12 replies to this topic

[Qowpel]

I wanted to know which supplements are best for inhibiting these processes?

 

I take benfotime at 750 mg a day

L carnosine at 1 gram per day.

I drink 3-6 cups of either white tea or green tea per day.

I take p5p 100 mg daily

I take 1 gram of ester c per day at meals

 

Is lutein good for glycatioN (I take it 20 mg a day)

Is pycnogenol at 90 mg a day good for glycation (I take this as well)

Is astaxanthin good for glycation at 4 mg a day (I take this too)

 

 

I would really like to know of all I listed, which ones are the best for anti glycation here from worst to best since I simply cannot draw a conclusion on this with my research it is so mind boggling.....

 

 

 

 

And lastly, am I missing much by NOT taking metformin, pyridoxamine, and aminoguanidine, and alpha lipoic acid (especially since ALA apparently recycles vitamins C and E), ginger, rutin, and licorice?

 

 

 

LASTLY, do these substnces ALL definetely or at least probably work on glycation AND do they all neccessarily work on skin glyction, or glycation in other parts of the body?

[ta5]

I don't have your answers. But, I just thought I would add some more to the list: Quercetin, N-Acetyl-L-Carnosine, Beta Alanine, Limonene, Olive Leaf, Ferulic Acid, Aspirin, PBN/NtBHA, Alagebrium, Luteolin, Green Tea, Rosemary, Garlic, Chebulic Acid, Fucoidan, Fisetin, Betanin, Taurine, Lysine, Glycine, Niacin, Milk Thistle, Cinnamon.

 

Many of those are just inhibitors, not breakers.

 

Then, you could get in to things to increase insulin sensitivity, ways to keep blood sugar low, and consuming fewer AGEs from cooked foods. 

 

Vitamin D may also be of some value. This showed up a few days ago:

 

Cardiovasc Diabetol. 2015 Jul 16;14:89.
Vitamin D status is associated with skin autofluorescence in patients with type 2 diabetes mellitus: a preliminary report.

Krul-Poel YH, Agca R, Lips P, van Wijland H, Stam F, Simsek S.

BACKGROUND:

Skin autofluorescence is a non-invasive measurement of advanced glycation end products (AGE), which are suggested to be one of the major agents in the pathogenesis and progression of diabetes related cardiovascular complications. Recently, low vitamin D status has been linked to the progression of type 2 diabetes mellitus (T2DM) and cardiovascular disease. The aim of this study is to investigate the association between vitamin D status and skin autofluorescence in patients with T2DM.

METHODS:

In this preliminary report skin autofluorescence was measured non-invasively with an AGE-reader in 245 patients with T2DM treated with lifestyle advice, metformin and/or sulphonylurea-derivatives. All patients were randomly assigned to receive either vitamin D 50,000 IU/month or placebo for 6 months.

RESULTS:

Skin autofluorescence was significantly higher in patients with a serum 25(OH)D <50 nmol/l compared to patients with a serum 25(OH)D >75 nmol/l (2.81 versus 2.41; p < 0.001). Mean serum 25(OH)D was 60.3 ± 23.4 nmol/l and was independently associated with skin autofluorescence (β -0.006; p < 0.001). Mean vitamin D increased from 60.8 to 103.6 nmol/l in the intervention group, however no effect was seen on accumulation of skin AGEs after 6 months compared to placebo.

CONCLUSIONS:

Vitamin D status is independently associated with skin auto fluorescence in patients with well-controlled T2DM. No effect was seen on the amount of skin AGEs after a short period of 6 months vitamin D supplementation. Further research with longer follow-up and measurement of circulating advanced glycation end products is needed to elucidate the causality of the association.

PMID: 26173772

Edited by ta5, 24 July 2015 - 01:55 AM.

[Darryl]

Maintain insulin sensivity, so glycemic spikes are brief. A low saturated fat, low fructose diet, avoiding obesity (a low BMI ~20 is ideal), CR/intermittent fasting, and exercise are all helpful here.

 

Though post-prandial fructose levels are  lower than those for glucose, fructose is an order of magnitude more potent initiator of the Maillard reaction. Avoid added sugars containing fructose (table sugar, HFCS, and esp. honey and agave) and high consumption of fruit juices.

