Health Benefits of Glycine

Laura

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As I approach the end of my antibiotic protocol, I've been poking around and looking at other things that might undo the damage done by years of being colonized by critters. One of these is glycine. So, for everyone's consideration, here is a run-down. _http://valtsus.blogspot.fr/2013/12/glycine.html

Some highlights:

A French-Spanish research group, in their review article (2009), wrote that humans can usually synthesize 3 grams of glycine, and they usually get 1.5-3.0 additional grams from the diet, so the total yield is 4.5-6 grams.

On the other hand, they stated that this amount doesn't satisfy the daily need of 10-13 grams for collagen synthesis in various tissues (bone, muscle, skin), and therefore glycine should be considered a semi-essential amino acid.[1]

"This result supports earlier suggestions in the literature that glycine is a semi-essential amino acid and that it should be taken as a nutritional supplement to guarantee a healthy metabolism"[1]

In the animal studies I could find, the results were surprisingly good. Glycine

protects rats from diabetes-induced harmful effects on kidneys[2], eyes[3], blood sugar, immune function and total mortality[4]

slows tumor growth in rats[5,6] and mice[7,26]

dramatically decreases the negative effects of sucrose[8,9,73] and ethanol[20,96] in rats

prolongs the lifespan of rats, possibly by mimicking the effect of methionine restriction[10]

protects rats from the harmful effects of excess methionine[45,67,68,79,113]

protects dogs[11], rats[12-14,69] and rabbits[70] from ischemia (lack of oxygen in the tissue)

protects rats[15,16,81] and mice[17] from endotoxin-induced damage

protects rats from lethal sepsis[54]

protects rats from liver injury caused by methionine or choline restriction[18], alcohol[19,20], chemotherapy[21], bile duct ligation[22], hemorrhagic shock[23], sepsis[54], Cyclosporin A[71] or corn oil[114]

protects rats (and increases survival) from hemorrhagic shock[24]

protects rats from acid reflux esophagitis[25]

protects mice from cancer cachexia (cancer wasting syndrome)[26]

protects rats from high blood pressure and vascular dysfunction caused by a low-protein diet (9% casein) during pregnancy[58,59]

protects rats from hypercholesterolemia induced by casein and cholesterol[77]

protects rabbits from hypercholesterolemia and atherosclerosis induced by casein[77]

protects chickens from body fat gain caused by a low-protein diet (supplemented w/glutamic acid)[65]

protects rats from lead toxicity[80]

protects rats from dental caries[92]

protects rats from experimental colitis, and gastric ulcers/lesions[101-105]

protects rats from experimental arthritis[64]

protects rats from Achilles tendon inflammation[111,112]

reduces platelet aggregation in rats[27]

reduces the birth defects caused by Tretinoin[28], cadmium[94] or hyperglycemia[95]

reduces the production of pro-inflammatory cytokines (TNF-α, IL-6) and increases adiponectin in mice[56,57]

Notice above that they admit that casein can INDUCE atherosclerosis

According to human study data, glycine

appears to mildly improve varioous health markers (HbA1c, IFN-gamma, TBARS, blood pressure etc.) in patients with metabolic syndrome or diabetes.[29,30] Diabetic patients have 26% lower serum glycine levels than "normal" population.[61]

dramatically increases (with cysteine) the insufficient glutathione synthesis, improves mitochondrial fat and carbohydrate oxidation and reduces excessive lipid peroxidation in diabetic patients[31], elderly humans[62] and older patients with HIV[72,115]. In elderly humans and HIV patients, the same combination also significantly improves insulin sensitivity and reduces fasting NEFA and F2-isoprostanes (not measured in diabetic patients).[63]

powerfully protects from neurological damage caused by stroke, with a mere 1 or 2 grams of glycine a day taken sublingually for five days after the stroke decreasing the risk of moderate to severe disability by 66%, cerebrospinal fluid lipid peroxides by 50% and mortality by 40% compared to placebo.[32]

improves sleep quality in some subjects[33,34]

improves schizophrenia symptoms in large doses (usually 0.8g/kg/d)[46-52], though it doesn't seem to augment the effect of clozapine[53]

improves the absorption of aspirin, and dramatically decreases the gastrointestinal side effects[108,109]


One large study, which hasn't been published in a scientific journal but has been reported on a news site, showed that glycine relieves arthrosis, osteoporosis and related diseases very effectively:

The work of De Paz Lugo was developed at the Cellular Metabolism Institute (CMI) in Tenerife, where researchers studied the effect of the glycine supplement on the diet of a group of 600 volunteers affected by different diseases related to the mechanical structure of the organism such as arthrosis, physical injuries or osteoporosis. The patients analysed were aged 4-85, and the average age was 45.

