Alternavita Daily© September 2018

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Alternavita Daily

September 20, 2018©

Milk Whey Protein Combats Iron Overload Oxidative Stress And DNA Damage

Whey protein comprises 20 % of total milk protein and it is rich in branched and essential amino acids, functional peptides, antioxidants and immunoglobulins. It provides benefits against a wide range of metabolic diseases.

Protein is the most satiating macronutrient and protein-rich diets are known to exert beneficial effects on body composition and metabolism. Increasing numbers of studies are reporting that the protein fraction in diet is insufficient, creating widespread PEM (Protein Energy Malnutrition). Protein deficiency is a major public health concern.

Whey protein is globular protein its main components are  β-lactoglobulins (35–65 %) and α-lactalbulins (12–25 %). The minor ingredients include immunoglobulins (8 %), serum albumins (5 %) and lactoferrin (1 %). Whey protein is a rich source of branched-chain amino acids (leucine, isoleucine, and valine), essential amino acids (cysteine) and peptides as well. Leucine is abundant (50–75 % higher than other protein sources) and it plays key role in the regulation of skeletal muscle protein synthesis. Whey protein is rich in sulfhydryl amino acid cysteine, a precursor of glutathione, the non-enzymatic thiol antioxidant.

Glutathione plays key role in reducing oxidative stress, regulating cellular processes, an imbalance of which can trigger diseases.

Lactoperoxidase enzymes, glycomacropeptides (12 %) and lactose are other important components of whey.

A broad range of functional properties have been attributed to whey protein and its derivatives, such as:

  • reduction of oxidative stress
  • promotion of muscle growth and lean body mass
  • appetite suppression
  • hyperglycemia
  • cardiovascular risk mitigation
  • phenylketonuria management (cheese whey)
  • protection from ultraviolet (UV) radiation

Inflammatory or oxidative stress begets cystic fibrosis, pneumonia, diabetes, cancer, atherosclerosis, myocardial infarction, aging and a host of other degenerative diseases.

As precursor of the antioxidant glutathione, whey protein is superior in nullifying the adverse effects of oxidative stressors.

  • Whey protein increased lymphocyte glutathione (GSH) in humans.
  • Oral administration of substantive amounts of bovine whey protein enhances the glutathione content in the liver, heart and spleen. This change is moderate but sustained over time and biologically significant.

This property is restricted to the undenatured conforma­tion of whey protein.

Whey protein reversed iron overload-induced DNA damage in leukocytes and colonocytes

The effect of whey protein on oxidative stress was studied. Test animals subjected to iron overload were given placebo or whey protein. After 6 weeks, the iron overload group showed a reduction in radical scavenging capacity with an increase in lipid peroxidation. The concentration of blood glutathione level was significantly higher in the iron overload supplemented with whey group compared to only iron overload group. Iron is a known genotoxic agent, capable of DNA aberration and consequent carcinogenesis. Whey protein reversed the iron overload-induced DNA damage in leukocytes and colonocytes. As the detrimental effect of iron is ROS-mediated, whey protein combatted ROS.

September 14, 2018©

The Gut-Skin Axis

The intestinal microbiome provides important metabolic and immune benefits to the host. Gut flora contribute to the breakdown of indigestible complex polysaccharides and are vital to the production of certain nutritional components. The gut microbiome’s influence on the host immune system is vast, and the relationship is intricately regulated to enable immune tolerance of dietary and environmental antigens and provide protection. The intestinal microbiome protects against invasion by exogenous pathogens directly, by competitively binding to epithelial cells, and indirectly, by triggering immunoprotective responses.

Many human and animal studies stress the the intestinal microbiome’s influence extends beyond the gut, and in fact greatly contributes to the function, and dysfunction, of distant organ systems. The gut microbiome’s influence clearly extends beyond the GI system.

DNA of intestinal bacteria has been successfully isolated from the plasma of psoriatic patients

One distant organ known to have a particularly complex connection with the gut is the skin

In cases of disturbed intestinal barriers, intestinal bacteria as well as intestinal microbiota metabolites have been reported to gain access to the bloodstream and accumulate in the skin disrupting skin homeostasis. DNA of intestinal bacteria has been successfully isolated from the plasma of psoriatic patients. These findings represent evidence of a more direct link between the gut microbiome and skin that has just begun to be explored.

