Ray's View On Cinnamon ?

burtlancast

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Cinnamon is an old folk remedy used to lower hyperglycemia in type 2 diabetes.

Ray recommends to treat it with niacinamide, aspirin, thyroid, pregenolone, progesterone, thiamin, vit D and K, coffee.
He mentions too that the tens and tens of herbs able to lower glycemia are (most often than not) toxic, so he doesn't advise them.

But i wonder if this includes cinnamon ? I wasn't able to find (by google) anything about this.
 

honeybee

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There are anecdotal stories regarding cinnamon and pcos. It has some impact on normalizing female hormones.
 

Kasra

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Lol this was so easy to find:

http://www.ncbi.nlm.nih.gov/pubmed/24019277

"In a meta-analysis of 10 RCTs (n = 543 patients), cinnamon doses of 120 mg/d to 6 g/d for 4 to 18 weeks reduced levels of fasting plasma glucose (-24.59 mg/dL; 95% CI, -40.52 to -8.67 mg/dL), total cholesterol (-15.60 mg/dL; 95% CI, -29.76 to -1.44 mg/dL), LDL-C (-9.42 mg/dL; 95% CI, -17.21 to -1.63 mg/dL), and triglycerides (-29.59 mg/dL; 95% CI, -48.27 to -10.91 mg/dL). Cinnamon also increased levels of HDL-C (1.66 mg/dL; 95% CI, 1.09 to 2.24 mg/dL)."
 

jyb

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http://www.ncbi.nlm.nih.gov/pubmed/25553481

Cinnamon is a traditional herb used for treatment of many human diseases. The most important chemical compounds of the essential oil are cinnamaldehyde and eugenol. Oleum cinnamomi (OCM, cinnamon oil) is increasingly used as a feed additive to animal diets. Beneficial effects of OCM in protecting tissues from inflammation and injury by endogenous and exogenous agents (such as hydrogen peroxide and lipopolysaccharide (LPS)) may result, in part, from its action on regulating amino acid metabolism in cells to favor the synthesis of glutathione (a major low-molecular-weight antioxidant) from cysteine, glycine and glutamate. In support of this notion, results of recent studies indicate that supplementing OCM (50 mg/kg diet) to a corn- and soybean meal-based diet for piglets weaned at 21 days of age enhances intestinal anti-oxidative capacity and reduces the incidence of diarrhea. Additionally, dietary supplementation with OCM ameliorates LPS-induced mucosal barrier dysfunction and mucosal damage in the small intestine. OCM holds great promise for protecting the gut from injury under conditions of inflammation, infections, and oxidative stress.

Is this hormesis type response? It reminds me of the studies on tobacco showing up regulation of important anti-oxidants.
 

tara

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jyb said:
http://www.ncbi.nlm.nih.gov/pubmed/25553481

Additionally, dietary supplementation with OCM ameliorates LPS-induced mucosal barrier dysfunction and mucosal damage in the small intestine. OCM holds great promise for protecting the gut from injury under conditions of inflammation, infections, and oxidative stress.
Looks like a winner for this effect.
 
T

tca300

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ME: Ceylon cinnamon seems to be much lower in harmful substances than the typical store bought type. Do you think ceylon cinnamon is safe and or beneficial for consumption? Thank you!

Ray Peat: I think it might be safer to use the metabolite, benzoic acid, because of the reactivity of the cinnamaldehyde, which I suspect might react with larger molecules to produce allergens.

