I honestly didn't bat an eye. Woah, no pun intended there... Seriously, that just came out...
ehem...
Actors, especially successful actors, are living out the greatest biggest hugest mindfuck in all of mankind's history. And the only thing wrong with this past incident is that people, other people, non-famous-actor people think that actors are somehow NORMAL, that they live in the same mental-emotional-physical-spiritual space that everyday people do. And I can't blame them because for the average human it's not POSSIBLE to imagine what it's like to live in such a severely different world, their brains aren't capable of the complete rewiring it would take to honestly empathize with living in a glass bubble.
I honestly don't think I would be able to consider it either, except I've done a lot of weird drugs, and during those weird drug trips have reflected on this question many times, so I feel like I'm a little closer to understanding it, not to mention incredibly empathetic anyhow.
Christian lives in a world where he could walk to the nearest video store and pick up a movie with him in it. But he can't because he would get stormed by paparazi and commoners. He lives in a world where just down the street is a movie theater with a gigantic picture of him wallpapered across the bannister. He lives in a world where EVERYONE thinks they KNOW HIM. We know more about his social life, personal quirks, eating habits and inner struggles than we even know about OUR SPOUSES, BEST FRIENDS, OR SIBLINGS. And yet we don't know him, nor do we have EXPLICIT permission to know him/be in his space. He has no space. In one inhale he is royalty and entitled to anything he wants/ has absolutely no boundaries, and in a deep exhale he is a caged creature borne from the industry that feeds him, a spectacle to be prodded and poked. He's a spoiled brat who always gets his way, and yet he's not granted the simple privilege of walking down a street and breathing fresh air.
What does this have to do with him flipping his lid, getting irate? EVERYTHING. Granted I also believe that acting in general plays a huge role in the decay of self and a complete transformation into a narcissistic paradigm (imagine thinking everything you do people are focussed solely on you, and to actually have it BE TRUE). But then you also throw in the huge amount of money, the low consequence of living a destructive life and not dealing with your demons, and then this idol worship. Voilah, you got someone who probably already came into the field a pretty eccentric if not neurotic person and have just put them into a social experiment the likes of which rhesus monkeys with their eyelids sewn open don't even know how to comprehend.
And then we're shocked when they act out. It's like people at the zoo throwing bananas into the monkey cages and then acting disgusted when the monkey gets diareah and tries to dismember their four year old. We've created these people and then sit back in awe when they beat their cage doors.
Saturday, February 7, 2009
Friday, February 6, 2009
Trans-Resveratrol poorly bioavailable
There has been a huge amount of buzz about Trans-resveratrol, the compound in red wine that is said to extend life by activating the sirt-1 gene. But one thing's for sure - we haven't figured out yet how to make it very bioavailable. Study results released today showed a very low plasma concentration of Trans-resveratrol after giving it to people (in doses of 25, 50, 100 or 150 milligrams six times a day) and then testing their blood (3.89, 7.39, 23.1 and 63.8 respectively). I know that some manufacturers are using bioperine, a chemical extracted from black pepper that aids absorption of certain nutrients, but how much this is helping is not very well known.
There are some people experimenting with transdermal versions and it seems that would be a much better route to take. Trans-Resveratrol is the right molecular weight and possesses enough lipophilicity (absorbable into fat) to make it through the cutaneous layer and into the bloodstream. I look forward to seeing how this turns out.
1: Mol Nutr Food Res. 2009 Feb 4. [Epub ahead of print]
Pharmacokinetic and safety profile of trans-resveratrol in a rising multiple-dose study in healthy volunteers.
Almeida L, Vaz-da-Silva M, Falcão A, Soares E, Costa R, Loureiro AI, Fernandes-Lopes C, Rocha JF, Nunes T, Wright L, Soares-da-Silva P.
Department of Research and Development, BIAL - Portela & Co SA, S Mamede do Coronado, Portugal. Fax: +351-22-9866192.
