Fatty Liver Support

Endotoxemia and Chlorella

December 14, 2017

Dear Friends

Chlorella HZ 2

Chlorella and inulin reduce endotoxemia and protect the intestinal mucosa barrier.

What is an endotoxin, and what causes endotoxemia? How does chlorella reduce endotoxemia, and how does inulin produce a healthy microbiome?  Let’s take a look at a few studies.

An endotoxin is often used synonymously with LPS.  Lipopolysaccharides (LPSs) are the major components of the outer membrane of Gram-negative bacteria. Rietschel et al. found in 1994 that LPSs induce strong inflammatory responses from the immune systems of all animals.

Liver Diseases are associated with leaky gut syndrome, which allows for the passage LPS molecules into the systemic circulation, causing chronic inflammation, and a condition called endotoxemia. A large enough load of LPSs in the systemic circulations can cause septic shock.

In fact, severe sepsis is a common and frequently fatal condition, with as many deaths annually as those from acute myocardial infarction. It is especially common in the elderly and is likely to increase substantially as the U.S. population ages (Angus et al., 2001)

Bedirli et al. (2009) investigated the role of different microalgae (Chlorella sp. and Spirulina sp.) extracts in intestinal barrier function and oxidative stress in experimentally jaundice rats.

The main outcomes measured were endotoxin concentrations in plasma [e.g. LPS levels], evidence of bacterial translocation in mesenteric lymph nodes and liver oxidative stress, and histology.

Their findings: A Chlorella sp. supplemented diet significantly demonstrated protective effects on the intestinal mucosa barrier in obstructive jaundice, and reduced intestinal translocation of bacteria and endotoxin.  Spirulina had no significant effect.

Original copyCani et al. (2008) found that a high animal fat diet changes the GI tract microbiome into a population of increasing numbers of Gram-negative bacteria, which raises the level of LPS endotoxins within the gut lumen and allows their passing through the GI tract membrane into the plasma.

The research team concluded that the plasma concentration of lipopolysaccharides (LPS) controls the inflammatory tone of the body.  This means that high concentrations of LPS set the stage for endotoxemia, resulting in metabolic diseases (obesity, diabetes, CVD) and cancer.

They further demonstrated in the study that increased fibers in the diet, such as inulin, increase the populations of Bifidobacterial sp. and Lactobacillus sp. which reduce both the load of Gram-negative bacteria and the permeability of the gastrointestinal membrane.

Our Suggestion: Take 4 to 8 tablets of Organic Chlorella daily.
Take 1 tsp. of Original Synbiotic daily.
References:

  • Angus, D. C., Linde-Zwirble, W. T., Lidicker, J., Clermont, G., Carcillo, J., & Pinsky, M. R. (2001). Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Critical care medicine, 29(7), 1303-1310.
  • Bedirli, A., Kerem, M., Ofluoglu, E., Salman, B., Katircioglu, H., Bedirli, N., … & Pasaoglu, H. (2009). Administration of Chlorella sp. microalgae reduces endotoxemia, intestinal oxidative stress and bacterial translocation in experimental biliary obstruction. Clinical nutrition, 28(6), 674-678.
  • Cani et al. (2008). Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat induced obesity and diabetes in mice, Diabetes; 57:1470-8.
  • Rietschel, E. T., Kirikae, T., Schade, F. U., Mamat, U., Schmidt, G., Loppnow, H., … & Di Padova, F. (1994). Bacterial endotoxin: molecular relationships of structure to activity and function. The FASEB Journal, 8(2), 217-225.

Sincerely yours,

Seann

We have developed our products based on scientific research and/or the practical experience of many healthcare practitioners. There is a growing body of literature on food based nutrition and supplements and their application in support of our health. Please use our products under the advisement of your doctor.

Green Facts:

Globe_Home 3
What kind of world do you want to wake up to 30 years from now?
The Biomimicry Institute aspires to a world where what we make is inspired by, and connected to, the natural world.  This means cities are resilient, emission targets are achieved, and industrial processes create healthy air, water, and soil.  It also means all species are thriving because our human designs restore the planet as nature’s desgns do.
 

©2005 – 2017 BioImmersion Inc. All Rights Reserved

Chlorella for fatty liver

November 29, 2017

Dear Friends

Chlorella HZ 2

Can Chlorella supplementation help with Non-Alcoholic Fatty Liver Disease (NAFLD)?

