Histidine for fat loss

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    Histidine for fat loss


    Histidine supplementation improves insulin resistance through suppressed inflammation in obese women with the metabolic syndrome: a randomised controlled trial.

    Increased inflammation and oxidative stress are associated with insulin resistance (IR) and metabolic disorders. Serum histidine levels are lower and are negatively associated with inflammation and oxidative stress in obese women. The objective of this study was to evaluate the efficacy of histidine supplementation on IR, inflammation, oxidative stress and metabolic disorders in obese women with the metabolic syndrome (MetS).

    METHODS:
    A total of 100 obese women aged 33-51 years with BMI ≥ 28 kg/m(2) and diagnosed with MetS were included following a health examination in the community hospital in this randomised, double-blinded, placebo-controlled trial. Participants were allocated to interventions by an investigator using sequentially numbered sealed envelopes and received 4 g/day histidine (n = 50) or identical placebo (n = 50) for 12 weeks. Participants then attended the same clinic every 2 weeks for scheduled interviews and to count tablets returned. Serum histidine, HOMA-IR, BMI, waist circumference, fat mass, serum NEFA, and variables connected to inflammation and oxidative stress were measured at baseline and 12 weeks. Participants, examining physicians and investigators assessing the outcomes were blinded to group assignment. In addition, the inflammatory mechanisms of histidine were also explored in adipocytes.

    RESULTS:
    At 12 weeks, a total of 92 participants completed this trail. Compared with the placebo group (n = 47), histidine supplementation significantly decreased HOMA-IR (-1.09 [95% CI -1.49, -0.68]), BMI (-0.86 kg/m(2) [95% CI -1.55, -0.17]), waist circumference (-2.86 cm [95% CI -3.86, -1.86]), fat mass (-2.71 kg [95% CI -3.69, -1.73]), serum NEFA (-173.26 μmol/l [95% CI -208.57, -137.94]), serum inflammatory cytokines (TNF-α, -3.96 pg/ml [95% CI -5.29, -2.62]; IL-6, -2.15 pg/ml [95% CI -2.52, -1.78]), oxidative stress (superoxide dismutase, 17.84 U/ml [95% CI 15.03, 20.65]; glutathione peroxidase, 13.71 nmol/ml [95% CI 9.65, 17.78]) and increased serum histidine and adiponectin by 18.23 μmol/l [95% CI 11.74, 24.71] and 2.02 ng/ml [95% CI 0.60, 3.44] in histidine supplementation group (n = 45), respectively. There were significant correlations between changes in serum histidine and changes of IR and its risk factors. No side effects were observed during the intervention. In vitro study indicated that histidine suppresses IL6 and TNF mRNA expression and nuclear factor kappa-B (NF-κB) protein production in palmitic acid-induced adipocytes in a dose-dependent manner, and these changes were diminished by an inhibitor of NF-κB.

    CONCLUSIONS/INTERPRETATION:
    Histidine supplementation could improve IR, reduce BMI, fat mass and NEFA and suppress inflammation and oxidative stress in obese women with MetS; histidine could improve IR through suppressed pro-inflammatory cytokine expression, possibly by the NF-κB pathway, in adipocytes.


    PMID: 23361591
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    Histidine supplementation suppresses food intake and fat accumulation in rats.

    Abstract

    OBJECTIVE:
    Histamine, a derivative of histidine, decreases food intake and body fat by activation of histamine neurons. Our objective was to clarify the effect of dietary histidine, in particular, on food intake and/or body fat accumulation in rats.

    METHODS:
    Male Wistar rats were assigned to one of four groups after acclimation and allowed free access to diets containing 20% casein (0% histidine), 20% casein plus 1.0% histidine, 20% casein plus 2.5% histidine, or 20% casein plus 5% histidine for 8 d.

    RESULTS:
    Food intake and body weight were recorded daily and compared between groups. During the experimental period, food intake decreased according to the increases in dietary histidine. There was a negative and significant (P < 0.01) correlation between dietary histidine (grams per 8 d) and retroperitoneal fat pad (grams per 100 g of body weight). Uncoupling protein-1 mRNA in brown adipose tissue increased with increases in dietary histidine.

    CONCLUSION:
    Our results indicate that dietary histidine suppresses food intake and fat accumulation in rats.

    PMID: 15561489
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    This is pretty interesting in the first one considering you would think we all have plenty without supplementation.

    Edit: can't help but speculate about supplementation of histidine along side beta-alanine...
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    I thought histidine increases histamine which increases inflammatory response, unless metabolic disease and insulin resistance is correlated with an excess of methylation capacity and the extra histamine can be easily metabolized.

