Multiple Chemical Sensitivity Etiology
Airway Genetics and Ambient Combustion Aerosol
Endotoxemia: sugar, oil, refined flour
Journal of Chiropractic Humanities
Toxins, Toxicity, and Endotoxemia: A Historical and Clinical Perspective for Chiropractors
Abstract
Body toxicity has been viewed as a health risk since the time of ancient Egypt, when it was believed that stool putrefaction would lead to systemic disease.1 The ancient Greek humoral theory of disease extended the concept of putrefaction to bile, phlegm, blood, and residues of food. In the late 1800s, Metchnikoff hypothesized that intestinal toxins shortened lifespan.1 Modern medicine embraced toxicity until at least the 1920s, when a colectomy was viewed as a cure for autointoxication.1 Clearly, the notion of “body toxicity” as a health risk for disease development has been part of patient care for a long time. It therefore might be expected that various sectors of health care, and individuals within health care, might still embrace and promote the issue of body toxicity as a treatment target.
The purpose of this commentary is to discuss the issue of toxicity in the context of chiropractic practice, including Daniel David Palmer’s impression of toxicity, a consideration of toxicity regarding the liver and colon, bacterial endotoxemia, and a rational approach to dietary detoxification in the context of addressing bacterial endotoxemia.
Toxins From the Perspective of Early Chiropractic History: Daniel David Palmer
The notion that toxins are related to chiropractic and subluxation is attributed to Palmer. Chiropractors routinely cite Palmer in this regard: “In his 1910 text, The Chiropractor’s Adjuster, DD Palmer identified the causes of vertebral subluxation as the Three T’s—thoughts, trauma and toxins.”2 Although this statement is commonly attributed to Palmer, did he actually mention the so-called 3 T's?
Senzon explains that “thoughts, trauma, and toxins have been described for years as the three
Toxicity of the Colon in Relation to Chiropractic Practice
Colon cleansing for the purpose of reducing intestinal toxicity and improving systemic health was popularized by a DC, Bernard Jensen, who wrote a text titled Tissue Cleansing Through Bowel Management.10 The 1-week cleansing process involved taking several doses of psyllium husk powder per day, consuming vegetable broths, and supplementing with chlorella. The ingested psyllium is claimed to remove built-up toxic debris, aided by a daily colema, which is a variation of an enema and colonic.
Toxicity of the Liver in Relation to Chiropractic Practice
The liver has also been targeted as an organ in need of detoxification to help reduce chronic fatigue, food allergies, migraine headaches, fibromyalgia, and generalized arthralgias, which are common presentations in chiropractic practice. Practitioners in both the medical and chiropractic professions are guilty of embracing the concept of liver toxicity, despite the lack of scientific evidence. To date, no studies have ever identified specific toxins in the liver that are detoxified by a
Bacterial Endotoxin in Relation to Chiropractic Practice
As outlined earlier, the issue of toxicity as a cause of spinal dysfunction, and as an intestinal and liver condition, is of therapeutic interest to DCs. The general topic of body cleansing and detoxification also appears to be of great interest to the general public. A Google search performed on June 20, 2016, using the phrases “detox diet” and “body detoxification” resulted in 13 100 000 and 12 900 000 results, respectively. The challenge thus far, from a scientific and clinical perspective, is
Measuring Bacterial Endotoxin Levels
Although assessing bacterial endotoxin levels is performed in the research setting, a clinical laboratory test is not available. This should not dissuade clinicians from embracing endotoxin as a candidate toxin in need of detoxification for a few reasons. First, as described earlier, we know that the consumption of refined sugar, flour, and oil leads to postprandial low-grade endotoxemia that has been measured in the clinical research setting.37, 38, 39 In other words, a patient who regularly
Managing Bacterial Endotoxin by Detoxifying the Diet
As described earlier, circulating levels of bacterial endotoxin are directly influenced by diet. Sugar and flour serve to promote bacterial growth, which has been referred to as an inflammatory microbiota.31 Thereafter, the consumption of refined carbohydrate and lipid calories from refined oils and animal products will stimulate the release of endotoxin from small intestine gram-negative bacteria, leading to the development of systemic low-grade endotoxemia and related low-grade chronic
Hepatology, VOL. 73, NO. 6, 2021 Steatohepatitis/Metabolic Liver Disease
Fructose Promotes Leaky Gut,
Endotoxemia, and Liver Fibrosis Through
Ethanol-Inducible Cytochrome
P450-2E1–Mediated Oxidative
and Nitrative Stress
Young-Eun Cho,1,2* Do-Kyun Kim,3
* Wonhyo Seo,4
Bin Gao,4
Seong-Ho Yoo,5
and Byoung-Joon Song1
Fructose intake is known to induce obesity, insulin resistance, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). We aimed to evaluate the effects of fructose drinking on gut leakiness, endotoxemia, and NAFLD and study the underlying mechanisms in rats, mice, and T84 colon cells.