Ebrahimi-Mameghani et al. (2016) sought to answer this question in their study entitled, Glucose homeostasis, insulin resistance and inflammatory biomarkers in patients with non-alcoholic fatty liver disease:  Beneficial effects of supplementation with microalgae Chlorella vulgaris: A double-blind placebo-controlled randomized clincial trail.

The authors researched the effects of C. vulgaris supplementation on glucose homeostasis, insulin resistance and inflammatory biomarkers in patients with NAFLD.

70 non-alcoholic fatty liver disease (NAFLD) patients confirmed by ultra-sonographic findings were randomly assigned into intervention group (four 300 mg tablets of C. vulgaris) or placebo group (four 300 mg tablets of placebos) for 8 weeks.

Anthropometric measurements, liver enzymes, fasting serum glucose (FSG), insulin, high sensitive C-reactive protein (hs-CRP), and tumor necrosis factor-alpha (TNF-a) were assessed and homeostatic model assessment (HOMA) score for insulin resistance was estimated before and after the intervention.

The results show the following:

  • Mean reduction in weight was significantly higher in C. vulgaris- treated group compared to placebo group.
  • Serum concentrations of liver enzymes, FSG and hs-CRP also significantly decreased.
  • Serum insulin concentration and HOMA score increased significantly only in C. vulgaris-treated group (insulin secretion was balanced).
  • Mean change in serum glucose and TNF-a levels were significant between the groups even after adjusting for the serum insulin and baseline values of variables.

The authors conclusion was that L. vulgaris supplementation could be considered as an adjunctive therapy to decrease weight and improve glycemic status and reducing hs-CRP as well as improving liver function in patients with NAFLD.

Take 3 tablets a day, 1500mg of Organic Chlorella, to meet the researched amounts of 1200mg a day.

References:

  • Ebrahimi-Mameghani, M., Sadeghi, Z., Farhangi, M. A., Vaghef-Mehrabany, E., & Aliashrafi, S. (2016). Glucose homeostasis, insulin resistance and inflammatory biomarkers in patients with non-alcoholic fatty liver disease: Beneficial effects of supplementation with microalgae Chlorella vulgaris: A double-blind placebo-controlled randomized clinical trial. Clinical Nutrition; 36(4): 1001-1006.
  • Ebrahimi-Mameghani, M., Aliashrafi, S., Javadzadeh, Y., & AsghariJafarabadi, M. (2014). The effect of chlorella vulgaris supplementation on liver enzymes, serum glucose and lipid profile in patients with non-alcoholic fatty liver disease. Health Promotion Perspectives, 4(1), 107.
  • Care, D. (2007). Insulin sensitivity and insulin secretion determined by homeostasis model assessment (HOMA) and risk of diabetes in a multiethnic cohort of women: the women’s health initiative observational study. Diabetes Care, 30(7), 1747-1752.

Sincerely yours,

Seann

We have developed our products based on scientific research and/or the practical experience of many healthcare practitioners. There is a growing body of literature on food based nutrition and supplements and their application in support of our health. Please use our products under the advisement of your doctor.

Globe_Home 3One bottle of BioImmersions Organic Chlorella contains 120 tablets, with each tablet containing 500 mgs of pure organic chlorella.  Therefore, according to the above researched dose of 1200 mgs per day for NAFLD, the BioImmersion equivalent dose would be three tablets/d.
 

©2005 – 2017 BioImmersion Inc. All Rights Reserved

Weight-Less

September 22, 2017

Dear Friends                                                                                                                                                      WL Low Cropped Jpeg

Recent research has shown the link between chronic hyperglycemia, oxidative stress, and weight gain. Hyperglycemia puts our body into a state of oxidative stress, which leads to many pathologies such as diabetes mellitus, obesity, cancer, and cardiovascular diseases (Domingueti et al., 2016).

Ingredients of Weight-Less per capsule

  • 7-Keto DHEA- 25mg (helps to burn fat)
  • 2 Brown Seaweed extracts- 200mg (help to lower and prevent high blood sugar levels, offers a strong anti-inflammatory, and supports weight loss)

Take 1 – 2 capsules of Weight-less one-half hour before meals, especially important before your carbohydrate (or meat) laden meals.* (See Green Facts on meat and diabetes)

Food Science

The ingredients in Weight-less have been shown to reduce both the states of hyperglycemia and oxidative stress. The Kelp and Bladderwrack polyphenol extracts (phlorotannins) offer organic-certified bioactive ingredients that (1) act on amylase and glucosidase enzymes to optimize post-meal blood glucose and insulin responses and (2) demonstrate that they have a high total antioxidant activity as verified by the Total ORAC 6.0 assay.