 

D-galactose (a product of lactose) is also a potent glycation initiator, so much so that its widely used as an aging mimetic. Avoid nonfermented dairy products.

 

Free serum iron catalyzes autooxidation of glucose, an initial step in AGE formation. Its likely that many glycation inhibitors (pyridoxamine, carnosine, aminoguanidine, metformin, tenilsetam, temocaprilat) function primarily via metal chelation.  I've chosen to regularly donate blood till my transferrin saturation is in the low-normal range (15-25%).

 

The phenols/phenol sources ta5 mentions (green tea, quercetin, olive Leaf, ferulic acid, luteolin, rosemary, fucoidan, fisetin,  licorice, milk thistle, pycnogenol, rutin) likely owe their benefits to upregulating endogenous antioxidant response via hormetic activation of Nrf2. Its possible to go overboard to hepatoxic levels with extracts.

 

ta5 mentioned all of the other widely available glycation inhibitors I'm aware of. I believe the evidence for aspirin/salicylates, carnosine/β-alanine, glycine and taurine in vivo is stronger than for most of the other compounds. Benfotiamine was so promising given its point of action, but clinical trials in diabetics have been disappointing.

 

Carotenoids like lycopene are superb at physical quenching of UV generated singlet oxygen, and do prevent skin photoaging (lutein and astaxanthin are available to the retina/cornea). However, they're only mediocre as chemical quenching antioxidants, so to my understanding have limited utility in preventing the Maillard reaction.  

 

There are no AGE breakers for the most important endogenous AGEs, like glucosepane. At present, its entirely a matter of prevention.

Edited by Darryl, 24 July 2015 - 07:11 AM.

[ImmortalSpace]

Here's my 2 cents. Taking care of blood sugar generally done by going on a low carb diet which is basically Atkins. Your body will start go into Ketosis (It produces ketones) and uses fat as energy for fuel (lyposis). 80% of calroies come from protein and fat, 20% or less from carbs. No bread. Instead, try making bread with cashew flower (grind up cashews in a coffee grounder, cashew flour)

 

Avoid Poly-Unsaturated Fats. Monounsaturated fats great, Saturated fats excellent. Mainly because of rapid oxidation in Poly Unsaturated Fats. Hmmm... I wonder why people who eat fast food are unhealthy? Could it be those highly oxidative Poly-Unsaturated Canola Oil's, let me think.

 

Keep in mind that Fat does not produce an insulin spike, so meat is great for this- protein barely produces changes in blood sugar. Carbs however do a LOT- well a considerable amount depending on the type.

 

 

Look into Qi-Gong, please be open minded. There is research that it is effective, and science is all about enquiry. The evidence is promising. I've noticed that people who live a long time, and have great skin eat a lot of herbs. Li chin Yuen for example is said to live 256 years and there are documents from the Chinese that congratulate him on his 200th birthday- which is likely. He Did Qi-Gong. Lots of Qi-Gong masters are in perfect health, even though they likely don't have the best diet sometimes. Research.

 

Genistein is important as a Granzyme B inhibitor and messes with skin, L-Lysine of course. Probiotics. Probiotics. Probiotics. Take them, but not in supplement- Sauerkraut. It has hundreds of times more than any supplement, and affects your microbiome positively. Your gut bacteria plays a Huge Role in your immune system. You need an excellent immune system for great skin. (Dr. Perlmitter-  Brain Maker, Grain Brain)

Edited by ImmortalSpace, 24 July 2015 - 04:39 PM.

[Darryl]

The unfortunate thing about keto is that all the post-prandial chylomicron remnants are precisely the thing that causes muscular insulin resistance. It takes very little carbs (~10% E) before you start seeing keto & "ancestral" diet advocates fretting about their blood glucose.

 

Mei S et al.  2014. A Small Amount of Dietary Carbohydrate Can Promote the HFD-Induced Insulin Resistance to a Maximal Level. 

 

It seems keto is only pragmatic in childhood epilepsy and metastatic cancer, where overriding health concerns favor an otherwise unpalatable diet, where numerous healthy foods are excluded.  