In all cases, there was a notable improvement in the symptomology. "Thefore -- according to De Paz Lugo -- we concluded that many degenerative diseases such as arthrosis can be treated as deficiency diseases due to the lack of glycine, since supplementing a diet with this amino acid leads to a notable improvement in symptomology without the need to take pain-killers."

In his book, Broda Barnes wrote that high-protein diets decrease thyroid function. Biologist Ray Peat's take on the subject is that insufficient protein intake is one of the main causes of low thyroid function, but muscle meats have a large amount of antimetabolic amino acids. Therefore he suggests that a large part of daily protein intake could be in the form of gelatin.

A popular health author Denise Minger has argued that the "harmfulness" of animal protein (or methionine) could actually be caused by the insufficient glycine intake on high-methionine diets that include muscle meat, milk and eggs. As shown above, some studies have demonstrated that glycine can decrease the possible harms of casein and methionine. Some animal proteins (scallop, cod) seem to have important health-promoting effects due to their high glycine and taurine content.[83-85,93]

"In conclusion, intake of scallop muscle as the sole dietary protein source completely prevented high-fat, high-sucrose-induced body mass gain and fat accretion without affecting lean body mass. Furthermore, scallop feeding improved plasma lipid profile in C57BL/6J mice compared to mice fed diets with protein from chicken, cod or crab. Correlation analyses revealed strong, highly significant inverse correlations between intake of taurine and glycine and body fat mass, as well as strong, highly significant correlations between glycine and especially taurine intake and improved plasma lipid profiles."
[83]

Well, I love scallops!

Anyway, read the whole article and do some research on your own. Seems to me that some of us need more glycine. It's very sweet, so I'm putting it in my tea several times a day.

Also, note that cysteine was mentioned above to be taken in combination. That's NAC - N-Acetyl cysteine,
 

Laura

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Another post about it here: _http://www.diethealthclub.com/dietary-supplements/glycine.html

Highlights:

In a study on the use of glycine for anxiety, injections containing glycine were administered to the gray matter of the brain in animal subjects. The results showed reduced anxiety levels. In another study, adults who received glycine doses daily showed an improvement in symptoms of obsessive compulsive disorder, an anxiety-related disorder.

Some studies have shown that amino acids like glycine may help to reduce the occurrence of asthma attacks.

Imbalances of glycine and another amino acid neurotransmitter, glutamate, may be a trigger for autism, according to some researchers.

Glycine supplements may help to increase attention and improve focus in children and adults who suffer from ADHD and other hyperactivity problems. Glycine enhances memory and mood and hence may be an effective treatment for such behavioral issues.

Glycine was found to restrict the growth of tumors in rats by blocking the formation of new blood vessels that may feed the tumors.

Due to its neuro-inhibitory effect, glycine calms the brain and is thus helpful in treating depression and anxiety. Glycine also helps in supplying glucose to the body and thus helps to alleviate fatigue and listlessness that often accompanies depressive disorders.

Glycine may help in reducing swelling of the prostate gland. Studies on glycine for prostatitis have shown that when taken in combination with alanine and glutamic acid, glycine helps in treating swollen prostate tissue.

Some health experts recommend glycine for psychosis. High doses of the amino acid help to alleviate psychosis and other symptoms of schizophrenia. Recent studies have shown that symptoms such as disinterest and avoidance of activities in people, reduced when the levels of glycine increased in the body.

Intake of glycine supplements helps to bring about considerable improvement in back pain. One of the reasons of back pain could be inadequate intake of glycine through the diet. Glycine also serves as an inhibitory neurotransmitter and thus induces a feeling of calmness. Glycine also promotes collage growth and release of the growth hormone, both of which aid in wound healing.

