Feature: The Gut Liver Axis©


The Gut Liver Axis Is Crucial For Detox

Why is the gut liver axis crucial for health?

The liver has over 500 functions in human metabolism.

These responsibilities include, among others, the formation and secretion of bile, the conversion of monosaccharides to glycogen, glycogenolysis, gluconeogenesis, fatty acid breakdown, recovery and deamination of amino acids, the formation of plasma proteins and gc proteins, vitamin synthesis as well as the detoxification, and excretion of toxic metabolites.

Glycogenolysis is the biochemical breakdown of glycogen to glucose whereas glycogenesis is the opposite, the formation of glycogen from glucose. Glycogenolysis takes place in the cells of muscle, and liver tissues in response to hormonal and neural signals.

NAFLD is one of the most important causes of liver disease worldwide

NAFLD is one of the most important causes of liver disease worldwide and will probably emerge as the leading cause of end-stage liver disease in the coming decades, with the disease affecting both adults and children. The epidemiology and demographic characteristics of NAFLD vary worldwide, usually parallel to the prevalence of obesity, but a substantial proportion of patients are lean. The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy. Furthermore, individuals with NAFLD have a high frequency of metabolic comorbidities and could place a growing strain on health-care systems from their need for management. While awaiting the development effective therapies, this disease warrants the attention of primary care physicians, specialists and health policy makers.

Notable Toxin Producers

A particularly toxic metabolite is ammonia, which is produced once during the bacterial degradation of proteins in the gut and in the degradation of amino acids in the liver itself. Ammonia is degraded in the healthy liver via the urea cycle to urea or detoxified via glutamic acid.

The Small Intestine And The Liver

Bacteria, fungi, and actinomycetes release hydrogen sulfide during the decomposition of sulfur-containing proteins and by the direct reduction of sulfate (SO4 2-).

In the body, H2S must be detoxified by oxidation. While H2S can be produced in large quantities (up to 12 liters per day) by sulfate-reducing bacteria in the colon, it is normally rapidly metabolized by a specialized detoxification system in the colonic mucosa. The small intestine is much less efficient at detoxifying this gas.If the detoxification system is overwhelmed, H2S would escape the gut to enter the portal vein. In the portal vein, a small amount of H2S is detoxified by oxygen bound to hemoglobin. The majority then enters the liver.

Gasotransmitters operate independently of immune receptors. Previously researchers have thought of signaling pathways as entailing a ligand binding to a receptor. However, gases can also trigger signaling cascades in the body. The best known is nitric oxide, or NO, which regulates a host of functions, notably blood pressure. H2S has a high co-morbidity with seizure activity.

A dysfunctional autophagic mechanism leads to chronic intestinal inflammation in IBD.

The maintenance of gut mucosal equilibrium requires a balance between enterocyte loss by apoptosis and the generation of new cells by proliferation from stem cell precursors at the base of the intestinal crypts. Macrophages functions change during infection and inflammation. The intestinal macrophage pool requires continual renewal from circulating blood monocytes, unlike most other tissue macrophages, which derive from primitive precursors that subsequently self-renew.

Neutrophils reside in three different groups, or pools, known as the proliferative, circulating, and marginating pools, with numbers in each influenced by the maturational development of the cell and the individual’s state of health.

The liver has long been recognized as the primary organ of detoxification but, there is now growing evidence that the gut also plays a central role in the detoxification process. Given that the small intestine functions predominantly as an absorptive organ its significance in the metabolism of non-nutritive dietary constituents and xenobiotics seems to have been significantly underestimated. This is in spite of the fact that the small intestine is the first site of xenobiotic exposure and that, over the course of a lifetime, is presented with the largest load of antigens and xenobiotics confronting the human body.

The pathogenesis of the liver manifestation of IBD is related to gut inflammation that results in inflamed portal tracts of the enterohepatic circulation of lymphocytes from the gut to the liver.