 

Ideally, one could engineer a diet strictly around short chain fatty acids and resistant starch for these disorders, as its not fats in general that cause insulin resistance, but just the longer saturated fats (esp ceramide generating palmitate (16:0) and equally TLR4 activating stearate (18:0)).

 

For myself, 75% carbs (but no added sugars or fruit juice) seems to be working, with fasting glucose around 75 mg/dL and HbA1 below 5%. These were normal levels in parts of the world with starch based diets, before Western high-fat diets and Western diabetes risks arrived.

 

It seems paradoxical, but to reduce fasting glucose, one minimizes long-chain saturated fat intake.

 

---

 

This isn't the ideal venue for it, but I feel like doing an info dump for ImmortalSpace's benefit, as I find the ignorance of some of the keto/low-carb gurus galling. The evidence that long-chain saturated fat intake is a primary cause of insulin resistance is overwhelming. Fructose has similar associations with other elements of metabolic syndrome, both saturated fats and excess fructose impair intestinal barrier function and bring endotoxemia, and there's much more detailing the connection between long-chain saturated fats, TLR4 activation, and inflammation in the etiology of insulin resistance, but I'll save those topics for another day.

 

Human studies

Roden M et al. 1996. Mechanism of free fatty acid-induced insulin resistance in humans. Journal of Clinical Investigation, 97(12), 2859.

Krssak M et al. 1999. Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1H NMR spectroscopy study. Diabetologia, 42(1), 113-116.

Santomauro AT et al. 1999. Overnight lowering of free fatty acids with Acipimox improves insulin resistance and glucose tolerance in obese diabetic and nondiabetic subjects. Diabetes, 48(9), 1836-1841.

Maron DJ  et al. 1991. Saturated fat intake and insulin resistance in men with coronary artery disease. Circulation, 84(5), 2020-2027.

Parker DR et al. 1993. Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study. The American journal of clinical nutrition, 58(2), 129-136.

Vessby B et al. 1994. Insulin sensitivity is related to the fatty acid composition of serum lipids and skeletal muscle phospholipids in 70-year-old men. Diabetologia, 37(10), 1044-1050.

Marshall JA et al. 1997. High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population: the San Luis Valley Diabetes Study. Diabetologia, 40(4), 430-438.

Jacob S et al. 1999. Association of increased intramyocellular lipid content with insulin resistance in lean nondiabetic offspring of type 2 diabetic subjects. Diabetes,48(5), 1113-1119.

Perseghin G et al. 1999. Intramyocellular triglyceride content is a determinant of in vivo insulin resistance in humans: a 1H-13C nuclear magnetic resonance spectroscopy assessment in offspring of type 2 diabetic parents. Diabetes,48(8), 1600-1606.

Roden M et al. 1999. Rapid impairment of skeletal muscle glucose transport/phosphorylation by free fatty acids in humans. Diabetes, 48(2), 358-364.

Manco M et al. 2000. Insulin resistance directly correlates with increased saturated fatty acids in skeletal muscle triglycerides.Metabolism, 49(2), 220-224.

Vessby B et al. 2001. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Diabetologia, 44(3), 312-319.

Lovejoy JC. et al. 2002. Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults. Diabetes care, 25(8), 1283-1288.

Summers L et al. 2002. Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity. Diabetologia, 45(3), 369-377.

Sparks LM et al. 2005. A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle. Diabetes, 54(7), 1926-1933.

Kusunoki M et al. 2007. Relationship between serum concentrations of saturated fatty acids and unsaturated fatty acids and the homeostasis model insulin resistance index in Japanese patients with type 2 diabetes mellitus. The Journal of Medical Investigation, 54(3, 4), 243-247.

Anderson EJ et al. 2009. Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans. The Journal of clinical investigation, 119(3), 573.

Das M et al. 2010. Association of metabolic syndrome with obesity measures, metabolic profiles, and intake of dietary fatty acids in people of Asian Indian origin. Journal of cardiovascular disease research, 1(3), 130-135.

Ebbesson SO et al. 2010. Individual saturated fatty acids are associated with different components of insulin resistance and glucose metabolism: the GOCADAN study. International journal of circumpolar health, 69(4), 344.

