DHEA therapy has provided benefit in autoimmune disease. IN this study they review the previous articles and physiology behind DHEA's proposed benefit in autoimmune disease.
Don't get to excited about this article. It is just a meta-analysis. Second, they looked at BMI and BMI is a notoriously bad estimater of muscle mass versus fat content. I am the perfect example, my BMI has me as obese, yet my measured fat % is 16%.
My read on this, is most of the individuals that are "overweight" are actually at a health weight with a higher muscle mass percentage not picked up with the BMI measurement.
This study finds most "western" diseases are the result of environment and only <5% genetic. Evidence is growing that the environment is the largest contributor to disease. The greatest environment contributor is diet. This is great, because we can change diet...if one wants too.
This article also shows are current understanding on how dietary inflammation results in insulin/glucose disruption.
great review article on the relationship between gut dysbiosis and type I diabetes--particularly the bacteroidetes and Veillonella species; in contrast, Prevotella and Akkermansia special protects and maintains a healthy gut epithelium.
A study by Bosi and colleagues suggested that the increased gut permeability preceded the clinical onset of T1D
gut permeability may be an important player in the development of T1D but, as yet, the findings in human studies have shown association but causation will be more difficult to prove.
Early childhood (≤ 3 month) introduction to cereals [10, 11] and cow's milk [48] were shown to promote beta cell autoimmunity
These findings suggest that prebiotics and probiotics could be potential therapeutic tools to improve gut integrity in various intestinal inflammatory and autoimmune diseases including T1D
review article of anti-inflammatory effects of Boswellia. Boswellia inhibits 5-LOX and resultant leukotrienes. 3-actyl-11-keto-Beta-boswellic acid is the most potent inhibitor of 5-LOX. As it relates to disease states and symptoms, Boswellia reduces pain in OA and RA. Boswellia also shown to inhibit NF-kappa B: a potent nuclear transcription factor for inflammation. In prostate cancer, Boswellia inhibits prostate tumor growth.
Mycotoxins deplete glutathione production and this depletion of glutathione is a portion go the toxicity/ill effects related to mycotoxins. This article also points to evidence that glutathione can actually be employed in the treatment of mycotoxin related conditions/illnesses.
The starting dose was 500 mg/day and if no toxicity was noted, the dose was then escalated to another level in the order of 1,000, 2,000, 4,000, 8,000, and 12,000 mg/day. There was no treatment-related toxicity up to 8 g/day but the bulky volume of the drug was unacceptable to the patients beyond 8 g/day.
The serum concentration of curcumin usually peaked at 1 to 2 hours after oral intake of curcumin and gradually declined within 12 hours
PUFA shown to effect GI bacterial balance. Altering adhesion of lactobacillus to intestinal surface. Also, lactobacilli species shown to alter PUFA metabolism in GI. This article reveals the effect that diet can have on GI bacterial balance.
acute GC secretion during stress mobilizes peripheral amino acids from muscle as well as fatty acids and glycerol
from peripheral fat stores to provide substrates for glucose synthesis by the liver
chronically elevated GC levels
alter body fat distribution and increase visceral adiposity as well as metabolic abnormalities in a fashion reminiscent of
metabolic syndrome
This local production may
play an important role in the onset of obesity and insulin resistance.
In adipocytes, cortisol inhibits lipid mobilization in the presence of insulin, thus leading to triglyceride accumulation
and retention.
Since the density of GC receptors is higher in intra-abdominal (visceral) fat than in other fat depots, the
activity of cortisol leading to accumulation of fat is accentuated in visceral adipose tissue (24, 158), providing a mechanism by which excessive endogenous or exogenous GC lead to abdominal obesity and IR
obese patients generally have normal or subnormal
plasma cortisol concentrations
This may be explained by an increased intratissular/cellular concentration of cortisol in adipose tissues
Intracellular GC may be produced from recycling of GC metabolites such as cortisone in adipose tissues
Local GC recycling metabolism is mediated by 11β-hydroxysteroid dehydrogenase enzymes (11β-HSD1 and 11β-HSD2
Cortisol also increases 11β-HSD1 expression in human adipocytes
In humans, elevated 11β-HSD1 expression in visceral adipose tissue is also associated with obesity
even if obese patients generally have normal or subnormal plasma cortisol concentrations
(131, 158), triglyceride accumulation in visceral adipose tissue may be due, at least in part, to the local production of GC in insulin-
and GC-responsive organs such as adipose tissue, liver, and skeletal muscle