Biol Psychiatry. 2014 May 1;75(9):678-85.
Benzoate, a D-amino acid oxidase inhibitor, for the treatment of early-phase Alzheimer disease: a randomized, double-blind, placebo-controlled trial. Lin CH(1), Chen PK(2), Chang YC(3), Chuo LJ(4), Chen YS(5), Tsai GE(6), Lane HY(7).
(1)Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan. (2)Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan; Department of Neurology, Lin-Shin Hospital, Taichung, Taiwan. (3)Department of Mathematics, Tamkang University, Taipei, Taiwan. (4)Department of Psychiatry, Taichung Veterans General Hospital, Taichung, Taiwan. (5)Department of Mathematics, Tamkang University, Taipei, Taiwan; Department of Psychiatry, China Medical University Hospital, Taichung, Taiwan. (6)Department of Psychiatry, Harbor-UCLA Medical Center, Torrance,
California. (7)Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; Department of Psychiatry, China Medical University Hospital, Taichung, Taiwan. Electronic address: [email protected].
BACKGROUND: N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission is vital for learning and memory. Hypofunction of NMDAR has been reported to play a role in the pathophysiology of Alzheimer disease (AD), particularly in the early phase. Enhancing NMDAR activation might be a novel treatment approach. One of the
methods to enhance NMDAR activity is to raise the levels of NMDA coagonists by blocking their metabolism. This study examined the efficacy and safety of sodium benzoate, a D-amino acid oxidase inhibitor, for the treatment of amnestic mild cognitive impairment and mild AD.
METHODS: We conducted a randomized, double-blind, placebo-controlled trial in four major medical centers in Taiwan. Sixty patients with amnestic mild cognitive impairment or mild AD were treated with 250-750 mg/day of sodium benzoate or placebo for 24 weeks. Alzheimer's Disease Assessment Scale-cognitive subscale (the primary outcome) and global function (assessed by Clinician Interview Based Impression of Change plus Caregiver Input) were measured every 8 weeks. Additional cognition composite was measured at baseline and endpoint.
RESULTS: Sodium benzoate produced a better improvement than placebo in Alzheimer's Disease Assessment Scale-cognitive subscale (p = .0021, .0116, and .0031 at week 16, week 24, and endpoint, respectively), additional cognition composite (p = .007 at endpoint) and Clinician Interview Based Impression of Change plus Caregiver Input (p = .015, .016, and .012 at week 16, week 24, and endpoint, respectively). Sodium benzoate was well-tolerated without evident side-effects.
CONCLUSIONS: Sodium benzoate substantially improved cognitive and overall functions in patients with early-phase AD. The preliminary results show promise for D-amino acid oxidase inhibition as a novel approach for early dementing processes.

Aliment Pharmacol Ther. 2011 Oct;34(7):687-701.
Review article: cinnamon- and benzoate-free diet as a primary treatment for orofacial granulomatosis.
Campbell HE, Escudier MP, Patel P, Challacombe SJ, Sanderson JD, Lomer MC.
BACKGROUND:
Orofacial granulomatosis is a rare chronic granulomatous inflammatory disease of the lips, face and mouth. The aetiology remains unclear but may involve an allergic component. Improvements have been reported with cinnamon- and benzoate-free diets.
AIMS:
To explore the prevalence of compound and food sensitivity and examine the dietary treatments used in orofacial granulomatosis.
METHODS:
A comprehensive literature search was carried out and relevant studies from January 1933 to January 2010 were identified using the electronic database search engines; AGRIS 1991-2008, AMED 1985-2008, British Nursing and Index archive 1985-2008, EMBASE 1980-2008, evidence based medicine review databases (e.g. Cochrane DSR), International Pharmaceutical and Medline 1950-2008.
RESULTS:
Common sensitivities identified, predominantly through patch testing, were to benzoic acid (36%) food additives (33%), perfumes and flavourings (28%), cinnamaldehyde (27%), cinnamon (17%), benzoates (17%) and chocolate (11%). The cinnamon- and benzoate-free diet has been shown to provide benefit in 54-78% of patients with 23% requiring no adjunctive therapies. A negative or positive patch test result to cinnamaldehyde, and benzoates did not predict dietary outcome. The most concentrated source of benzoate exposure is from food preservatives. Use of liquid enteral formulas can offer a further dietary therapy, particularly in children with orofacial granulomatosis.
CONCLUSION:
Management of orofacial granulomatosis is challenging but cinnamon- and benzoate-free diets appear to have a definite role to play.