This was a double-blind, randomised, placebo-controlled study to investigate the pharmacokinetics and safety of trans-resveratrol. In four groups of ten healthy adult subjects (five males and five females), two subjects were randomized to receive placebo and eight subjects to receive trans-resveratrol 25, 50, 100 or 150 mg, six times/day, for thirteen doses. Peak plasma concentrations of trans-resveratrol were reached at 0.8-1.5 h postdose. Following the 13th dose of trans-resveratrol 25, 50, 100 and 150 mg, mean peak plasma concentration (C(max)) was 3.89, 7.39, 23.1 and 63.8 ng/mL and mean area under the plasma concentration-time curve (AUC(0-tau)) was 3.1, 11.2, 33.0 and 78.9 ng.h/mL. Interindividual variability was high, with coefficients of variation >40%. Trans-resveratrol half-life was 1-3 h following single-doses and 2-5 h following repeated dosing. Trough (C(min)) concentrations were less, not double equals1 ng/mL following 25 and 50 mg, 3 ng/mL following 100 mg and <>
There are some people experimenting with transdermal versions and it seems that would be a much better route to take. Trans-Resveratrol is the right molecular weight and possesses enough lipophilicity (absorbable into fat) to make it through the cutaneous layer and into the bloodstream. I look forward to seeing how this turns out.
1: Mol Nutr Food Res. 2009 Feb 4. [Epub ahead of print]
Pharmacokinetic and safety profile of trans-resveratrol in a rising multiple-dose study in healthy volunteers.
Almeida L, Vaz-da-Silva M, Falcão A, Soares E, Costa R, Loureiro AI, Fernandes-Lopes C, Rocha JF, Nunes T, Wright L, Soares-da-Silva P.
Department of Research and Development, BIAL - Portela & Co SA, S Mamede do Coronado, Portugal. Fax: +351-22-9866192.
This was a double-blind, randomised, placebo-controlled study to investigate the pharmacokinetics and safety of trans-resveratrol. In four groups of ten healthy adult subjects (five males and five females), two subjects were randomized to receive placebo and eight subjects to receive trans-resveratrol 25, 50, 100 or 150 mg, six times/day, for thirteen doses. Peak plasma concentrations of trans-resveratrol were reached at 0.8-1.5 h postdose. Following the 13th dose of trans-resveratrol 25, 50, 100 and 150 mg, mean peak plasma concentration (C(max)) was 3.89, 7.39, 23.1 and 63.8 ng/mL and mean area under the plasma concentration-time curve (AUC(0-tau)) was 3.1, 11.2, 33.0 and 78.9 ng.h/mL. Interindividual variability was high, with coefficients of variation >40%. Trans-resveratrol half-life was 1-3 h following single-doses and 2-5 h following repeated dosing. Trough (C(min)) concentrations were less, not double equals1 ng/mL following 25 and 50 mg, 3 ng/mL following 100 mg and <>
Thursday, February 5, 2009
Arginine, Fat Loss, Muscle Gain
Arginine is probably one of my favorite amino acids. Arginine is responsible for that famous "Pump" feeling you get after you've been working out hard. Well, that and the water pressure in muscle cells if you've been consuming a lot of carbohydrates. A lot of people knock the "pump" because it's only cosmetic. I disagree. Well first of all it may only be cosmetic. BUT SO WHAT? If something makes you feel good or gives you a positive impression (looking into a mirror, even for a non-narcissist, and seeing a bulging muscle can be very very rewarding) then that will only further help you focus in on your intention, and that in turn feeds your connection with what you're doing. But if that's all that Arginine did for us I'd probably not mention it. It has a few nifty other effects too. It enhances sexual activity, erection response and even activates the part of the brain that is aroused by sexual thought. It also constitutes the major amino acid of sperm, so there is a good replenishment going on there.
For some people arginine is a great anti-depressant. Arginine's major metabolite is agmatine. Agmatine is an NMDA antagonist. What this means essentially is that it helps calm the excitatory parts of our brain. This can be good for mental peace as well as protecting our brains from excess stimulation and also helping to curb addiction. I can speak for it's mellowing effects. I've given some arginine to a few other people as well and they all seem to come back with a resounding relaxation response to it.
But what recently caught my eye was a study done, albeit with rats, which are by no means a great replacement for humans. In this study though they found that arginine protected rats from gaining excess weight. Rats do tend to be metabolic powerhouses though. They have shorter lives and faster metabolisms. They are an exagerated version if you will of the human metabolism. If it sounds too good to be true, then it was probably done on rats is what I seem to see over and over again.