The phenols in the kelp and bladderwrack have superior antioxidant activity – a neutralizing effect – on the primary free radical superoxide anion. Superoxide  anion is known as the “mother of  free radicals” because  it also can become a hydroxyl ROS, a nitrogen RNS and a hydrogen peroxide ROS.

Thus, Weight-Less helps prevent post-meal hyperglycemia and has a direct scavenging action on excess free radical generation.  The key is not to totally neutralize all free radical activity but to bring about a healthy redox homeostasis.

References:

  • Domingueti, C. P., Dusse, L. M. S. A., das Graças Carvalho, M., de Sousa, L. P., Gomes, K. B., & Fernandes, A. P. (2016). Diabetes mellitus: The linkage between oxidative stress, inflammation, hypercoagulability and vascular complications. Journal of diabetes and its complications, 30(4), 738-745.
  • Hulsmans, M., & Holvoet, P. (2010). The vicious circle between oxidative stress and inflammation in atherosclerosis. Journal of cellular and molecular medicine, 14(1‐2), 70-78.
  • InterAct Consortium. (2013). Association between dietary meat consumption and incident type 2 diabetes: the EPIC-InterAct study. Diabetologia, 56(1), 47-59
  • Gutowski, M., & Kowalczyk, S. (2013). A study of free radical chemistry: their role and pathophysiological significance. Acta Biochimica Polonica, 60(1), 1-16.
  • Valko, M., Rhodes, C., Moncol, J., Izakovic, M. M., & Mazur, M. (2006). Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-biological interactions, 160(1), 1-40.

Sincerely yours,

Seann

We have developed our products based on scientific research and/or the practical experience of many healthcare practitioners. There is a growing body of literature on food based nutrition and supplements and their application in support of our health. Please use our products under the advisement of your doctor.

Green Facts:

Globe_Home 3High meat intake is also shown in research to generate oxidatative stress and hyperglacemia. We will discuss this in another email but meanwhile, see Dr. Greger’s informative video on Why is meat a risk factor for diabetes?
 

©2005 – 2017 BioImmersion Inc. All Rights Reserved

Fatty Liver

February 9, 2016

Dear Friends

Nonalcoholic fatty liver disease (NAFLD), defined by excessive lipid accumulation in the liver, is the hepatic manifestation of insulin resistance and the metabolic syndrome. Due to the epidemics of obesity, NAFLD is rapidly becoming the leading cause of altered liver enzymes in Western countries (Blachier et al., 2004).   A fatty liver may lead to a fatty pancreas which leads to diabetes (Lichtenstein, Schwab., 2000).

Valenti et al. (2013) explain how steatosis (fatty liver) may be associated with oxidative hepatocellular damage, inflammation, and activation of fibrogenesis, defining nonalcoholic steatohepatitis (NASH).  And, NASH is potentially a progressive liver disease leading to cirrhosis and hepatocellular carcinoma.

Therapeutic Foods support for Nonalcoholic Fatty Liver Disease:
Fatty Liver Protocol 3

  • Blueberry Extract– one daily
  • Phyto Power– two daily
  • Cruciferous Sprouts Complex– two daily
  • Original Synbiotic– one tsp. daily

Food Science:

Anthocyanins decrease hepatic lipid accumulation and counteract oxidative stress and hepatic inflammation (Valenti, 2013; Zhu  et al., 2012; Guo et al., 2011).

Blueberry Extract contains pure anthocyanin extract from Vaccinium corymbosum– a North American blueberry cultivar with an exception broad spectrum of anthocyanins.  It takes us 80 pounds of blueberries to get one pound of this precious extract.

Phyto Power contains four species of wild-crafted Alaskan blueberries (the whole berry), with an exceptionally high concentration of anthocyanins. Plus, it contains the flavonoids of three species of whole wild-crafted rose hips (including seeds) and four species of wild-crafted Alaskan dandelion (including roots, leaves and flowers).  The roots increase liver bile flow.

Dietary supplementation with broccoli sprout extract containing sulforaphane precursor glucoraphanin is likely to be highly effective in improving liver function through reduction of oxidative stress (Kikuchi, 2015).

Cruciferous Sprouts Complex contains broccoli sprouts, daikon radish sprouts, red radish sprouts, water cress sprouts, kale sprouts, mustard sprouts and cabbage sprouts; all together containing high levels of not only glucosinolates, but also high levels of myrosinase (from red radish), the enzymes necessary for high production of sulforaphanes.