The complex connection between acne and GI dysfunction may also be mediated by the brain, an idea first postulated in 1930. Supporting this hypothesis is the association of both psychological comorbidities – anxiety and depression – and GI distress with various skin disorders. The gut-brain-skin axis hypothesis remained dormant for several decades but has been validated by recent advances in microbiome research and our understanding of its effect on health and disease.

Low levels of acidity allows for the migration of colonic bacteria to distal parts of the small intestine, creating a state of intestinal dysbiosis and small intestinal bacterial overgrowth (SIBO).

The link may originate with GI dysfunction which then leads to psychological and cutaneous disorders. Hypochlorhydria is frequently associated with acne. Low levels of acidity allows for the migration of colonic bacteria to distal parts of the small intestine, creating a state of intestinal dysbiosis and small intestinal bacterial overgrowth (SIBO).

A larger bacterial population competes for nutrients and impairs the absorption of:

  • fats

  • proteins

  • carbohydrates

  • vitamins

Malabsorbed nutrients, including folic acid, zinc, chromium, selenium, and ω-3 fatty acids have been shown to influence one’s psychological state and, along with systemic oxidative stress, have been implicated in the pathophysiology of acne vulgaris.

SIBO also results in the production of toxic metabolites, which can injure enterocytes, increase intestinal permeability, and ultimately lead to systemic inflammation.

SIBO-caused conditions include:

  • irritable bowel syndrome
  • fibromyalgia
  • chronic pelvic pain syndrome
  • chronic fatigue syndrome
  • depression
  • impaired mentation
  • impaired memory
  • halitosis
  • tinnitus
  • sugar craving
  • autism
  • attention deficit/hyperactivity disorder
  • drug sensitivity
  • an autoimmune disease, for example MS or SLE Lupus
  • and Crohn’s disease

 – Cedars-Sinai Medical Center

Various immunodeficiency syndromes, such as IgA deficiency, common variable immunodeficiency, AIDS and others, are complicated by miscellaneous infection complications, including SIBO.

SIBO is often misdiagnosed and generally underdiagnosed. Clinical symptoms might be non-specific (dyspepsia, bloating, abdominal discomfort). Nevertheless, SIBO can cause severe malabsorption, serious malnutrition and deficiency syndromes. Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Infants who are not breastfed are at an early stage with SRB (and with methane-forming bacteria) settled (Baquero et al, 1988;. Hudson, Roberts, 1993).

Infants fed formula are also more likely to develop necrotizing enterocolitis.

September 8, 2018©

Resetting microbiota by Lactobacillus reuteri inhibits autoimmunity 

Regulatory T (T reg) cells maintain immune homeostasis. Forkhead box protein 3 (Foxp3) is a major transcription factor that is associated with T reg cell function. Mutations or deletions of the Foxp3 gene result in IPEX syndrome (immunodysregulation, polyendocrinopathy, and enteropathy, with X-linked inheritance) in humans. Transplantation of donor T reg cells and stem cells is promising, but the procedure is limited by the availability of a suitable donor; and the ultimate outcome can be fatal or associated with chronic health problems.

IPEX syndrome is an autoimmune disease associated with:

  • eczema
  • severe enteropathy
  • type I diabetes
  • thyroiditis
  • hemolytic anemia
  • thrombocytopenia.
  •  inflammatory bowel disease (IBD)
  • onset dermatitis
  • progressive multiorgan inflammation

The life expectancy of patients with IPEX syndrome without hematopoietic stem cell transplant rarely extends beyond infancy.

This study will spur future application of probiotic L. reuteri in many autoimmune diseases, such as IPEX syndrome, many of which are linked to inborn immune defects.

Intestinal microbial dysbiosis related diseases and syndromes

The intestinal microbiota drives host immune homeostasis by regulating the differentiation and expansion of T reg cells. Intestinal microbial dysbiosis can develop as a result of:

  • an abnormal diet (including infant formula)
  •  infection
  • inflammation
  • altered host genetics

Gut microbial dysbiosis can lead to autoimmune diseases including:

  • IBD
  • autoimmune arthritis
  • type I diabetes
  • experimental autoimmune encephalomyelitis (EAE)(mouse model MS)

It is hypothesized that T reg cell deficiency caused by a Foxp3 mutation disrupts the gut microbiota; and T reg cell deficiency–mediated autoimmune disease can be treated by targeting gut microbiota.