Amino acid supplementation is known to help in bodybuilding since it aids in muscle growth. The best time to take amino acids is soon after training when the muscles receive nutrients easily. Blood flow to the muscles also improves.

Adequate doses of glycine help to regulate the levels of blood sugar in the body thus ensuring healthy metabolism.

Side Effects Of Glycine

Like any other supplement, glycine too may trigger certain side effects. Some of the side effects which are often reported after intake of glycine supplements include nausea, vomiting, slight drowsiness and mild digestive problems. Some of the less common side effects which are, however, more serious include aggravation of schizophrenia symptoms especially if glycine is taken along with certain other schizophrenia medications and symptoms of an allergy such as wheezing, skin rash, itching, swelling of the mouth, swallowing difficulties and problems in breathing.
 

Laura

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Here's still another:

http://openheart.bmj.com/content/1/1/e000103.full

The cardiometabolic benefits of glycine: Is glycine an ‘antidote’ to dietary fructose?
Mark F McCarty1 and James J DiNicolantonio2

Glycine is a biosynthetic precursor for creatine, haeme, nucleic acids and the key intracellular antioxidant glutathione. Measures which raise or conserve intracellular glutathione levels may be of benefit from the standpoint of oxidant-mediated mechanisms that impair vascular health. A recent clinical study reports that concurrent supplementation of elderly participants with glycine and cysteine (100 mg/kg/day of each, cysteine administered as its N-acetyl derivative) reverses the marked age-related reduction in erythrocyte glutathione levels while lowering the serum markers of oxidative stress28; the authors, however, did not prove that the supplemental glycine was crucial for this effect.

With respect to diabetes, it is of interest that high intakes of glycine have the potential to oppose the formation of Amadori products, precursors to the advanced glycation endproducts (AGEs) that mediate diabetic complications.29 ,30 Indeed, supplementation of human diabetics with glycine—5 g, 3-4 times daily—is reported to decrease haemoglobin glycation.31 ,32 A similar effect has been reported in streptozotocin-treated diabetic rats.33 These studies did not measure AGEs per se, so their findings should be interpreted cautiously. Nonetheless, glycine supplementation has delayed the progression of cataract, inhibited microaneurysm formation, normalised the proliferative response of blood mononuclear cells and aided the humoral immune response in diabetic rats, effects which suggest that glycine may have potential for prevention of some diabetic complications.34–36 In a recent controlled but unblinded study, patients with diabetes experiencing auditory neuropathy achieved improvements in hearing acuity and auditory nerve conduction while ingesting 20 g glycine daily for 6 months.37

TWENTY GRAMS A DAY FOR SIX MONTHS!!! Yikes!

Of particular interest are studies showing that high glycine intakes can counteract many of the adverse effects of a high-sucrose diet on the liver, adipose mass and vascular function in rats.38 ,39 Glycine decreased the elevated non-esterified fatty acid content of the liver of sucrose-fed rats, increased the state IV oxidation rate of hepatic mitochondria, corrected an elevation of blood pressure, normalised the serum triglycerides and insulin, prevented an increase in abdominal fat mass and, in the vasculature, boosted glutathione, decreased oxidative stress and normalised endothelium-dependent vasodilation. Of likely relevance to these findings is a recent clinical report that supplemental glycine (15 g daily in three divided doses) administered to patients with metabolic syndrome lessened indices of oxidative stress in erythrocytes and leucocytes, while lowering systolic blood pressure.40 These findings are of considerable interest, particularly in the light of evidence that high dietary fructose intakes can promote metabolic syndrome and non-alcoholic fatty liver disease in humans and increase LDL cholesterol.

FIFTEEN GRAMS A DAY. That's like a level teaspoon three times a day. Not bad, and it's sweet, so just have three cups of tea a day sweetened with glycine!

Oral administration of glycine in humans (75 mg glycine/kg lean mass) has also been reported to stimulate an increase in glucagon secretion by pancreatic α-cells.55 This response is negated if glucose is ingested simultaneously,

So it doesn't help if you keep eating sugar/glucose.