But nonetheless what they found was interesting. They took two groups of rats and fed one group a High Fat Diet (HF) and the other group eate a Low Fat diet. They kept this diet going for 15 weeks. Then they introduced arginine into their diet at the amount of 1.51% L-Arginine or Alanine (for the control group). This was added to their drinking water. At the end of the study the arginine group lost 30% of their fat in their white pads (rats have pads of white fat, humans ARE pads of white fat). AND the soleus muscle was increased by 13%!
"Serum concentrations of insulin, adiponectin, growth hormone, corticosterone, triiodothyronine, and thyroxine did not differ between control and arginine-supplemented rats. However, arginine treatment resulted in lower serum concentrations of leptin, glucose, triglycerides, urea, glutamine, and branched-chain amino acids, higher serum concentrations of nitric-oxide metabolites, and improvement in glucose tolerance. "
Now, what shocked me was how nothing really changed here in the serum. But, leptin, glucose, AND triglycerides were all lower. As we know, leptin lowering is actually a good thing in the obese. It usually means there is a return to normal sensitivity to leptin. Usually people that are overweight have developed a tolerance, or insensitivity to leptin's signals.
So what's the take home message? Well, for one thing, don't stop taking arginine. And if you aren't taking it, there's no need to rush out and buy up the store, but if you're looking for something to add to your regimen to increase overall health, and possibly help you in the pursuit of leanness then pick up some arginine. You can take it on an empty stomach preferably, or you can be your own experimental rat and put it in your drinking water.
1: J Nutr. 2009 Feb;139(2):230-7. Epub 2008 Dec 23. Links
Dietary L-arginine supplementation reduces white fat gain and enhances skeletal muscle and brown fat masses in diet-induced obese rats.
Jobgen W, Meininger CJ, Jobgen SC, Li P, Lee MJ, Smith SB, Spencer TE, Fried SK, Wu G.
Department of Animal Science, Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Previous studies showed that dietary L-arginine supplementation decreased white fat mass in genetically obese rats. This study tested the effectiveness of L-arginine in diet-induced obesity. Male Sprague-Dawley rats were fed for 15 wk a high-fat (HF) (40% energy) or low-fat (LF) (10% energy) diet beginning at 4 wk of age, resulting in 18% higher body weight gains and 74% higher weights of major white fat pads (retroperitoneal, epididymal, subcutaneous, and mesenteric adipose tissues) in HF than in LF fed rats. Starting at 19 wk of age, rats in each dietary group were supplemented for 12 wk with 1.51% L-arginine-HCl or 2.55% L-alanine (isonitrogenous control) (n = 8 per treatment) in drinking water and arginine groups were individually pair-fed to alanine controls. Despite similar energy intake, absolute weights of white fat pads increased by 98% in control rats over a 12-wk period but only by 35% in arginine-supplemented rats. The arginine treatment reduced the relative weights of white fat pads by 30% and enhanced those of soleus muscle by 13%, extensor digitorum longus muscle by 11%, and brown fat by 34% compared with control rats. Serum concentrations of insulin, adiponectin, growth hormone, corticosterone, triiodothyronine, and thyroxine did not differ between control and arginine-supplemented rats. However, arginine treatment resulted in lower serum concentrations of leptin, glucose, triglycerides, urea, glutamine, and branched-chain amino acids, higher serum concentrations of nitric-oxide metabolites, and improvement in glucose tolerance. Thus, dietary arginine supplementation shifts nutrient partitioning to promote muscle over fat gain and may provide a useful treatment for improving the metabolic profile and reducing body white fat in diet-induced obese rats.
PMID: 19106310 [PubMed - in process
For some people arginine is a great anti-depressant. Arginine's major metabolite is agmatine. Agmatine is an NMDA antagonist. What this means essentially is that it helps calm the excitatory parts of our brain. This can be good for mental peace as well as protecting our brains from excess stimulation and also helping to curb addiction. I can speak for it's mellowing effects. I've given some arginine to a few other people as well and they all seem to come back with a resounding relaxation response to it.