Lactobacillus reuteri major component of the gut microbiota

Lactobacillus reuteri is a Gram-positive bacterium that naturally inhabits the gut of mammals and birds. First described in the early 1980s, some strains of L. reuteri are used as probiotics.

In the early 1980s scientists began to find L. reuteri in many natural environments. It has been isolated from many foods, including milk.

Interest in L. reuteri began to increase when scientists found it colonizing the intestines of healthy animals.

A study searching for 18 major species in the gut microbiota, found that L. reuteri was the only species to constitute a “major component” of the Lactobacillus species present in the gut of each of the tested host animals. It is one of the most ubiquitous members of the mammalian gut microbiota.

In a related discovery, each host seems to have a host-specific strain of L. reuteri, e.g. a rat strain for rats, a pig strain for pigs, etc. The universality of L. reuteri, in conjunction with this evolved host-specificity, led scientists to make inferences about its importance in promoting the health of the host organism.

Lactobacillus reuteri DSM17938 is a human breast milk derived probiotic sold by BioGaia.

L. reuteri is marketed by Swedish company BioGaia AB, which owns patents on several strains as well as other patents regarding commercial usage of L. reuteri.

Probiotics have the capacity to not only induce large-scale changes in the host microbiota composition but also modulate the global metabolic function of intestinal microbiomes. Lactobacillus reuteri (L. reuteri) demonstrates beneficial attributes caused by a mutualistic relationship between microbe and host. L. reuteri DSM17938 is effective in treating and preventing diseases that affect infants and children, including:

  • necrotizing enterocolitis
  • diarrhea
  • infantile colic 

L. reuteri modulates the abnormal microbial communities associated with these diseases.

Mechanisms of Lactobacillus reuteri protection against T reg cell deficiency–mediated autoimmunity

T reg cell deficiency shapes gut microbiota and induces autoimmunity resulting in multiorgan inflammation and early death. L. reuteri remodels gut microbiota, alters the metabolites, and protects against T reg cell deficiency–induced autoimmunity by suppressing Th1/Th2 cells via inosine–adenosine A2A interaction.

T cells differ from mast cells, platelets, or macrophages in that T cells express A2A as their main adenosine receptor. A2Aknockout mice data strongly suggest the effects of inosine are dependent on the A2A receptor on T cells. Knockout models provide more solid evidence than in vitro studies with A2A antagonists.

Metabolites produced by bacteria promote or suppress immune cell functions. Microbiota-modulated metabolites accompanying the introduction of L. reuteri into T reg cell–deficient mice may play a critical role in regulating immune responses. We discovered that the purine metabolite inosine is reduced in plasma by T reg cell deficiency and is completely restored by L. reuteri treatment. L. reuteri does not generate large amounts of purine/inosine in culture. Based on the evidence of recovery of plasma levels of inosine we postulate that L. reuteri may promote inosine absorption in the intestine by improving overall gut health through multiple mechanisms (for example by improving villus length) and/or by modulating the gut microbial community. As shown, we measured the small intestinal villi in SF mice compared with SF mice after oral feeding and showed that orally feeding L. reuteri improves the length of villi and depth of crypts. The increased expression of ENT transporters after L. reuteri feeding would also be predicted to correlate with improved absorption.

An enterocyte is a type of cell that absorbs water and nutrients from the digestive tract.  Enterocytes originate inside intestinal glands, or crypts, in the small intestine and colon. In the small intestine, they produce and secrete digestive enzymes, which bind to their brush borders and help break down sugars and proteins, making them smaller and easier to absorb. Enterocytes in the large intestine absorb water and electrolytes.

The wall of the small intestine is arranged into finger-like projections called villi. After being formed inside crypts at the bottom of the villi, enterocytes migrate all the way to the tips, maturing as they go. At the tips of the villi, cell death occurs and the enterocytes are sloughed off into the gut. The life cycle of an enterocyte lasts for only a few days, and in the small intestine the resulting rate of renewal of the lining is more rapid than for any other body tissue. In the colon, there are no villi, but there are crypts where enterocyte formation takes place.

Microvilli on the apical surface increase surface area for the digestion and transport of molecules from the intestinal lumen.

