichever preparation you use, the effects seem to be similar. Recommended doses tend to fall anywhere from 200mg/day - 400mg/day as a general “preventative” dose, and all the way up to 3,000mg/day of Korean red ginseng to achieve max potency for certain disease states. However, many benefits for health and performance measures have been noted with doses of 400mg daily—especially cognitive benefits. This dose will typically yield about 2% - 3% total active ginsenosides.

Certain nootropic supplements are a great way to consume ginseng along with several other bioactive and beneficial ingredients. Specifically, the combination of caffeine and L-theanine may help provide a calm yet alert feeling to keep you focused and energized all day long.

Is Ginseng Safe?

At the recommended doses and even higher, ginseng appears to be well-tolerated by most and safe for nearly everyone. A review published on the safety of ginseng found a low incidence of adverse effects in over 57 randomized trials.30 Even doses as high as 2,000mg, 4,500mg and all the way up to 6,000mg for several weeks appear to yield few side effects.

When effects are present, they tend to include symptoms like nausea, vomiting, diarrhea, and stomach cramps. And, since ginseng can lower blood sugar levels, hypoglycemia has sometimes been observed.

Uncommon ginseng “overdoses” may lead to bleeding, excitation, fidgeting, headache, increased body temperature, dizziness, and insomnia. As stated before, even high amounts of ginseng are generally well-tolerated and overdosing would require what might be considered a “heroic” dose of ginseng.

Ginseng may have drug interactions of which you should be aware. Some stimulant drugs that speed up the nervous system (caffeine, epinephrine) may cause jitteriness if taken with ginseng. Blood thinners such as Warfarin, immunosuppressants, and Lasix might have decreased effectiveness if taken alongside ginseng. Furthermore, diabetes medications like insulin, if taken with ginseng, may lower blood sugar levels a dangerous amount.

Due to these various interactions, if you’re planning on supplementing with ginseng and are taking any medication, talk to your healthcare professional to ensure safe use and maximal benefit.

While ginseng has been advised against for pregnant women, studies have shown that ginseng is not associated with adverse effects in women who use it during pregnancy.31 However, there is some advice to refrain from use during the first trimester and during lactation. If you’re pregnant and wanting to use ginseng, consult a healthcare professional.

CAN STEM CELL THERAPY HELP WITH DEGENERATIVE DISC DISEASE IN MY BACK?

CAN STEM CELL THERAPY HELP WITH DEGENERATIVE DISC DISEASE IN MY BACK?

[original article]

 

Degenerative disc disease is a problem for a large portion of America. Sadly, one third of people aged 40-59 have some form of degenerative disc disease. This is a huge problem that needs to be addressed as the aging population in the United States continues to grow. Stem cell treatments have the potential to completely revolutionize how the medical community treats degenerative disc disease.

The condition

Degenerative disc disease occurs when the discs between the bones in your spine wear out. The spine will lose flexibility and the patient will likely begin to feel pain in their lower back. The issue is that anyone’s discs are going to be less effective over time. Spinal discs are more or less the shock absorbers between the vertebrae in the spine. Cars also have shock absorbers, just like the discs in your back. The discs in your spine, however, cannot be easily changed out like shock absorbers in a car. That is why so many patients have looked for other treatment options, such as stem cells.

An orthopedic surgeon has seen incredible results by using stem cells to treat patients with degenerative disc disease. About 85% of their patients saw an improvement in their condition after utilizing a stem cell treatment. There are several other research projects that have showcased stem cells are a potential treatment option for patients with degenerative disc disease.

Research

A research team at the University of Pennsylvania has been investigating creating bioengineered discs that would be made out of a patient’s own stem cells. The discs would be easily accepted into the body as the body is already familiar with the cells that are being implanted. They have already successfully tested the stem cell discs in both rats and goats. Goats have a very similar cervical spine to humans.

The bioengineered disc was able to integrate seamlessly into the surrounding tissue compared to the artificial discs that are typically used. The researchers hope to test the bioengineered discs on human patients as soon as possible.

There was another study released in 2015 that looked into how mesenchymal stem cells in bone marrow would affect patients with degenerative disc disease. 26 patients with degenerative disc disease were treated with bone marrow injections into the areas where the discs were worn out.

21 out of 26 patients showed a substantial improvement in both pain and impairment. The patients that had the most dramatic improvements unsurprisingly had the highest stem cell counts in the problematic areas. This is great news as patients who did not see a substantial improvement can potentially go back and receive more stem cells to see a real recovery.  

A deep analysis of several different studies where stem cells were used in treating back disc problems showed the state of the treatment. The overall results of the studies were not strong enough to identify that stem cells can be used as a real treatment for disc pain as of today.

There needs to be more conclusive studies of stem cell treatments on back discs for the treatment to be widely accepted in the medical community. Studies are currently underway all around the world to continue to evaluate the effectiveness of stem cell treatments on back discs.

Stem cells have the potential to completely change how the medical community treats problematic back discs. Researchers will continue to push the boundaries for stem cell treatments for degenerative disc disease. Patients could completely rid themselves of back pain and improve their quality of life.