But what recently caught my eye was a study done, albeit with rats, which are by no means a great replacement for humans. In this study though they found that arginine protected rats from gaining excess weight. Rats do tend to be metabolic powerhouses though. They have shorter lives and faster metabolisms. They are an exagerated version if you will of the human metabolism. If it sounds too good to be true, then it was probably done on rats is what I seem to see over and over again.
But nonetheless what they found was interesting. They took two groups of rats and fed one group a High Fat Diet (HF) and the other group eate a Low Fat diet. They kept this diet going for 15 weeks. Then they introduced arginine into their diet at the amount of 1.51% L-Arginine or Alanine (for the control group). This was added to their drinking water. At the end of the study the arginine group lost 30% of their fat in their white pads (rats have pads of white fat, humans ARE pads of white fat). AND the soleus muscle was increased by 13%!
"Serum concentrations of insulin, adiponectin, growth hormone, corticosterone, triiodothyronine, and thyroxine did not differ between control and arginine-supplemented rats. However, arginine treatment resulted in lower serum concentrations of leptin, glucose, triglycerides, urea, glutamine, and branched-chain amino acids, higher serum concentrations of nitric-oxide metabolites, and improvement in glucose tolerance. "
Now, what shocked me was how nothing really changed here in the serum. But, leptin, glucose, AND triglycerides were all lower. As we know, leptin lowering is actually a good thing in the obese. It usually means there is a return to normal sensitivity to leptin. Usually people that are overweight have developed a tolerance, or insensitivity to leptin's signals.
So what's the take home message? Well, for one thing, don't stop taking arginine. And if you aren't taking it, there's no need to rush out and buy up the store, but if you're looking for something to add to your regimen to increase overall health, and possibly help you in the pursuit of leanness then pick up some arginine. You can take it on an empty stomach preferably, or you can be your own experimental rat and put it in your drinking water.
1: J Nutr. 2009 Feb;139(2):230-7. Epub 2008 Dec 23. Links
Dietary L-arginine supplementation reduces white fat gain and enhances skeletal muscle and brown fat masses in diet-induced obese rats.
Jobgen W, Meininger CJ, Jobgen SC, Li P, Lee MJ, Smith SB, Spencer TE, Fried SK, Wu G.
Department of Animal Science, Faculty of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Previous studies showed that dietary L-arginine supplementation decreased white fat mass in genetically obese rats. This study tested the effectiveness of L-arginine in diet-induced obesity. Male Sprague-Dawley rats were fed for 15 wk a high-fat (HF) (40% energy) or low-fat (LF) (10% energy) diet beginning at 4 wk of age, resulting in 18% higher body weight gains and 74% higher weights of major white fat pads (retroperitoneal, epididymal, subcutaneous, and mesenteric adipose tissues) in HF than in LF fed rats. Starting at 19 wk of age, rats in each dietary group were supplemented for 12 wk with 1.51% L-arginine-HCl or 2.55% L-alanine (isonitrogenous control) (n = 8 per treatment) in drinking water and arginine groups were individually pair-fed to alanine controls. Despite similar energy intake, absolute weights of white fat pads increased by 98% in control rats over a 12-wk period but only by 35% in arginine-supplemented rats. The arginine treatment reduced the relative weights of white fat pads by 30% and enhanced those of soleus muscle by 13%, extensor digitorum longus muscle by 11%, and brown fat by 34% compared with control rats. Serum concentrations of insulin, adiponectin, growth hormone, corticosterone, triiodothyronine, and thyroxine did not differ between control and arginine-supplemented rats. However, arginine treatment resulted in lower serum concentrations of leptin, glucose, triglycerides, urea, glutamine, and branched-chain amino acids, higher serum concentrations of nitric-oxide metabolites, and improvement in glucose tolerance. Thus, dietary arginine supplementation shifts nutrient partitioning to promote muscle over fat gain and may provide a useful treatment for improving the metabolic profile and reducing body white fat in diet-induced obese rats.
PMID: 19106310 [PubMed - in process
Wednesday, February 4, 2009
Obey These 2 Rules for Fat Loss
Obey These 2 Rules for Fat Loss
Obey This 1 Rule for Fat Loss
obeying this one old rule.
ON AND ON AND ON!!!
THESE SITES ARE A SCAM!!!
Have you been seeing sites that start out with this?
YOU ARE BEING LIED TO...