Intriguingly, peptide drugs with dual agonism for GLP-1 and glucagon receptors have been developed recently, and these agents have shown markedly beneficial effects in mice with diet-induced obesity.75–77 They can induce a weight loss of 15–20%, modestly decrease calorie intake while boosting thermogenesis, decrease hepatic triglyceride levels and serum levels of triglycerides and LDL cholesterol, improve insulin sensitivity and glucose tolerance and counteract leptin resistance. These beneficial metabolic effects are only partially attributable to the associated weight loss and are considerably greater than the benefits seen with GLP-1 agonists alone. These agents provide continual stimulation of their target receptors, and hence understandably achieve more potent effects than dietary glycine, which at best could only boost GLP-1 and glucagon levels episodically. Nonetheless, while glycine does not induce weight loss or suppress calorie intake in sucrose-fed mice, it reduces visceral fat stores by over 50%, increases the thermogenic potential of hepatic mitochondria by increasing state 4 respiration, alleviates hepatic steatosis and improves insulin sensitivity and serum lipids. Hence, its effects are homologous to, if not as dramatic, as those seen with the coagonist drugs.

If supplemental glycine does indeed boost secretion of GLP-1, this may have interesting implications for the prevention and treatment of diabetes, and for the preservation of vascular health.

ETC.
 

Oxajil

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Thank you for sharing, very interesting! Found this doing a search on glycine:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC98707/#B35

Dietary glycine prevents peptidoglycan polysaccharide-induced reactive arthritis in the rat: role for glycine-gated chloride channel.

Peptidoglycan polysaccharide (PG-PS) is a primary structural component of bacterial cell walls and causes rheumatoid-like arthritis in rats. Recently, glycine has been shown to be a potential immunomodulator; therefore, the purpose of this study was to determine if glycine would be protective in a PG-PS model of arthritis in vivo. In rats injected with PG-PS intra-articularly, ankle swelling increased 21% in 24 to 48 h and recovered in about 2 weeks. Three days prior to reactivation with PG-PS given intravenously (i.v.), rats were divided into two groups and fed a glycine-containing or nitrogen-balanced control diet. After i.v. PG-PS treatment joint swelling increased 2.1 +/- 0.3 mm in controls but only 1.0 +/- 0.2 mm in rats fed glycine. Infiltration of inflammatory cells, edema, and synovial hyperplasia in the joint were significantly attenuated by dietary glycine. Tumor necrosis factor alpha (TNF-alpha) mRNA was detected in ankle homogenates from rats fed the control diet but not in ankles from rats fed glycine. Moreover, intracellular calcium was increased significantly in splenic macrophages treated with PG-PS; however, glycine blunted the increase about 50%. The inhibitory effect of glycine was reversed by low concentrations of strychnine or chloride-free buffer, and it increased radiolabeled chloride influx nearly fourfold, an effect also inhibited by strychnine. In isolated splenic macrophages, glycine blunted translocation of the p65 subunit of NF-kappaB into the nucleus, superoxide generation, and TNF-alpha production caused by PG-PS. Further, mRNA for the beta subunit of the glycine receptor was detected in splenic macrophages. This work supports the hypothesis that glycine prevents reactive arthritis by blunting cytokine release from macrophages by increasing chloride influx via a glycine-gated chloride channel. [...]

Glycine, a dietary nutrient, is anti-inflammatory and has protective effects in experimental arthritis by reducing TNF-α production (Fig. ​(Fig.3).3). Since dietary glycine is easily administered, inexpensive, and nontoxic, it could supplement current therapies for arthritis.

And:

http://www.ncbi.nlm.nih.gov/pubmed/11212343/

Glycine: a new anti-inflammatory immunonutrient.

The mechanism of the immunosuppressive effects of glycine and its pathophysiological applications are discussed in this review. Glycine has been well characterized in spinal cord as an inhibitory neurotransmitter which activates a glycine-gated chloride channel (GlyR) expressed in postsynaptic membranes. Activation of the channel allows the influx of chloride, preventing depolarization of the plasma membrane and the potentiation of excitatory signals along the axon. Glycine has recently been shown to have similar inhibitory effects on several white blood cells, including hepatic and alveolar macrophages, neutrophils, and lymphocytes. Pharmacological analysis using a GlyR antagonist strychnine, chloride-free buffer, and radiolabeled chloride has provided convincing evidence to support the hypothesis that many white blood cells contain a glycine-gated chloride channel with properties similar to the spinal cord GlyR. Molecular analysis using reverse transcription-polymerase chain reaction and Western blotting has identified the mRNA and protein for the beta subunit of the GlyR in total RNA and purified membrane protein from rat Kupffer cells. Dietary glycine is protective in rat models against endotoxemia, liver ischemia-reperfusion, and liver transplantation, most likely by inactivating the Kupffer cell via this newly identified glycine-gated chloride channel. Glycine also prevents the growth of B 16 melanomas cell in vivo. Moreover, dietary glycine is protective in the kidney against cyclosporin A toxicity and ischemia-reperfusion injury. Glycine may be useful clinically for the treatment of sepsis, adult respiratory distress syndrome, arthritis, and other diseases with an inflammatory component.