    Also, I have no idea what I'm talking about........
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    I've seen some other things that suggested a positive use for histidine before, although the whole potential of increasing my already crappy allergic hayfever response sucks.
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    The real question is whether or not histidine increases lipolysis independent of the adrenergic pathway. Im guessing its adrenergic through H1 neuronal depolarization
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    http://primaladvisor.com/tag/obesity/

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    I am interested in the increase in insulin sensitivity aspect, having type II diabetes. I know Vinegar can also do this as well as grapefruit IIRC, however I cannot eat grapefruit (/sadface) because it has a enzyme that blocks metabolism of one of my meds.
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    How would this affect those who take antihistamines for allergies?
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    Quote Originally Posted by McBurly View Post
    How would this affect those who take antihistamines for allergies?
    It would appear that histamine induced lipolysis is directly through H2 receptor and cAMP accumulation. Thus your antihistamines which work on the H1 receptor will not inhibit histamine induced lipolysis.
    jpet.aspetjournals.org/content/195/1/176

    Anyone tried this stuff yet?
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    Quote Originally Posted by nidhogg View Post
    It would appear that histamine induced lipolysis is directly through H2 receptor and cAMP accumulation. Thus your antihistamines which work on the H1 receptor will not inhibit histamine induced lipolysis.
    jpet.aspetjournals.org/content/195/1/176

    Anyone tried this stuff yet?
    Increasing l-histidine intake has the paradoxical effect of alleviating common allergies, though it does seem counter intuitive. Sure it's a precursor to histamine, but I suspect it has more to do with it's influence on Th-2 interleukins. For example, forget it's effect on NF-kB and look what it does to IL-10 and IL-12. That in itself might explain most of the anti-inflammatory results.

    I played with it many years ago and found about 16g/d to be an impressive anorectic. One might naturally expect to see changes like reduced insulin resistance and exaggerated lipolysis with caloric restriction, but I'm not sure l-histidine has any unique intrinsic quality in that regard. However, it does improve consolidation of memory retrieval in reduced inhibitory avoidance by H2 activation, so there may be some profound central mechanism which contributes to it's effect as well. H2 manipulation could result in multiple effects, so it all starts to get complicated and very subjective depending on your genes and the rest of your brain chemistry.

    So it's one of those things you just may have to try yourself if you really wanna know if it works. The dose made it impractical IMO.
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    Quote Originally Posted by DR.D View Post
    Increasing l-histidine intake has the paradoxical effect of alleviating common allergies, though it does seem counter intuitive. Sure it's a precursor to histamine, but I suspect it has more to do with it's influence on Th-2 interleukins. For example, forget it's effect on NF-kB and look what it does to IL-10 and IL-12. That in itself might explain most of the anti-inflammatory results.

    I played with it many years ago and found about 16g/d to be an impressive anorectic. One might naturally expect to see changes like reduced insulin resistance and exaggerated lipolysis with caloric restriction, but I'm not sure l-histidine has any unique intrinsic quality in that regard. However, it does improve consolidation of memory retrieval in reduced inhibitory avoidance by H2 activation, so there may be some profound central mechanism which contributes to it's effect as well. H2 manipulation could result in multiple effects, so it all starts to get complicated and very subjective depending on your genes and the rest of your brain chemistry.

    So it's one of those things you just may have to try yourself if you really wanna know if it works. The dose made it impractical IMO.
    HOLY CRAP! I havent seen you post since bacl when I first joined.

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    Thanks, Josh. It's been awhile, but I trust you've been winning tournaments and your belts are increasing steadily.
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    Quote Originally Posted by taman6886 View Post
    I am interested in the increase in insulin sensitivity aspect, having type II diabetes. I know Vinegar can also do this as well as grapefruit IIRC, however I cannot eat grapefruit (/sadface) because it has a enzyme that blocks metabolism of one of my meds.
    For DM2, focus on losing weight as your first through tenth priority. Insulin resistance is directly related to adipose tissue content, AND insulin is coexpressed with a protein which forms local amyloid deposits in the pancreas, destroying it. So, as you get bigger you need to produce more insulin, which in a vicious cycle necessarily destroys your pancreas' ability to produce insulin.

    Depending on your relative level of insulin resistance and residual beta cell function, some people can actually -- at least for some period of time -- reverse their diabetes with weight loss alone.

    Vinegar might slightly affect the p-ratio in a way that bodybuilders at least hypothetically benefit from, but it's unlikely to be satisfactory as a means of blood sugar control for the vast majority of diabetics.
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    Quote Originally Posted by trn450 View Post

    For DM2, focus on losing weight as your first through tenth priority. Insulin resistance is directly related to adipose tissue content, AND insulin is coexpressed with a protein which forms local amyloid deposits in the pancreas, destroying it. So, as you get bigger you need to produce more insulin, which in a vicious cycle necessarily destroys your pancreas' ability to produce insulin.

    Depending on your relative level of insulin resistance and residual beta cell function, some people can actually -- at least for some period of time -- reverse their diabetes with weight loss alone.

    Vinegar might slightly affect the p-ratio in a way that bodybuilders at least hypothetically benefit from, but it's unlikely to be satisfactory as a means of blood sugar control for the vast majority of diabetics.
    Nice post, thank you. Before I was hospitalized, my A1c was 5.9 @265lbs, which is a really good number for a type II.
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    Quote Originally Posted by taman6886 View Post
    Nice post, thank you. Before I was hospitalized, my A1c was 5.9 @265lbs, which is a really good number for a type II.
    Awesome, great job! Now, keep working on getting that bodyfat content down as far as possible and you might start be able to peeling off meds; I'm especially optimistic if your A1c is 5.9.
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    im trying to cut weight I do my share of cardio but more on on weights high rep side is there a good cycle for helping with faster results. I do fish and a lot of veg just need help on a cycle plz
  

  
 

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