God this makes me so angry. I am usually pretty laid back and I am ALL about people making a living on the internet. I don't even mind people who want to write a get lean fast ebook and charge for it, even if it's not life changing.
But these websites are all completely false, misleading and plain out creepy.
Just a couple of bullet points for everyone out there looking at these sites.
1) These sites are NOT made by women who found an honest way to lose weight. Most likely these AREN'T EVEN WOMEN AT ALL. In actuality ANYONE can set up one of these sites, throw up a few pictures of some woman, write a quick blurb about how they struggle to lose weight and then add....
2) FAKE PICTURES OF OPRAH AND DR OZ. Ok so the pictures are real. But never in a million years would Oprah or Dr Oz stand behind these scandalous liars.
3) Then they claim to have "Found" two different products that have changed their lives! The truth is though, they only copied and pasted marketing material and then linked to companies THAT PAY THEM MONEY every time someone like yourself visits their site or god forbid buys their products!!!
SO TO RECAP!
These diet blogs all over the place are a SCAM. Even the comments that are on the blog that seem to be written by people just like you and me - It's all a setup. They just add those comments themselves!!
If you want one simple rule to obey to lose weight? Eat less and exercise more!
If you want to try Acai Berry Then go to Vitacost.com and use this code to save five dollars off your first order.
HIZ683
Yes, you use this code and save five dollars off your first order. I in turn get bonus points to buy future purchases from them. I am honest about this, but I really recommend vitacost.com anyways. It's a very reasonable store.
You will get a far better deal from vitacost for Acai berry and Colon Cleanse products. A FAR BETTER DEAL. And you won't be making these scamming liars any more money than they've already made.
Please pass this blog along to anyone you know so that they won't fall into this trap!!
The one simple rule to obey? Don't buy into this SCAM!
Monday, February 2, 2009
Once Lean Always Lean (well not quite, but....)
Yet another study on tryptophan and eating behaviors. My comments follow.
1: Eat Behav. 2009 Jan;10(1):36-41. Epub 2008 Oct 30.
Acute tryptophan depletion and sweet food consumption by overweight adults.
Pagoto SL, Spring B, McChargue D, Hitsman B, Smith M, Appelhans B, Hedeker D.
Department of Medicine, Division of Preventive and Behavioral Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
Serotonergic involvement has been implicated in preferential consumption of treat foods. We tested the effect of acute tryptophan depletion (ATD) on food consumption by overweight and lean adults with and without a history of recurrent major depressive disorder (MDD). ATD and taste-matched placebo challenges were administered double-blind in counter-balanced order. Participants were classified as lean (n=36) or overweight (n=19) on the basis of body mass index (BMI). Total calorie, carbohydrate, protein, and sweet food consumption were assessed via a test meal 8-h following ATD. Four food items of comparable palatability were offered as a part of the test: two sweet (one carbohydrate-rich, and one protein-rich) and two non-sweet (one carbohydrate-rich, and one protein-rich). As compared to the placebo challenge, ATD significantly increased sweet calorie intake among overweight participants and increased their propensity to consume sweet food first before any other type of food. Lean participants' sweet calorie intake and food preference were unaffected by ATD. Findings suggest serotonergic involvement in the sweet food consumption by overweight individuals.
So what do we have here? To break it down for the non-scientists: Researchers found that overweight people have a sweet tooth! After they were depleted of tryptophan (which is the feel good chemical involved in serotonin formation) overweight people found the temptation to eat sweets overwhelming. They gorged on sweet things until, presumably, that tryptophan imbalance was corrected. And what about lean people? They didn't feel affected by the tryptophan depletion. They ate pretty much normally.
So the bottom line is if you are fat (I'm going to cut the formalities here, as I have some cake waiting for me, lol) then you are going to have to battle cravings which have a very strong biological basis. Your own body is working against you in a way. It WILL BE HARDER to fight against the current of indulgence early on in your pursuits to slim down.
But is that where our story ends? A song of defeat and an invitation to gorge and claim that you're helpless against the beast and that you are a victim? NOPE.
The take home message I get from it is this: Your battle early on will be hard won. But once you get your weight under control those beasts that once dictated your every thought, those little goblins that kept tempting you with sweets will be banished to their own little hell, leaving you FREE to feel complete and utter contentment with a balanced eating plan.