Corella D et al. 2011. A high intake of saturated fatty acids strengthens the association between the fat mass and obesity-associated gene and BMI. The Journal of nutrition, 141(12), 2219-2225.

Perez-Martinez P et al. 2011. Calpain-10 interacts with plasma saturated fatty acid concentrations to influence insulin resistance in individuals with the metabolic syndrome. The American journal of clinical nutrition, 93(5), 1136-1141.

González-Muniesa P. 2013. Differential proinflammatory and oxidative stress response and vulnerability to metabolic syndrome in habitual high-fat young male consumers putatively predisposed by their genetic background. International journal of molecular sciences, 14(9), 17238-17255.

Lee S et al. 2013. Effects of an overnight intravenous lipid infusion on intramyocellular lipid content and insulin sensitivity in African–American versus Caucasian adolescents. Metabolism, 62(3), 417-423.

Mayneris-Perxachs J et al. 2014. Plasma fatty acid composition, estimated desaturase activities, and their relation with the metabolic syndrome in a population at high risk of cardiovascular disease.Clinical nutrition, 33(1), 90-97.

 

 

Ceramides

Schmitz-Peiffer C et al. 1999. Ceramide generation is sufficient to account for the inhibition of the insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate. Journal of Biological Chemistry, 274(34), 24202-24210.

Chavez JA et al. 2003. A role for ceramide, but not diacylglycerol, in the antagonism of insulin signal transduction by saturated fatty acids. Journal of Biological Chemistry, 278(12), 10297-10303.

Chavez JA. & Summers SA. 2003. Characterizing the effects of saturated fatty acids on insulin signaling and ceramide and diacylglycerol accumulation in 3T3-L1 adipocytes and C2C12 myotubes. Archives of biochemistry and biophysics, 419(2), 101-109.

Kelpe CL el al. 2003. Palmitate inhibition of insulin gene expression is mediated at the transcriptional level via ceramide synthesis. Journal of Biological Chemistry, 278(32), 30015-30021.

Powell D et al. 2004. Intracellular ceramide synthesis and protein kinase Czeta activation play an essential role in palmitate-induced insulin resistance in rat L6 skeletal muscle cells. Biochem. J, 382, 619-629.

Turpin SM et al. 2006. Apoptosis in skeletal muscle myotubes is induced by ceramides and is positively related to insulin resistance. American Journal of Physiology-Endocrinology and Metabolism, 291(6), E1341-E1350.

Holland WL et al. 2007. Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistance. Cell metabolism, 5(3), 167-179.

Pickersgill L et al. 2007. Key role for ceramides in mediating insulin resistance in human muscle cells. Journal of Biological Chemistry, 282(17), 12583-12589.

Holland WL et al. 2011. Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid–induced ceramide biosynthesis in mice. The Journal of clinical investigation,121(5), 1858.

Chavez JA et al. 2014. Ceramides and glucosylceramides are independent antagonists of insulin signaling. Journal of Biological Chemistry, 289(2), 723-734.

 

Other studies

Hunnicutt JW et al. 1994. Saturated fatty acid–induced insulin resistance in rat adipocytes. Diabetes,43(4), 540-545.

Lee JS et al. 2006. Saturated, but not n-6 polyunsaturated, fatty acids induce insulin resistance: role of intramuscular accumulation of lipid metabolites.Journal of applied physiology, 100(5), 1467-1474.http://dx.plos.org/1...al.pone.0100875

Matsuzaka T et al. 2007. Crucial role of a long-chain fatty acid elongase, Elovl6, in obesity-induced insulin resistance. Nature medicine, 13(10), 1193-1202.

Alkhateeb H et al. 2007. Two phases of palmitate-induced insulin resistance in skeletal muscle: impaired GLUT4 translocation is followed by a reduced GLUT4 intrinsic activity.American Journal of Physiology-Endocrinology and Metabolism, 293(3), E783-E793.

Matsuzawa-Nagata N et al. 2008. Increased oxidative stress precedes the onset of high-fat diet–induced insulin resistance and obesity. Metabolism,57(8), 1071-1077.

Hommelberg PP et al. 2009. Fatty acid-induced NF-κB activation and insulin resistance in skeletal muscle are chain length dependent. American Journal of Physiology-Endocrinology and Metabolism, 296(1), E114-E120.