J Immunol. 2009 Nov 1; 183(9): 5917–5927.
Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Reduces Microglial and Astroglial Inflammatory Responses1
Saurav Brahmachari, Arundhati Jana, and Kalipada Pahan2
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available free at J Immunol
See other articles in PMC that cite the published article.
Activation of glial cells (microglia and astroglia) has been implicated in the pathogenesis of a variety of neurodegenerative diseases, including Alzheimer's disease (AD), 3 Parkinson's disease, Creutzfeld-Jacob disease, HIV-associated dementia (HAD), stroke, and multiple sclerosis (MS) (1, 2). It has been found that activated microglia and astroglia accumulate at sites of injury or plaques in neurodegenerative CNS (1–7). Although activated microglia scavenge dead cells from the CNS and secrete different neurotrophic factors for neuronal survival, it is believed that severe activation causes various autoimmune responses leading to neuronal death and brain injury (1–7). During activation, microglia and astroglia express various genes related to inflammation, such as proinflammatory cytokines, proinflammatory enzymes, and proinflammatory adhesion molecules (1–9). Therefore, characterization of signaling pathways required for the activation of glial cells is an active area of investigation since compounds capable of antagonizing such signaling steps may have therapeutic effect in neurodegenerative disorders.

Cinnamon contains three major compounds (cinnamaldehyde, cinnamyl acetate and cinnamyl alcohol), which are converted into cinnamic acid by oxidation and hydrolysis, respectively. In the liver, this cinnamic acid is β-oxidized to benzoate (10) that exists as sodium salt (sodium benzoate; NaB) or benzoyl-CoA. It has been reported that minor amount of NaB is also excreted in the urine of humans (11, 12). NaB is of medical importance because it is a component of Ucephan, a Food and Drug Administration (FDA)-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia such as urea cycle disorder in children (13, 14). It is also widely used as a preservative in broad range of foods and cosmetic products (15). It is nontoxic and can be administered as a solution in drinking water. It has been reported that 2% solution of NaB in drinking water is safe for lifelong treatment in mice without any noticeable side effects (16). Because Ayurvedic as well as Yunani medicines have been using cinnamon as vital medicines for inflammatory diseases like arthritis for centuries, we were prompted to test the effect of NaB on the expression of proinflammatory molecules in glial cells.

Here we provide the first evidence that NaB attenuates the expression of inducible NO synthase (iNOS) and proinflammatory cytokines in microglia, astrocytes, and macrophages. Although NaB reduced the level of cholesterol in vivo in mice, it was not the cause behind the anti-inflammatory activity of NaB. Alternatively, hydroxymethylglutaryl-CoA (HMG-CoA), mevalonate, and farnesylpyrophosphate reversed NaB-mediated inhibition of iNOS, indicating the involvement of intermediates, but not the end product, of the mevalonate pathway in the anti-inflammatory effect of NaB. Consistently, inhibition of the expression of iNOS and the production of NO by farnesylpyrophosphate transferase inhibitor, suppression of p21ras activation by NaB and induction of iNOS by the activated p21ras alone suggest that NaB exerts its anti-inflammatory effect in glial cells via modulating farnesylation and activation of p21ras. Our findings raise a possibility that NaB, a component of a prescribed drug for human urea cycle disorder and a widely used food preservative, may find further application in neuroinflammatory and neurodegenerative disorders.
 

golder

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Take a look at haidut's first post on his Oxidal thread where he talks about benzoic acid. I have been guided by that.
Thanks. Just to note - Haiduts taken the benzoic acid away in the latest oxidal formula? Any ideas why?
 

SQu

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I don't I'm afraid. It would be good to know. I do remember him saying benzoic acid is very closely related to salicylic acid. A form of which has replaced it? Perhaps it's just another name for it.
 

Mauritio

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Mauritio

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Never got any idea of dosages, so no.
You could just use some ceylon cinnamon as per this post :
Ammonia symptoms are very much like low thiamine - fatigue, inability to sleep well or concentrate on tasks for too long, trouble with short-term memory, etc. Based on the studies I have seen pretty much anybody over the age of 30 has some ammonia problems due to sluggish liver and/or kidneys. You can check by taking some ceylon cinnamon (1g-2g) before going to bed. If you state improves then it's likely ammonia and not low thiamine that is the problem.
 

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