Levels of ileum junctional proteins, oxidative stress markers, and apoptosis-related proteins in rodents, T84 colonic cells, and human ileums were determined by immunoblotting, immunoprecipitation, and immunofluorescence analyses. Fructose drinking caused microbiome change, leaky gut, and hepatic inflammation/fibrosis with increased levels of nitroxidative stress marker proteins cytochrome P450-2E1 (CYP2E1), inducible nitric oxide synthase, and nitrated proteins in small intestine and liver of rodents. Fructose drinking significantly elevated plasma bacterial endotoxin levels, likely resulting from decreased levels of intestinal tight junction (TJ) proteins (zonula occludens 1, occludin, claudin-1, and claudin-4), adherent junction (AJ) proteins (β-catenin and E-cadherin), and desmosome plakoglobin, along with α-tubulin, in wild-type rodents, but not in fructose-exposed Cyp2e1-null mice.
Consistently, decreased intestinal TJ/AJ proteins and increased hepatic inflammation with fibrosis were observed in autopsied obese people compared to lean individuals. Furthermore, histological and biochemical analyses showed markedly elevated hepatic fibrosis marker proteins in fructose-exposed rats compared to controls.
Immunoprecipitation followed by immunoblot analyses revealed that intestinal TJ proteins were nitrated and ubiquitinated, leading to their decreased levels in fructose-exposed rats.
Conclusion: These results showed that fructose intake causes protein nitration of intestinal TJ and AJ proteins, resulting in increased gut leakiness, endotoxemia, and steatohepatitis with liver fibrosis, at least partly, through a CYP2E1-dependent manner. (Hepatology 2021;73:2180-2195).
Sub-noxious Intravesical Lipopolysaccharide Triggers Bladder Inflammation and Symptom Onset in A Transgenic Autoimmune Cystitis Model: A MAPP Network Animal Study
1Abstract
Patients with interstitial cystitis/bladder pain syndrome (IC/BPS) can potentially develop symptom flares after exposure to minor bladder irritants such as subclinical bacterial infection. To reproduce this symptom onset, we intravesically instilled a sub-noxious dose of uropathogenic E. coli component lipopolysaccharide (LPS) in young URO-OVA/OT-I mice, a transgenic autoimmune cystitis model that spontaneously develops bladder inflammation at ≥10 weeks of age.
Female URO-OVA/OT-I mice (6-weeks old) were treated intravesically with phosphate-buffered saline (PBS) or PBS containing a sub-noxious dose (1 μg) of LPS. Mice were evaluated for bladder inflammation, pelvic pain, and voiding dysfunction at days 1, 7, and 14 post-treatment. Mice treated with LPS but not PBS developed early bladder inflammation with increased macrophage infiltration. Accordingly, the inflamed bladders expressed increased levels of mRNA for proinflammatory cytokines (IL-1β and IL-6) and pain mediator (substance P precursor). In addition, LPS-treated mice exhibited pelvic pain and voiding dysfunction such as increased urinary frequency and reduced bladder capacity. These functional changes sustained up to day 14 tested. Our results indicate that a single sub-noxious dose of intravesical LPS triggers early bladder inflammation and symptom onset in URO-OVA/OT-I mice, providing a useful model for IC/BPS symptom flare study.
Multiple Chemical Sensitivity: 2021 Consensus Criteria
Baseline, Diagnosis, Patient Rights, Etiology - 4 Parts:
II. Diagnosis, Patient Rights, Etiology
III. Baseline: Nutrition and Exercise
IV. Baseline: Nutrition and Exercise
22. Fructose Lipogenesis
There are potential difficulties in replacing SJF: multiple units of glucose (not sweet tasting) - preferred fuel blood sugar - make up the starch of whole grain, metabolized with insulin release and a temporary rise in blood glucose and triglycerides; on contrast glucose as a simple sugar and fructose (recognized by its sweetness) - or in combination as sucrose, such as in white table sugar, sweetened beverages, and fruit juice - even at low to moderate consumption are shown to impair glucose and lipid metabolism, increase inflammation - and fructose intake is an independent predictor of a proatherogenic increase of smaller LDL particles (Aeberli 2011, 2007).
Excessive fructose (10% of US calories, 20% among America's youth), high fat, and refined grain of SJF - action on bacterial flora, even if not in a weight gain situation may result in alteration or bloom of bacteria, lower scores on tight junction protein measures, impacts on intestinal wall integrity, increase in microbrial translocation (MT) from the gastrointestinal tract to the liver - endotoxemia - high plasma endotoxin concentrations (inflammatory cell wall components of gram negative bacteria) involving soluble CD-14 LPS (lipopolysaccharide endotoxin) receptors and LPS binding protein (LBP-1), large elevations in c-reactive protein and liver enzymes: alanine transferase, alkaline phosphatase, and y-glutamyl transpeptidase; LPS overwhelming local and innate immune mechanisms reaching kupffer (liver macrophages) and non immune liver cells producing periportal inflammatory infiltrates - liver damage - which if accompanied by extra calories leads to Hepatic Steatosis (HS) - today's epidemic of nonalcoholic fatty liver disease (NAFLD) afflicting nearly 1/3 of the US population - fructose participation in lipogenesis, unlike glucose, not involving insulin - fructose 90% uptake by the liver promoting insulin resistance adversely affecting glucose metabolism disposing to the development of type 2 diabetes and cardiovascular disease (Kavanagh 2013, Hellerstein 2012).
Fructose - small amounts okay in nutritious vegetables such as kale, brussels sprouts, cauliflower; but high in fructose low in nutrients, fruit becomes the junk food of a good diet; not bad as SJF, fruit now and then better than starving in a pinch; fructose is 75% of calories apple, 50% grape and orange, 25% of calories bananas.
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