Nolan CJ & Larter CZ. 2009. Lipotoxicity: why do saturated fatty acids cause and monounsaturates protect against it?. Journal of gastroenterology and hepatology, 24(5), 703-706.

Nakamura S et al. 2009. Palmitate induces insulin resistance in H4IIEC3 hepatocytes through reactive oxygen species produced by mitochondria. Journal of Biological Chemistry, 284(22), 14809-14818.

Jornayvaz FR et al 2010. A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain. American Journal of Physiology-Endocrinology and Metabolism, 299(5), E808-E815.

Van den Berg SA et al. 2010. High levels of dietary stearate promote adiposity and deteriorate hepatic insulin sensitivity. Nutr Metab (Lond),7(24.2010).

Hirabara SM. et al. 2010. Saturated fatty acid‐induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells. Journal of cellular physiology, 222(1), 187-194.

Clegg DJ et al. 2011. Consumption of a high-fat diet induces central insulin resistance independent of adiposity. Physiology & behavior, 103(1), 10-16.

Hommelberg PP et al. 2011. Palmitate-induced skeletal muscle insulin resistance does not require NF-κB activation. Cellular and Molecular Life Sciences, 68(7), 1215-1225.

Sawada K et al. 2012. Ameliorative effects of polyunsaturated fatty acids against palmitic acid-induced insulin resistance in L6 skeletal muscle cells. Lipids Health Dis, 11(1), 36.

Talukdar S et al. 2012. Neutrophils mediate insulin resistance in mice fed a high-fat diet through secreted elastase. Nature medicine, 18(9), 1407-1412.

Eguchi K et al. 2012. Saturated fatty acid and TLR signaling link β cell dysfunction and islet inflammation

Junior SAO et al. 2013. Extensive impact of saturated fatty acids on metabolic and cardiovascular profile in rats with diet-induced obesity: a canonical analysis. Cardiovasc Diabetol, 12(1), 65.

Salvado L et al. 2013. Oleate prevents saturated-fatty-acid-induced ER stress, inflammation and insulin resistance in skeletal muscle cells through an AMPK-dependent mechanism. Diabetologia, 56(6), 1372-1382.

Galbo T et al. 2013. Saturated and unsaturated fat induce hepatic insulin resistance independently of TLR-4 signaling and ceramide synthesis in vivo. Proceedings of the National Academy of Sciences, 110(31), 12780-12785.

Mei S et al. 2014. A small amount of dietary carbohydrate can promote the HFD-induced insulin resistance to a maximal level.  PLoS ONE, 9(7).

 

Reviews

Boden G. 1997. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes, 46(1), 3-10.

McGarry JD & Dobbins RL. 1999. Fatty acids, lipotoxicity and insulin secretion. Diabetologia, 42(2), 128-138.

Riccardi G et al. 2005. Dietary fat, insulin sensitivity and the metabolic syndrome. Clinical nutrition, 23(4), 447-456.

Haag M & Dippenaar NG. 2005. Dietary fats, fatty acids and insulin resistance: short review of a multifaceted connection. Medical Science Monitor Basic Research, 11(12), RA359-RA367.

Schrauwen P.  2007. High-fat diet, muscular lipotoxicity and insulin resistance. In Proceedings - Nutrition Society of London. Vol. 66, No. 1, p. 33

Ye J. 2007. Role of insulin in the pathogenesis of free fatty acid-induced insulin resistance in skeletal muscle. Endocrine, Metabolic & Immune Disorders-Drug Targets, 7(1), 65-74.

Corcoran MP et al.2007. Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. The American journal of clinical nutrition, 85(3), 662-677.

Galgani JE et al. 2008. Effect of the dietary fat quality on insulin sensitivity. British Journal of Nutrition, 100(03), 471-479.

Fessler MB et al. 2009. Toll-like receptor signaling links dietary fatty acids to the metabolic syndrome. Current opinion in lipidology, 20(5), 379.

Chavez JA & Summers SA. 2010. Lipid oversupply, selective insulin resistance, and lipotoxicity: molecular mechanisms. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids, 1801(3), 252-265.