Gelatin (from bone broth for example) is also rich in glycine:

_http://butternutrition.com/bone-broth-a-gelatin-rich-elixir/

So why gelatin? Gelatin has a unique and very non-inflammatory amino acid profile, primarily consisting of glycine, glutamic acid, proline & alanine. These particular amino acids are lacking in the Standard American Diet, due to the heavy consumption of muscle meats and exclusion of the other 50% of the animal. Over time, this greater consumption can produce more inflammation when not balanced by non-inflammatory proteins like gelatin. Although gelatin is primarily made up of non-essential amino acids (meaning your body CAN make them), many over-stressed livers are not able to manufacture all the non-essential amino acids in the amounts demanded by the body. The liver needs an abundance of these proteins to keep the liver functioning optimally. Gelatin helps fuel the liver to help your body “take out the trash” in our toxic world!

Laura said:
FIFTEEN GRAMS A DAY. That's like a level teaspoon three times a day. Not bad, and it's sweet, so just have three cups of tea a day sweetened with glycine!

Good idea, I'm going to try it out!
 

Gaby

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Oxajil said:
Laura said:
FIFTEEN GRAMS A DAY. That's like a level teaspoon three times a day. Not bad, and it's sweet, so just have three cups of tea a day sweetened with glycine!

Good idea, I'm going to try it out!

Sounds doable and very effective! :)
 

Alana

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My husband and I have been taking glycine with our colostrum every night for about a month now, but nowhere near that dosage! I take half a teaspoon only and I've already seen in action how much it helps me to sleep. So I recommend it highly to anyone with sleep problems, even if it is that it takes you a lot of time to fall asleep. I will try the higher doses now that I know of the benefits!
 

Adobe

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Ive been taking 500 mg or Glycine before bed for a few months now. I had read that it helps stop "mind chatter" thus allowing you to sleep better. It does seem to have helped sleeping, but I cant be sure its not a placebo effect. After reading this thread it seems that maybe I should up the dosage. Thanks for the research.
 

riclapaz

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Thanks by this research, glycine supplements, had been taking for some time, but not the amount recommended by the articles, I will experiment with the recommended dose and see what happens. :flowers:
 

Lilou

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Besides gelatin being a good source of glycine (#1 actually) pork skins come in as the 2nd highest source - 11.917 grams of glycine per 100 grams! Good for all of you making flour out of pork skins!

I was reading about glycine precautions


So unless someone is supplementing glycine for a specific purpose, I think looking into a balance of amino acids may be important. And very cool that it can be used as a natural sweetener!! :D
 

Siberia

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Very interesting, thank you Laura.

My family has started taking glycine two weeks ago too, so I already know some basic info about its benefits, but this thread gives more valuable details and precious sharing of experience with others about glycine. We are taking it in a form of 100 mg pills. Our doctor says it's great for nervous system and suitable for any age due to its safeness. And its effect comes only after a certain amount of glycine has accumulated in the body after taking it for a period of time. Thank you all for your input. :flowers:
 

monotonic

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Lilou said:
Besides gelatin being a good source of glycine (#1 actually) pork skins come in as the 2nd highest source - 11.917 grams of glycine per 100 grams! Good for all of you making flour out of pork skins!

And good reason to find more uses for pork rhinds!
 