Previous studies demonstrated that inosine treatment reduces levels of inflammatory cytokines produced by LPS-stimulated macrophages in murine models of endotoxic shock. Inosine also attenuates the course of chronic autoimmune inflammatory diseases including type I diabetes and experimental colitis;  in association with a reduction of the production of proinflammatory cytokines and chemokines. Recently, investigators demonstrated antiinflammatory effects of inosine in mouse models of pleurisy and allergic lung inflammation. Our results confirm that inosine is sufficient to inhibit Th1/Th2 differentiation in vitro and autoimmunity in vivo by reducing Th1/Th2 cells and the associated cytokines in SF mice.

This research proposed that the gut environment activates enzymatic functions to help generate more inosine to be absorbed.

In conclusion

In a T reg cell–depleted model (Foxp3-DTR), inflammation in the small intestine of SPF (specific pathogen free) mice was more severe than in GF (germ free) mice, as shown by significantly increased:

  • gut lymphocyte infiltration
  • decreased body weight
  • increased % of IFN-γ–producing T helper cells

indicating that T reg cell deficiency–induced inflammation is related to gut microbiota.

Gut microbiota drives host immune homeostasis by regulating the differentiation and expansion of T cells

The gut microbiota drives host immune homeostasis by regulating the differentiation and expansion of T cells. We found that the development of Th1/Th2-drived autoimmunity was accompanied by microbial dysbiosis over the lifespan of SF mice. When this gut microbial dysbiosis was remodeled by L. reuteri, the autoimmunity was inhibited, as indicated by prolonged survival, reduced multiorgan inflammation, and decreased Th1/Th2 cytokines in SF mice. We have previously observed the same effects of L. reuteri in the setting of experimental necrotizing enterocolitis.

This proof-of-principle study will spur future application of probiotic L. reuteri, inosine, and A2A receptor agonists in other autoimmune diseases, such as IPEX syndrome, many of which are linked to inborn immune defects.

Did you know?

Milk: a postnatal imprinting system stabilizing FoxP3 expression and regulatory T cell differentiation.

Accumulating evidence underlines that milk is a complex signalling and epigenetic imprinting network that promotes stable FoxP3 expression and long-lasting Treg differentiation, crucial postnatal events preventing atopic and autoimmune diseases.

Human breast milk–derived Lactobacillus reuteri DSM17938 (L. reuteri) was provided by BioGaia AB for this research.

Lactobacillus reuteri is also found in many kefir products like Lifeway® kefir

*Note, probiotics are a natural product (no one has ever created an organism), patents are prohibited for natural products, proprietary methods for producing probiotics are not similar to patent prohibition of natural products and should not be equated. BioGaia AB likely gets a royalty for all commercial use of the L. reuteri that they ‘own’, it may influence your decision about research conducted with use their products.
Write your legislator if you feel this is misuse of the patent process which results in a forced payment system as opposed to selling a natural product produced via a proprietary method such as gcmaf (which cannot be patented, proprietary method patented only) or a few other examples, fermented cod liver oil (proprietary method patented only) or Bravo Yogurt™, (name trademarked only). It appears that many ‘probiotic owners’  have made huge profits by claiming ‘ownership’ of a probiotic. See wiki for more examples of common probiotics that have undergone such transformations leading to market confusion and more and more ‘patented’ strains such as those found in Digestive Advantage. 

 

 

 

September 5, 2018©

Fatty Liver and SIBO

Lab animals such as mice and rats have similar effects to humans upon high fructose intake. They are an acceptable model for research of NAFLD (non alcoholic fatty liver disease).

A high-fat diet experimentally induced weight gain in conventional mice but not all of them developed reduced glucose tolerance, hyperinsulinemia, and overt fatty liver. A study revealed that mice developing insulin resistance and fatty liver showed a decreased number of Lactobacilli. These alterations were not observed in mice resistant to diet-induced metabolic syndrome.

Gut microbiota could contribute to the development of fatty liver through the ethanol production. In genetically obese mice breath ethanol tested levels were significantly higher than in lean mice and antibiotic treatment could reduce by 50% the cumulative ethanol production.

Other proposed mechanisms through which gut microbiota could influence the susceptibility to develop NAFLD are the alteration of the choline and the bile acid metabolism.

More recently, the role of fructose-rich diet has been explored: the experimental administration of a 30% fructose solution, for 8 wk, to a group of mice, is associated to the development of hepatic steatosis and a significant increase of hepatic transaminases. The onset of fructose induced-NAFLD is associated with the development of small bowel bacterial overgrowth, increased intestinal permeability, increased circulating endotoxin and the subsequent activation of Kupffer cells mediated hepatic inflammation.