Samuel VT et al. 2010. Lipid-induced insulin resistance: unravelling the mechanism. The Lancet, 375(9733), 2267-2277.

Kewalramani G et al. 2010. Muscle insulin resistance: assault by lipids, cytokines and local macrophages. Current Opinion in Clinical Nutrition & Metabolic Care, 13(4), 382-390.

Chavez JA & Summers SA. 2012. A ceramide-centric view of insulin resistance. Cell metabolism, 15(5), 585-594.

Martins AR et al. 2012. Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function. Lipids Health Dis, 11(30), 1-11.

Estadella D et al. 2013. Lipotoxicity: effects of dietary saturated and transfatty acids. Mediators of inflammation, 2013.

Yang J et al. 2013. The mechanisms linking adiposopathy to type 2 diabetes. Frontiers of medicine, 7(4), 433-444.

Nourmohammdi M et al. 2014. Dietary fatty acid composition and metabolic syndrome: a review. Journal of Nutritional Sciences and Dietetics, 1(1), 28-36.

 

Note: the Talukdar et al 2012 study above exemplifies why one should avoid proinflammatory long-chain saturated fats in a skin preservation regimen. Elastase is enemy #1 in skin aging, and much of the harm of UV irradiation is due to elastase secretion.

 

 

Edited by Darryl, 24 July 2015 - 07:24 PM.

[Heisenburger]

Color me impressed. That's one hell of a post.

[Qowpel]

Color me impressed. That's one hell of a post.

 

Thanks everyone I do appreciate your input. But again I was wondering which inhibitors actually help to prevent glycation of skin specifically as I have gerd that benfotiamine isn't necessarily for skin gylcation but that carnosine is. I am getting very confused

[Heisenburger]

You do realize that the compliment was directed at Darryl, right?

[Qowpel]

You do realize that the compliment was directed at Darryl, right?

Yeah I know. It's just I am lucky that taking someone elses comments cannot get you banned here ... regardless I am still trying to find out which glycation inhibitors are the ones the target/at least are effective on, skin glycation

[ImmortalSpace]

 

Color me impressed. That's one hell of a post.

 

Thanks everyone I do appreciate your input. But again I was wondering which inhibitors actually help to prevent glycation of skin specifically as I have gerd that benfotiamine isn't necessarily for skin gylcation but that carnosine is. I am getting very confused

 

 

Theres a lot of scientific evidence of Carnosine and anti Glycation. Get carnosine. Also cinnamon is another one to get.

[Qowpel]

 

 

Color me impressed. That's one hell of a post.

 

Thanks everyone I do appreciate your input. But again I was wondering which inhibitors actually help to prevent glycation of skin specifically as I have gerd that benfotiamine isn't necessarily for skin gylcation but that carnosine is. I am getting very confused

 

 

Theres a lot of scientific evidence of Carnosine and anti Glycation. Get carnosine. Also cinnamon is another one to get.

 

Ok so are we all just concluding that benfotiamine is absolutely NOT helpful in stopping skin glycation?

 

Also are we Also concluding that carnosine is truly the ONLY one effective for skin glycation?

 

Is alpha lipoic acid effective for skin glycation, specifically? What about Metformin?

 

Is there ANYTHING else effective for skin glycation specifically?

[aribadabar]

 I've chosen to regularly donate blood till my transferrin saturation is in the low-normal range (15-25%).

 

It is slightly OT but I noticed your mentioning of bimonthly donation schedule in another post and given your vegan diet I wanted to ask you - how do you even keep your ferritin levels high enough?

Using the same frequency, I went from 80 (prior to adopting mostly vegan diet) to sub 15 after only 3 donations in the span of 6 months and have been unable to raise it beyond 20s range for over a year now(despite cessation of the donations).

[Darryl]

aribadabar:

 

I haven't been monitoring ferritin, just hemoglobin (required at each donation), and iron saturation on a yearly basis. I'm frankly surprised that my iron levels have stabilized at low-normal levels for 3 years and 4 gallons of donation, especially considering I eat few iron supplemented foods like enriched flour. My guess is that my intestinal iron absorption has adapted, but I suppose there may be concerns with how that adaptation effects absorption of less desirable divalent minerals like cadmium.