Lilou

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Looking into a balance of amino acids for effective glycine function, so far I've only found this

Glycine has a role in glutaminergic neurotransmission as the NMDA receptors* (a subset of glutamate receptors) tend to be tetramers composed of two glycine-binding units (the GluN1 subunits) and glutamate-binding units (GluN2)[22][23][24][25] with the GluN1 subunit having eight splice variants.[26]On the GluN1 receptors both glycine (D-serine may be used as well) and glutamate are required to induce signalling, which causes these glutamate receptors to be known as 'glycine dependent' and glycine as a 'coagonist'.[27][28]

As for glycine accumulation, it seems to only be problematic if there is a deficiency in Mg.
http://www.ncbi.nlm.nih.gov/pubmed/18031345

I agree, it should be classed as a semi-essential amino acid (rather than non-essential) and should be supplemented to daily requirements or more, if treating a specific condition. As the wave approaches, we need all the neuroprotection we can get!!

*The N-methyl-D-aspartate receptor (also known as the NMDA receptor or NMDAR), is a glutamate receptor and ion channel protein found in nerve cells. It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane.[2] The NMDA receptor is very important for controlling synaptic plasticity and memory function.[3] https://en.wikipedia.org/wiki/NMDA_receptor
 

mugatea

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Thanks Laura,

I have just started taking this from your post about it on Facebook and then through a post on Sott. I took 3 grams last night. Didn't have a great sleep (which I bought it for) but boy did I dream all night! Very interesting reading. What can this stuff not help with?. I suffer from anxiety/ocd and suffer from trich (hair pulling) my bro is schizophrenic/alcoholic and my mind is intense and non stop, I also have trouble focusing and sleeping all night long so I'm very interested in this Glycin.

Jamie
 

RedFox

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I tried glycine a few years back, with initial positive results followed by a worsening of symptoms.
I had a bunch left over so have been trying it again, and this time the results are markedly different.

Glycine is can be turned into choline and serine (extremely important for nerve health, myelination and some neurotransmitters). Glycine can also be made from breaking down choline and serine, so hypothetically low glycine levels may decrease choline and serine levels, leading to nerve degeneration.

http://www.vitaminstuff.com/amino-acid-serine.html
Serine is a non-essential amino acid derived from the amino acid glycine. It is important to overall good health, both physical and mental. Serine is especially important to proper functioning of the brain and central nervous system.

Serine helps form the phospholipids needed to make every cell in your body. It is also involved in the function of RNA and DNA, fat and fatty acid metabolism, muscle formation, and the maintenance of a healthy immune system. The proteins used to form the brain, as well as the protective myelin sheaths that cover the nerves, contain serine. Without serine, the myelin sheaths could fray and become less efficient at delivering messages between the brain and nerve endings in the body, essentially short circuiting mental function.

Serine is also needed to produce tryptophan, an amino acid that is used to make serotonin, a mood-determining brain chemical. Both serotonin and tryptophan shortages have been linked to depression, insomnia, confusion, and anxiety. Research suggests that low levels of serine may contribute to chronic fatigue syndrome (CFS) and fibromyalgia (FM).

Serine helps produce immunoglobulins and antibodies for a strong immune system, and also aids in the absorption of creatine, a substance made from amino acids that helps build and maintain all the muscles in the body, including the heart.


In order for serine to be manufactured in the body, sufficient amounts of vitamin B3 and vitamin B6, and folic acid must be present

So to start with, those who don't do well with (or react badly to) glycine the following may be the missing link:

http://www.jbc.org/content/221/1/501.full.pdf
In the liver of the normal poult there was a considerable synthesis of serine and choline from the alpha-carbon of glycine (Table I). With a deficiency of folic acid there was a marked reduction in the synthesis of serine, and choline synthesis was slightly reduced. A deficiency of vitamin B12 caused no reduction in serine synthesis, but there was a slight reduction in the synthesis of liver choline. The livers of folic acid-deficient poults utilized less of alpha-carbon of glycine than did those of the normal or vitamin B12-deficient birds

The same is true in rats, so a deficiency in folic acid/B12 (B12 levels reduce with age) will slow the rate of choline and serine production from glycine. Add in a glycine deficiency (not having lots of broth every day?) and/or a MTHFR mutation and this system stops working or so it seems.