The effects of probiotics and prebiotics have proven to be beneficial in NAFLD (Iacono, 2010; Yadav, 2007).

The Original Synbiotic contains 5 pedigreed strains of L. acidophilus, L. rhamnosus, L. plantarum, S. thermophilus and B. longum, plus inulin derived from organic chicory root.

Inulin is very bifidogenic, enhancing the growth of Lactobacillus as well.  These good bacterial produce copious amounts of butyrate upon the fermentation of inulin which facilitate the tightening of gut epithelial cell junctions—reducing leaky gut syndrome.  Delzenne and Kok (1999) demonstrated that FOS, modifying the gene expression of lipogenic enzymes, reduced the de novo liver fatty acid synthesis.

Lactobacillus acidophilus reduced liver oxidative stress and improved insulin resistance (Yadav et al., 2007).  Lactobacillus plantarum reduced liver  and serum cholesterol and triglycerides (Wang et al., 2009).  Lactobacillus rhamnosus reduced hepatic steatosis (Lee 2006).

Bibliography:

  • Blachier et al. (2004). The burden of liver disease in Europe: a review of available epidemiological data. Journal of Hepatology; 58(3): 593-608.
  • Browning et al. (2004). Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity. Hepatology; 40(6): 1387-1395.
  • Delzenne NM, Kok NN. (1999). Biochemical basis of oligofructose3-induced hypolipidemia in animal models. J Nutr; 129: 1467S-1470S.
  • Guo et al. (2011). Anthocyanin inhibits high glucose-induced hepatic mtGRAT1 activation and prevents fatty acid synthesis through PKC. Journal of Lipid Research;52(5): 908-922.
  • Iacono et al. (2010). Probiotics as an emerging therapeutic strategy to treat NAFLD: focus on molecular and biochemical mechanisms. JNB; 22(8): 699-711.
  • Johnson-Henry et al. (2008). Lactobacillus rhamnosus strain GG prevents enterohemorrhagic Escherichia coli 0157:H7- Induced changes in epithelial barrier function. Infect Immun; 76:1340-1348.
  • Kikuchi et al. (2015). Sulforaphane-rich broccoli sprout extract improves hepatic abnormalities in male subjects. World J Gastroenterol; 21(43): 12457-12467.
  • Lee et al. (2006). Human originated bacteria, Lactobacillus rhamnosus PL60, produce conjugated linoleic acid and show anti-obesity effects in diet-induced obese mice. Biochim Biophys Acta; 1761: 736-744.
  • Lichtenstein AH, Schwab US. (2000). Relationship of dietary fat to glucose metabolism. Atherosclerosis; 150(2): 227-243.
  • Valenti et al. (2013). Dietary Anthocyanins as Nutritional Therapy for Non alcoholic Fatty Liver Disease. Oxidative Medicine and Cellular Longevity; Volume 2013:Article ID 145421.
  • Vendrame et al. (2013a). Wild Blueberry (Vaccinium angustifolium)-enriched diet improves dyslipidaemia and modulates the expression of genes related to lipid metabolism in obese Zucker rats. British Journal of Nutrition; 111(2): 194-200.
  • Wang et al. (2009). Effects of Lactobacillus plantarum MA2 isolated from Tibet kefir on lipid metabolism and intestinal microflora of rats fed on high-cholesterol diet. Appl Microbiol Biotechnol; 84: 341-347.
  • Yadav et al. (2007). Antidiabetic effect of probiotic dahl containing Lactobacillus acidophilus and Lactobacillus casei in high fructose fed rats. Nutrition; 23: 62-68.
  • Zhu et al. (2012). The anthocyanin cyaniding-3-O-beta-glucoside, a flavonoid, increases hepatic glutathione synthesis and protects hepatocytes against reactive oxygen species during hyperglycemia: involvement of a cAMP-PKA-dependent signaling pathway. Free Radical Biology and Medicine; 52(2): 314-327.

Yours,

Seann Bardell

We have developed our products based on scientific research and/or the practical experience of many healthcare practitioners.  There is a growing body of literature on food based nutrition and supplements and their application in support of our health.  Please  use our products under the advisement of your doctor.

Green Facts:

Globe_Home 3

Michael Gregor in his educational series shows how saturated fat in the diet causes insulin resistance which leads to fatty muscles leading to fatty liver leading to fatty pancreas leading to diabetes: What Causes Insulin Resistance? and Diabetes as a Disease of Fat Toxicity.