Gut microbiota also exerts a role in the progression from fatty liver to non-alcoholic steatohepatitis (NASH) and the development of hepatic fibrosis. It has been observed that experimentally induced endotoxemia activates hepatic inflammatory response through the recruitment of Kupffer cells by TLR mediated signaling.

Recent studies have underlined the role of cytoplasmic multiprotein complexes, called inflammosomes, in the development of inflammatory liver injury. These inflammosomes are expressed in most liver cells, such as Kupffer cells, liver sinusoidal endothelial cells, periportal myofibroblasts and hepatic stellate cells. The activation of cytosolic inflammosomes, induced by the interaction with LPS or with other microbial antigens coming from bacteria circulating in the portal system, leads to the expression of the pro-inflammatory cascade and modulates hepatic fibrotic tissue deposition.

Although inflammosomes play a critical role in the pathogenesis of liver disease, inflammosome-deficient mice show a more severe hepatic injury and a faster progression to NASH, probably because these cytosolic complexes may contribute to modulate gut microbial composition, and their dysfunction leads to gut dysbiosis.

In conclusion, gut microbiota affects the susceptibility to develop fatty liver and NASH. Bacterial ethanol production, alterations of choline and bile acids metabolism, the stimulation of hepatocytes’ lipogenesis and the development of an increased intestinal permeability leading to metabolic endotoxemia are the main mechanisms involved. The complex interaction between microbial antigens and the cytosolic inflammosomes affects the activation of inflammatory cascade and the development of hepatic fibrosis.

September 4, 2018©

Acute pancreatitis

Acute pancreatitis (AP), a human disease in which the pancreas digests itself, has substantial mortality with no specific therapy.

Exogenous sugar removal does not help acute pancreatitis.

Acute pancreatitis (AP) originates in the exocrine pancreas, where inactive pancreatic proenzymes become prematurely activated inside the pancreatic acinar cells (PACs), digesting the pancreas.

The main causes of AP are:

  • excessive alcohol and fatty food intake
  •  gallstone disease

accounting for about 80% of all cases.

Stimulation of PACs with alcohol metabolites or bile acids (BAs) leads to aberrant calcium signaling due to excessive release from intracellular stores, followed by activation of massive Ca2+ entry through store-operated Ca2+ release–activated Ca2+ (CRAC) channels, causing intracellular Ca2+ overload.

Another cause of AP is treatment of acute lymphoblastic leukemia. According to Cancer Research UK, there were 832 new cases of ALL (acute lymphoblastic leukemia) diagnosed in the United Kingdom in 2015. The incidence rates for ALL are highest in children aged 0 to 4 (2012–2014). Antileukemic drugs based on l-asparaginase are currently used in the clinic as an effective treatment for childhood. However, in up to 10% of cases, the asparaginase treatment has to be truncated due to development of AP, a serious and incurable illness. Although asparaginase-based drugs have been used in the clinic for many years, the mechanism of this side effect has not been well explored and understood.

Galactose was tested for its effectiveness in protection against alcohol- and bile-induced pancreatic pathologies. Galactose very significantly reduced the ATP loss caused by the alcohol metabolites and also essentially prevented the necrosis induced by these agents. Pyruvate had a very similar effect. Both pyruvate and galactose almost entirely eliminated BA (bile acids)-induced necrosis.

Galactose could also be used preventively, which could be of particular importance in cases in which there is a significantly enhanced risk of acute pancreatitis.

Note:

Some genetically susceptible individuals may react badly to milk products but this is considered a very rare occurrence and is usually suspected and confirmed while the subject is very young. Intolerance can develop for many reasons later in life not related to severe inherent genetic problems. Galactosemia is one such genetic enzymatic dysfunction that can be investigated before undertaking any mammal milk therapy. Confirmed severe lactose or casein allergy can also prevent undertaking mammal milk therapeutics. Age related decline in tolerance is not a hindrance in most cases as the human body can recover lost digestive capability and humans can naturally eat a variety of foods. Bovine colostrum is generally not included among most milk intolerance problems but one should ensure avoidance of all mammal milk products if there is potential for a severe outcome due to an inherent, irreversible, genetic or other severe clinically confirmed allergic problem.

General widespread food intolerances, malabsorption and chronic malnutrition can become severe due to extensive intestinal damage such as found in SIBO, IBD and Crohn’s, prognosis is poor in these syndromes with current clinical approaches.