Some further interesting connection:

http://www.ncbi.nlm.nih.gov/pubmed/23615880
Glycine is a major amino acid in mammals and other animals. It is synthesized from serine, threonine, choline, and hydroxyproline via inter-organ metabolism involving primarily the liver and kidneys. Under normal feeding conditions, glycine is not adequately synthesized in birds or in other animals, particularly in a diseased state. Glycine degradation occurs through three pathways: the glycine cleavage system (GCS), serine hydroxymethyltransferase, and conversion to glyoxylate by peroxisomal D-amino acid oxidase. Among these pathways, GCS is the major enzyme to initiate glycine degradation to form ammonia and CO2 in animals. In addition, glycine is utilized for the biosynthesis of glutathione, heme {I'd be curiouse if glycine deficiency causes iron overload?}, creatine, nucleic acids, and uric acid. Furthermore, glycine is a significant component of bile acids secreted into the lumen of the small intestine that is necessary for the digestion of dietary fat and the absorption of long-chain fatty acids. {Problems with fat digestion?} Glycine plays an important role in metabolic regulation, anti-oxidative reactions, and neurological function. Thus, this nutrient has been used to: (1) prevent tissue injury; (2) enhance anti-oxidative capacity; (3) promote protein synthesis and wound healing; (4) improve immunity; and (5) treat metabolic disorders in obesity, diabetes, cardiovascular disease, ischemia-reperfusion injuries, cancers, and various inflammatory diseases. These multiple beneficial effects of glycine, coupled with its insufficient de novo synthesis, support the notion that it is a conditionally essential and also a functional amino acid for mammals (including pigs and humans).

http://180degreehealth.com/glycine-insulin-resistance/
Glycine and Insulin Resistance

For many of us, the downside of the holidays is the dread of adding a few pounds of abdominal fat that will take more than a New Year’s resolution to work off. Even worse, we all also know that it’s the extra abdominal fat that causes insulin resistance and eventually—or maybe already—type 2 diabetes.

But more recent research tells a more precise—and cheerful—story about what is really going on. It’s not the actual fat (adipose) tissue that causes the problem after all: It’s the immune cells—the macrophages, to be specific—that are embedded in the adipose tissue, that stir up the trouble.

So why do the macrophages get stirred up, and what do they do that’s so damaging as to ultimately cause diabetes and all the morbidity and mortality that follows? The last two decades of research has demonstrated that excess abdominal fat—because of the associated macrophages—causes a condition of “metabolic inflammation” in the whole body. This systemic inflammation is characterized by elevated inflammatory markers in the blood, most notably a hormone called Tumor Necrosis Factor-alpha (TNF-α). We now know that TNF-α does a double whammy by directly causing insulin resistance in skeletal muscle AND the inhibition and ultimate destruction of the beta cells of the pancreas (the cells that make insulin).

A little more background is in order here: Insulin is the hormone secreted by the beta cells of the pancreas in response to and/or the anticipation of the rise in blood glucose (blood sugar) that happens after a carb-rich meal. What insulin actually does is command mainly three types of tissue: liver, adipose (fat) and skeletal (voluntary) muscle to get that glucose out of the circulation as quickly as possible, by burning it or storing it. These tissues can store glucose as glycogen (aka “animal starch”) or fat. What insulin does is to turn on the enzymatic machinery to store (or burn, in the case of muscle), as well as to open up specialized channels (called “GLUTs”; short for “glucose transporters”—pun intended by the creative researchers that came up with the term) in the cell membranes of adipose and muscle cells, so that glucose can be taken up rapidly by these tissues.

Trouble is, TNF-α, secreted by the activated macrophages embedded in the adipose tissue, directly interferes with the muscles’ deployment of GLUTs in their cell membranes, so they cannot take up glucose readily. This is manifest as the pre-diabetic condition known as “insulin resistance”. As a result, the pancreatic beta cells respond by cranking out more and more insulin. But at the same time, TNF-α also directly interferes with the ability of the beta cells to make insulin, and ultimately induces their self-destruction, causing actual type-2 diabetes. The reason this takes some years to occur is the existence of other chemical control mechanisms—hormones and other factors secreted by muscle cells and other types of pancreatic islet cells that help to protect the existence and function of the beta cells. The complex interplay of such chemical signals is currently being elucidated by ongoing research. But the bottom line is that ultimately, the chronic inflammatory condition and unrelenting action of TNF-α (and likely other pro-inflammatory chemical signals) crashes the system, and diabetes ensues.