In other words, what was once thought an eternal struggle against cravings is now clear evidence that once you make it over the hill you will have a reset sense of serenity that will no longer need to be fed sugars to feel satiated. Tighten down your bootstraps knowing there is a craving-free pot of satisfaction at the end of your weightloss rainbow.
1: Eat Behav. 2009 Jan;10(1):36-41. Epub 2008 Oct 30.
Acute tryptophan depletion and sweet food consumption by overweight adults.
Pagoto SL, Spring B, McChargue D, Hitsman B, Smith M, Appelhans B, Hedeker D.
Department of Medicine, Division of Preventive and Behavioral Medicine, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
Serotonergic involvement has been implicated in preferential consumption of treat foods. We tested the effect of acute tryptophan depletion (ATD) on food consumption by overweight and lean adults with and without a history of recurrent major depressive disorder (MDD). ATD and taste-matched placebo challenges were administered double-blind in counter-balanced order. Participants were classified as lean (n=36) or overweight (n=19) on the basis of body mass index (BMI). Total calorie, carbohydrate, protein, and sweet food consumption were assessed via a test meal 8-h following ATD. Four food items of comparable palatability were offered as a part of the test: two sweet (one carbohydrate-rich, and one protein-rich) and two non-sweet (one carbohydrate-rich, and one protein-rich). As compared to the placebo challenge, ATD significantly increased sweet calorie intake among overweight participants and increased their propensity to consume sweet food first before any other type of food. Lean participants' sweet calorie intake and food preference were unaffected by ATD. Findings suggest serotonergic involvement in the sweet food consumption by overweight individuals.
So what do we have here? To break it down for the non-scientists: Researchers found that overweight people have a sweet tooth! After they were depleted of tryptophan (which is the feel good chemical involved in serotonin formation) overweight people found the temptation to eat sweets overwhelming. They gorged on sweet things until, presumably, that tryptophan imbalance was corrected. And what about lean people? They didn't feel affected by the tryptophan depletion. They ate pretty much normally.
So the bottom line is if you are fat (I'm going to cut the formalities here, as I have some cake waiting for me, lol) then you are going to have to battle cravings which have a very strong biological basis. Your own body is working against you in a way. It WILL BE HARDER to fight against the current of indulgence early on in your pursuits to slim down.
But is that where our story ends? A song of defeat and an invitation to gorge and claim that you're helpless against the beast and that you are a victim? NOPE.
The take home message I get from it is this: Your battle early on will be hard won. But once you get your weight under control those beasts that once dictated your every thought, those little goblins that kept tempting you with sweets will be banished to their own little hell, leaving you FREE to feel complete and utter contentment with a balanced eating plan.
In other words, what was once thought an eternal struggle against cravings is now clear evidence that once you make it over the hill you will have a reset sense of serenity that will no longer need to be fed sugars to feel satiated. Tighten down your bootstraps knowing there is a craving-free pot of satisfaction at the end of your weightloss rainbow.
Thursday, January 22, 2009
Sleep Apnea and Insulin Sensitivity
This is some pretty old research but it's really unique and I thought I'd share it for any of our readers with sleep apnea.
Continuous Positive Airway Pressure Treatment Rapidly Improves Insulin Sensitivity in Patients with Obstructive Sleep Apnea Syndrome
Department of Medicine I; Department of Medical Informatics, Biometrics, and Epidemiology, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen; Department of Medicine 3, Klinikum Nürnberg, Nuremberg, Germany The obstructive sleep apnea syndrome is typically associated with conditions known to increase insulin resistance as hypertension, obesity, and diabetes. We investigated whether obstructive sleep apnea itself is an independent risk factor for increased insulin resistance and whether continuous positive airway pressure (CPAP) treatment improves insulin sensitivity. Forty patients (apnea–hypopnea index > 20) were treated with CPAP. Before, 2 days after, and after 3 months of effective CPAP treatment, hyperinsulinemic euglycemic clamp studies were performed. Insulin sensitivity significantly increased after 2 days (5.75 ± 4.20 baseline versus 6.79 ± 4.91 µmol/kg · min; p = 0.003) and remained stable after 3 months of treatment. The improvement in insulin sensitivity after 2 days was much greater in patients with a body mass index less than 30 kg/m2 than in more obese patients. The improved insulin sensitivity after 2 nights of treatment may reflect a decreasing sympathetic activity, indicating that sleep apnea is an independent risk factor for increased insulin resistance. The effect of CPAP on insulin sensitivity is smaller in obese patients than in nonobese patients, suggesting that in obese individuals insulin sensitivity is mainly determined by obesity and, to a smaller extent, by sleep apnea.