Signs Of Liver Damage

1. Unexplained Fatigue

2. Loss Of Appetite

3. Upset Stomach

4. Digestion Issues

5. Urine Color Changes

6. Stool Color Changes

7. Abdominal Changes

8. Fluid Retention

9. Skin Itching

10. Abdominal Ache

11. Constipation, Intestinal Bleeding, Diarrhea

12. Jaundice

The Liver And Gc Protein

The vitamin D binding protein (DBP) was initially discovered as a major liver-derived polymorphic protein and called group-specific component or Gc.

Vitamin D Binding Protein is otherwise know as: VDBP Gc-Protein Glycoprotein Transport protein Gc-Globulin (GcMAF) Serum levels of Gc-globulin are often markedly reduced and the reduction correlates with the severity and the acuity of liver disease, since Gc-globulin concentrations were lowest among patients with ALF (acute liver failure), a condition characterized by massive hepatic necrosis.

  •  Patients with ALF often develop
  •  renal failure
  •  arterial hypotension
  •  severe infections
  • and occasionally pulmonary dysfunction

The most feared complication in ALF is the development of cerebral edema and intracranial hypertension. Liver failure is also associated with MOD (multi organ dysfunction).

In general, total Gc-globulin levels are decreased in all patients with hepatotoxicity. Patients with ALF have total Gc-globulin concentrations of approximately 100 mg/L which is less than one third of normal values.

In the industrialized countries large proportions of the population are chronically ill with some form of liver failure, including acute and chronic hepatitis, fatty liver and cirrhosis.

Hepatitis includes all hepatocellular diseases associated with an inflammatory response of the liver tissue due to viral and bacterial infections and/or drug associated or alcohol poisoning. When inactive only a moderate hepatocellular insufficiency occurs.The active form is characterized by dystrophic acute relapses or severe liver cell insufficiency up to the pre-coma or coma.In its most severe form, decompensated cirrhosis of portal hypertension, esophageal varices, and ascites is observed. The collapse of the liver features death which usually occurs by bleeding from Esophageal varices or coma.

Esophageal varicesare enlarged veins in the lower esophagus. They’re often due to obstructed blood flow through the portal vein, which carries blood from the intestine and spleen to the liver.

Portal encephalopathy occurs due to intoxication with ammonia and other breakdown products of proteins. Other neurological and psychopathological disorders that manifest themselves can be depression, fatigue, lack of energy or loss of consciousness up to hepatic coma. 30 to 40% of liver cirrhosis sufferers die in hepatic coma.

Acute liver failure (fulminant hepatic failure) and prognosis

It is safe to say that acute liver failure (ALF) is one of the most dramatic conditions in medicine. The failing liver leads by definition to hepatic encephalopathy within a short time after initial symptoms and may also lead to a cascade of organ failures including renal failure, circulatory collapse, and pulmonary dysfunction. Further, severe infections, deep coagulopathy, and the risk of cerebral edema, intracranial hypertension, and cerebral herniation adds to the picture of an extreme disease entity. Not surprisingly, the mortality rate in ALF has historically been very high, with survival being the exception to the rule.

The global prevalence of NAFLD is currently estimated to be 24%.

What effective supplement can you use to help detoxify the liver?


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Malnutrition  is the leading cause of death worldwide in children under the age of five, and is the focus of the first World Health Organization (WHO) Millennium Development Goal. Breastfeeding, food and water security are major protective factors against malnutrition and critical factors in the maturation of healthy gut microbiota, characterized by a transient bifidobacterial bloom before a global rise in anaerobes. Early depletion in gut Bifidobacterium longum, a typical maternal probiotic, known to inhibit pathogens, represents the first step in gut microbiota alteration associated with severe acute malnutrition (SAM). Later, the absence of the Healthy Mature Anaerobic Gut Microbiota (HMAGM) leads to deficient energy harvest, vitamin biosynthesis and immune protection, and is associated with diarrhea, malabsorption and systemic invasion by microbial pathogens. A therapeutic diet and infection treatment may be unable to restore bifidobacteria and HMAGM. Besides re-feeding and antibiotics, future trials including non-toxic missing microbes and nutrients necessary to restore bifidobacteria and HMAGM, including prebiotics and antioxidants, are warranted in children with severe or refractory disease.