So, getting back to the earlier key question, why do the macrophages embedded in the abdominal fat get stirred up in the first place? The answer, in a word, is glycine, or rather, insufficient glycine. Feel free to check out my earlier post (Diet and Inflammation, Part 2) on this blog for the details. But in short, glycine is the body’s most important regulator of inflammation, by keeping membrane channels open for the intake of chloride ions. A constant, low-level influx of chloride is needed to maintain the proper membrane voltage (0.07 volts): If the voltage deteriorates, the cell gets activated. That’s when these macrophages go into action to fight invading microbes. Normally, these cells only get activated when they detect the chemical signature of bacteria or viruses or fungi, but if the concentration of glycine is not high enough, the macrophages get activated to fight microbes that aren’t even there!
{Are we looking at a major cause of chronic infections here? If the immune system is always active, that would most likely lead to fatigue and reduced ability to fight infections (plus autoimmune disease).}


Now here’s a key error that the mainstream research and medical world is still laboring under: It is still generally thought that inflammation is also a natural response to tissue injury. I have discovered that–unequivocally—that is not true. When, for example, there is blunt injury—no microbes to kill—macrophages do need to be involved in gobbling up the mess of dead cells and cell debris. But they do not need to get activated, which involves the secretion of destructive chemicals like hydrogen peroxide and TNFα. They only cause damage and delay healing (That’s why it helps to put ice on such a wound, to inhibit inflammation.) And if you are not glycine-deficient, blunt injury does not cause inflammation, but just naturally heals quite quickly.

What about abdominal obesity? After all, there’s not even any tissue injury to activate the macrophages. It is not known what the signal is precisely that sets them off. But I can tell you that they do NOT get activated if glycine is adequate. So where’s the proof of this? Two lines of evidence provide confirmation: First, we find that insulin resistant (pre-diabetic) and type-2 diabetic patients have significantly lower blood levels of glycine than normal. Over the last few years, the evidence for this has been accumulating, thanks in some measure to the new technological advance known as metabolomics, which allows the simultaneous measurement of hundreds of metabolites from each blood sample collected, rather than just a few. So for example, in 2010, a study identified glycine as the single most reduced metabolite—among 485 different metabolites identified—in 143 insulin-resistant 30-60-year-old men and women from 13 European countries, compared to 256 subjects with normal insulin sensitivity. Similar results have been showing up in several other recent studies among subjects with insulin resistance and abdominal obesity, as well as subjects with type 2 diabetes, as had shown up in earlier studies on laboratory rats with diabetes.

Second, clinical trials are starting to show that when insulin resistant and diabetic patients’ diets are supplemented with glycine, the clinical markers of the condition improve markedly as was previously demonstrated in laboratory rats. So, for example, in a study in Mexico City in 2008 found that, in 3 dozen patients taking 15 g/day of glycine (v. placebo controls) mean fasting glucose went down from 183 mg/dL to 140: from way diabetic to right on the border of diabetes. In the same study, hemoglobin A1C (a standard measure of long-term blood sugar control) decreased from 8.3 to 6.9 (i.e., down to non-diabetic levels), and a measure of TNF-α decreased 4-fold! A clinical study of my own is also in the works.

Finally, let’s not underestimate the value of self-experimentation: My experience with my own 8g/day sweetamine supplement was that, with no change in weight, it reduced my fasting glucose–which had gone up over the years to 129; just over the border into diabetic territory–down to 110: the top of the normal range. (Some sweetamine users diagnosed with type 2 diabetes have also reported not needing their medication anymore to control their blood sugar.)

So we end where we began: Enjoy the holidays, and eat, drink and be merry—even if you do pick up a few pounds. Just don’t forget the glycine.
 

itellsya

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FOTCM Member
Interesting finds all! Much appreciated. Especially relating to sleep. Initially when trying bone broth a few years ago, i did find it made me feel quite sleepy (in a good way). So i'll get the powdered glyince and sup it in a chamomile tea and report back - i expect if you swill it around the mouth it could have a sublingual effect? On seeing the article on Sott, i made a trotters broth immediately :D It's probably been 2 months since i made the last one.
 
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