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Wednesday, January 21, 2009
Tryptophan ingestion and Circadian Rhythm
Speaking of Circadian Rhythm,
Take your tryptophan at 7pm.
1: Basic Clin Pharmacol Toxicol. 2009 Jan;104(1):52-59.
Circadian Levels of Serotonin in Plasma and Brain after Oral Administration of Tryptophan in Rats.
Mateos SS, Sánchez CL, Paredes SD, Barriga C, Rodríguez AB.
Department of Physiology, Neuroimmunophysiology Research Group, Faculty of Science, University of Extremadura, Badajoz, Spain.
: Serotonin, one of the most important neurotransmitters in the central nervous system, is synthesized by the amino acid, tryptophan. Given that this essential amino acid is consumed in the diet, the aim of this study was to evaluate the effect of orally administered L-tryptophan (125 mg/kg) on circadian variations in the levels of serotonin in brain and plasma. We used male Wistar rats of 14 +/- 2 weeks of age (n = 240), maintained under conditions of a 12-hr light:dark cycle, and food and water ad libitum. Tryptophan administration was by gavage in a daily single dose at 7 p.m. for 7 days. The serotonin levels were measured by ELISA every hour at night (8 p.m. to 8 a.m.) and every 4 hr during daytime (8 a.m. to 8 p.m.). The results show that in both the tryptophan-treated and untreated groups the highest values appeared during the beginning of the darkness with a peak at 9, 10 and 11 p.m. in controls, and at 9 p.m. in the tryptophan-treated group. After tryptophan administration, the levels of serotonin were significantly higher in the plasma and all the brain regions analysed than in the control group. This increase of serotonin levels was greater in the pineal gland than in other brain regions, and the least in plasma. In conclusion, oral administration of tryptophan during 7 days enhances serotonin levels over a 24-hr period, and produces an advance in the peak of serotonin in both plasma and different brain regions.
PMID: 19152552 [PubMed - as supplied by publisher]
Take your tryptophan at 7pm.
1: Basic Clin Pharmacol Toxicol. 2009 Jan;104(1):52-59.
Circadian Levels of Serotonin in Plasma and Brain after Oral Administration of Tryptophan in Rats.
Mateos SS, Sánchez CL, Paredes SD, Barriga C, Rodríguez AB.
Department of Physiology, Neuroimmunophysiology Research Group, Faculty of Science, University of Extremadura, Badajoz, Spain.
: Serotonin, one of the most important neurotransmitters in the central nervous system, is synthesized by the amino acid, tryptophan. Given that this essential amino acid is consumed in the diet, the aim of this study was to evaluate the effect of orally administered L-tryptophan (125 mg/kg) on circadian variations in the levels of serotonin in brain and plasma. We used male Wistar rats of 14 +/- 2 weeks of age (n = 240), maintained under conditions of a 12-hr light:dark cycle, and food and water ad libitum. Tryptophan administration was by gavage in a daily single dose at 7 p.m. for 7 days. The serotonin levels were measured by ELISA every hour at night (8 p.m. to 8 a.m.) and every 4 hr during daytime (8 a.m. to 8 p.m.). The results show that in both the tryptophan-treated and untreated groups the highest values appeared during the beginning of the darkness with a peak at 9, 10 and 11 p.m. in controls, and at 9 p.m. in the tryptophan-treated group. After tryptophan administration, the levels of serotonin were significantly higher in the plasma and all the brain regions analysed than in the control group. This increase of serotonin levels was greater in the pineal gland than in other brain regions, and the least in plasma. In conclusion, oral administration of tryptophan during 7 days enhances serotonin levels over a 24-hr period, and produces an advance in the peak of serotonin in both plasma and different brain regions.
PMID: 19152552 [PubMed - as supplied by publisher]
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