Maslinic Acid
Maslinic acid (which goes by thechemical name tongue-twister of 2-alpha, 3-beta-dihydroxiolean-12-en-28-oicacid) is what is called a triterpenoid compound, present in fruit and leaves ofOlea europaea. Cholesterol is one example of a triterpene. Phytosterols andphytoecdysteroids are also triterpenes. Now I know that animal studies don'talways translate into human studies, but at the same time, this is often wherewe find new cool ingredients. In this study, scientists investigated theeffects of maslinic acid on growth, protein-turnover rates and nucleic acidconcentration in trout white muscle. Yep, that's trout. As in fish. But theresults are rather intriguing. Five groups of 180 trout of a mean body mass of20 grams were fed for 225 days with diets containing zero, 1, 5, 25 and 250mgof maslinic acid per kg of diet. At the end of the experiment, white-muscleweight (which is their fast-twitch muscle) and protein-accumulation rate oftrout fed with maslinic acid were higher than in the control group. The totalcontent of DNA, RNA and protein in trout fed with 25 and 250mg of maslinic acidper kg bodyweight was significantly higher than in the control. The protein:DNAratio was also slightly higher than control.
It gets even better! In the samegroups of trout, protein synthesis rates increased to more than 80 percent overthe control values, while no differences were found in protein-degradationrate. Thus, maslinic acid can act as a growth factor when added to a standardtrout diet. What if we added it to a human diet? Maslinic acid has other veryintriguing properties as well. For instance, treatment with maslinic acidresults in a significant inhibition of cell proliferation and causes apoptoticdeath in colon cancer cells. And to top it off, another study showed thatmaslinic acid might modulate glucose metabolism partially through reducinginsulin resistance. So to summarize, maslinic acid may help promote skeletalmuscle hypertrophy, improve glucose metabolism and for you health nuts, fightcancer cells in the colon. Not a bad trifecta!
Semicarbazide
In organic chemistry, semicarbazide is a derivative of urea, where NH2on one side has been replaced with H2NNH2 hydrazine,yielding H2NNHC(=O)NH2. (http://en.wikipedia.org/wiki/Semicarbazide) Research has shown that inhibitionof semicarbazide-sensitive amine oxidases (SSAO) and monoamine oxidases (MAO) reducesfat deposition inobese rodents: chronic administration of the SSAO-inhibitor semicarbazide (S)in combination with pargyline (MAO-inhibitor) has also been shown to reducebodyweight gain in obese rats. So what happens in non-obese, non-diabetic rats?Prolonged treatment of non-obese rats with a high dose of S (900 micromol perkg bodyweight per day) reduced bodyweight gain and limited white adipose tissueenlargement. When chronically administered at a threefold lower dose, S alsoinhibited SSAO activity, but not fat depot enlargement, suggesting that effectsother than SSAO inhibition were involved in adipose tissue growth retardation.
Octopamine
Did you know that in mammals andhumans, noradrenaline is a key modulator of aggression? And that octopamine, aclosely related biogenic amine, has been proposed to have a similar function inflies? Octopamine, of course, has also been proposed as a substitution productof synephrine vis-a-vis weight loss. Octopamine is able to activate in-vitro(that's test tube) fat breakdown or lipolysis in rat fat cells viabeta-3-adrenergic receptor activation, while it activates glucose uptake inhuman fat cells via its oxidation by amine oxidases. Octopamine treatment wasfound to produce a 19 percent decrease in bodyweight gain, when compared to the177 grams gained by controls (rat study). The decrease in bodyweight gain wasnot due to a pronounced and sustainable anorectic (appetite lowering) effect ofoctopamine; also, elevated plasma insulin of obese rats was lowered byoctopamine. It would be interesting to see if a caffeine-octopamine stack wouldwork better than the traditional caffeine:synephrine combo.
Glabridin
Stay tuned for a new category ofweight-loss supplements based on the presence of glabridin. Kaneka, a Japanese firm, has a patent onthis new ingredient. The data on this to say the least, is very interesting. Inone investigation, scientists applied licorice flavonoid oil (LFO) to high-fat diet-inducedobese mice and investigated its effect. LFO contains hydrophobic flavonoidsobtained from licorice. Wow, sounds complicated. Well, get this. The oil is amixture of medium-chain triglycerides, having glabridin, a major flavonoid of licorice. Obesemice were fed on a high-fat diet containing LFO at zero (control), 0.5 percent,1.0 percent, or 2.0 percent for eight weeks. Compared with mice in the controlgroup, those in the 1 percent and 2 percent LFO groups efficiently reduced theweight of abdominal white adipose tissues and bodyweight gain. Their fat cellsshrunk and they found that in the liver, genes for beta-oxidation (fat burning)went up and those for fatty acid synthesis went down. Now that's a good trend,my friend. These findings proved that LFO prevented and reduced diet-inducedobesity.
