These protective effects are similar to those seen with trimethylglycine, since they both cause an increase in liver concentrations of phosphatidylcholine (PC, causing an increase in vLDL production and efflux of triglycerides from the liver). Both TMG and creatine are thought to work indirectly by preserving SAMe concentrations, since PC synthesis requires SAMe as well (via PEMT) and genes involved in fatty acid metabolism in the liver that were not affected by the diet (VLCAD and CD36) were unaffected by creatine.
According to research from the University of Stirling, for optimal protein growth, weight lifters need to eat 0.25 to 0.30 grams of protein per kilogram body weight per meal. For a 175-pound person, that works out to 20 to 24 grams of protein at every meal. You’ll get that in three to four eggs, a cup of Greek yogurt, or one scoop of protein powder.
The majority of studies have used nothing but a loading period and the duration, overall, was about a week. This is partially because one study that noted benefit with a loading period failed to note benefit with prolonged supplementation. Lowballing supplementation at 2g a day in high active swimmers does not appear to be sufficient to alter any function in skeletal muscle.
Before getting into the nitty-gritty details about supplements, it’s important to have a good understanding of how muscle growth works. When you take a muscle growth supplement, the role it plays in helping you reach your goals should be very clear. With the supplements available on the market, you can be sure that while some serve an important purpose, others are gimmicks. It’s easier to identify the money wasters if you know how muscle building works.
Due to a combination of its neuroprotective effects and dopaminergic modulatory effects, creatine has been hypothesized in at least one review article to be of benefit to drug rehabilitation. This study used parallels between drug abuse (usually methamphetamines) and traumatic brain injury and made note of creatine being able to reduce symptoms of brain trauma, such as headaches, fatigue, and dizziness in clinical settings in two pilot studies. No studies currently exist that examine creatine supplementation and drug rehabilitation.
Minor liver lesions (grade I, no grade II or III, pathology not indicative of toxicity) have been studied in SOD1 G93A transgenic mice (a research model for amyotrophic lateral sclerosis or ALS, but used in this study to assess a state of chronic pro-oxidative stress) for 159 days with 2% of feed intake and in CD-1 rats (seen as normal) over 56 days with 0.025-0.5mg/kg in CD-1 mice, although in Sprague-Dawley rats (normal controls) there were no significant differences noted even after 2% of feed intake for 365 days. These observations appear to be due to the strain of the rodents used, and human studies on amyotrophic lateral sclerosis (ALS; what the SOD1 G93A transgenic mice are thought to represent) lasting from nine to sixteen months with subjects supplementing with up to 10g of creatine daily have failed to find any abnormalities in serum biomarkers of liver or kidney health.
Homocysteine is produced after S-adenosyl methionine is used up (as donating a methyl group creates S-adenosylhomocysteine, which then produces homocysteine) mostly from phosphatidylcholine synthesis and its reduction (via either methylation from trimethylglycine via betaine:homocysteine methyltransferase, urinary excretion, or convertion into L-cysteine via cystathionine beta-synthase) is thought to be therapeutic for cardiovascular diseases.
Gain mass: One of the most popular reasons for people to take body building supplements is to gain weight and that is why protein powder is much sought after. Protein is the building block of muscles and therefore, bodybuilders use protein powder to help repair muscles, speed recoveries and preserve muscle mass. They usually consume 1 to 2 grams of protein per pound of body weight every day.
Most causes of brain injury (calcium influx, excitotoxicity, lipid peroxidation, reactive oxygen intermediates or ROIs) all tend to ultimately work secondary to damaging the mitochondrial membrane and reducing its potential, which ultimately causes cellular apoptosis. Traumatic brain injuries are thought to work vicariously through ROIs by depleting ATP concentrations. Creatine appears to preserve mitochondrial membrane permeability in response to traumatic brain injury (1% of the rat’s diet for four weeks), which is a mechanism commonly attributed to its ATP-buffering ability.
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter. In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency. More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources is the major source of neural creatine. However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded. These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.