This flavonoid has other amazingeffects. For instance, glabridin, isolated from the roots of Glycyrrhizaglabra, was tested for its effect on cognitive function. Indeed, glabridinappears to help with memory improvement. So, a fat-loss potentiator andsomething to help you find your car keys. A good duo, indeed!
N-butyldeoxynojirimycin
High doses ofN-butyldeoxynojirimycin (NB-DNJ) in healthy, lean and leptin-deficient obese(ob/ob) mice can promote weight loss, according to recent studies. The effectof NB-DNJ treatment on subcutaneous adipose tissue (i.e., fat under the skin)and on epididymal fat pads was measured. Lean mice treated with NB-DNJ admixedwith their diet lost weight in the form of adipose tissue. This resulted in a40 percent reduction in skin thickness and a reduction in epididymal fat padweights after five weeks of treatment. Following the depletion of adiposetissue mass, the mice grew normally and did not have any reduction in leanmass. Cool. Lose fat and keep your muscle! Sounds like caffeine-ephedra! Obesemice treated with NB-DNJ also lost weight or gained weight at a greatly reducedrate compared with nontreated controls. The cause of this weight loss? Apparently,NB-DNJ causes weight loss as a result of reduced food consumption due tocentral appetite suppression. That is, your brain tells you that enough isenough and to stop eating those French fries.
Protein Still Rules!
I still hear the nonsense fromclinicians that all calories are the same and it only matters how many caloriesyou eat during the day. To that I say, "You're an idiot." Read the literature.Protein, carbs and fats are not treated the same by your body. Try overeating doughnutsand overeating on skinless chicken. If you were to overeat by 500 caloriesdaily, are you going to tell me that you'd gain the same amount and kind ofweight eating doughnuts as chicken? You are a moron. Anyhow, this investigationassessed changes in resting energy expenditure and substrate oxidation inoverweight and obese women in response to a weight-loss intervention thatcombined a high-protein, reduced-calorie diet with increased physical activity.Sounds like some fitness competitors post-competition who go high on the hogand then end up saying, "Soooey!" OK, that was mean.
In this study, 39 overweight andobese women (mean age 30.9 years) participated in a 10-week weight-loss programin which they ate a reduced-calorie diet for which protein provided 30 percentof total energy and approximated 1.4 g/kg. That's not that high, but it's ahelluva lot higher than the stinkin' RDA. Subjects incrementally increasedphysical activity (i.e., steps walking) throughout the diet interventionperiod. They discovered that the weight-loss intervention combining consumptionof a high-protein, reduced-calorie diet with increased physical activitypromotes weight loss without negatively impacting resting energy expenditure(REE) in thispopulation of women. That is an amazing finding. Part of the problem with anydiet is the drop in REE. Kick up the protein intake and lift weights is whatI'd suggest.
Creatine-Carnosine Connection
Given its versatile biologicproperties, such as anti-oxidative, anti-glycation and pH-buffering capacity,carnosine has been implicated as a protective factor in the aging process. Canyou say, beta-alanine?! In this study, scientists looked at the age-relatedchanges in skeletal muscles as well as the effect of lifelong creatinesupplementation on mice. At 25 (young mice), but not at 60 weeks (old mice),oral creatine supplementation significantly increased carnosine (+88 percent)and anserine (+40 percent) content compared to age-matched control-fed animals.Intriguing indeed. However, taurine and total creatine content was not affectedby creatine supplementation at any age. Creatine-treated mice showed lessmuscle fatigue (soleus muscle) and enhanced force recovery (m. extensordigitorum longus [EDL]) compared to controls at 25 weeks, but not at 60 weeks.So, it looks like creatine supplementation is able to transiently, but potentlyincrease muscle carnosine and anserine content, which coincides with improvedresistance to contractile fatigue. But as you get older, you may need more thanjust creatine.
Allicin
What are the effects of allicinsupplementation on exercise-induced muscle damage (EIMD) in well-trainedathletes? Subjects were randomly assigned to an allicin supplementation group(AS group) and a control group and received either allicin or placebo for 14 daysbefore and two days after a downhill treadmill run. The results suggested thatallicin might be a potential agent to reduce EIMD. If you're wondering whereyou'd likely get allicin...that's right, from garlic.
Jose Antonio, PhD, is vice president of the NationalStrength and Conditioning Association. He has a PhD in muscle physiology and ischief executive of the International Society of Sports Nutrition.
References:
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