August 25, 2018©

Recap: Milk Proteins And Sugars

Milk serum proteins are defined as substances that remain soluble in milk serum. These proteins are naturally formed during the production of cheese and account for 20% of the all protein in milk, such as:

  • β-lactoglobulins
  • α-lactalbumin
  • immunoglobulins
  • lactoferrin
  • lactoperoxidase
  • glycomacropeptide
  • bovine serum albumin
  • and other proteins

Milk serum proteins are rapidly digested, and raise plasma amino acid concentrations. Therefore, milk serum proteins perform several functions, such as mineral absorption, improvement of protein synthesis, sensitivity to hormones, and decreased blood glucose and lipid levels.

Sweet whey is a byproduct produced during the manufacture of rennet types of hard cheese, like Cheddar or Swiss cheese. Acid whey (also known as sour whey) is a byproduct produced during the making of acid types of dairy products, such as cottage cheese or strained yogurt.

Components And Action Of Whey Proteins On Immune Function

Immunoglobulin (10–15%)

Four classes of immunoglobulins are present in serum: IgG, IgA, IgM, and IgE. It functions as an antioxidant protection and increases immunity.

  • IgM is in the first line of immune system defense.
  • IgA are common antibodies in mucosal areas such as the nose, lungs, eyes and ears. They prevent mucosal infections by causing microbes to agglutinate (clump). In the intestine, IgA is an immunosuppressant that inhibits proinflammatory responses to oral antigens. IgA deficiency is common.
  • IgG antibodies inactivate harmful infectious organisms by binding to them. This reduces or eliminates microbes’ ability to cause illness. IgG binds toxins.

Whey Protein Can Enhance Innate Immunity by Priming Normal Human Blood Neutrophils

Galactose

  • Severely ill diabetic patients have a decreased amount of galactose and sialic acid on their Easy Home Made Yogurtbuccal cells, compared with minimally ill patients and healthy controls.

Galactose has been shown to be a very beneficial sugar that is actually an essential nutrient for the human body.

Milk sugar aka lactose has been shown to be very beneficial for the human body though unlike sucrose, lactose is made up of glucose and galactose. There is no fructose in lactose. It is a healthy disaccharide sugar.

β-galactosidase, also called lactase is important for organisms as a key provider in the production of energy and a source of carbons through the break down of lactose to galactose and glucose. It is also important for the lactose intolerant as many adult humans lack the lactase enzyme, which has the same function of beta-gal, so they are not able to properly digest dairy products.

Kefir grains show β-galactosidase enzyme activity, which stays active when consumed. β galactosidase enzymes found in kefir and yogurt are able to convert gc globulin protein to macrophage activating factors during the fermentation process. β-Galactosidase treatment is a common first-stage modification of the three major subtypes of Gc protein to GcMAF (a popular and effective immune therapy treatment).

Galactose is known as the “brain sugar” and supports brain development of babies and children. Galactose helps triggers long-term memory formation. Galactose has been shown to inhibit tumor growth and stop its spread, particularly to the liver. This beneficial sugar can also enhance wound healing, decrease inflammation, enhances cellular communication, and increases calcium absorption.

  • Of the milk sugars, galactose, but not prebiotic galacto-oligosaccharide (GOS), improves insulin sensitivity. Intake of galacto-oligosaccharides (GOS) improved the gut microbial profile but did not improve insulin sensitivity.

Your Immune System Would Not Be Able To Function Without Galactose

  • Your body wouldn’t know which cells are “good” and what cells are “bad.” Your body wouldn’t know who the invaders were and which ones should be attacked by antibodies.

Acid whey contains more than twice the amount of galactose as ‘sweet’ or ‘cheese whey’ making it a beneficial addition to the control of insulin resistance, diabetes, metabolic syndrome and perhaps obesity.

Alpha-lactalbumin

How does whey protein enhance GSH? Alpha-lactalbumin, a whey protein, contains high levels of cysteine, an amino acid used to make glutathione.

Sulfur amino acids are linked but they are not entirely interchangeable. The bioavailability of cysteine is rate limiting for glutathione synthesis. Cysteine is generally considered a nonessential or dispensable amino acid in adults because it can be synthesized from the essential amino acid methionine. Methionine is central to 1-carbon metabolism, which requires folate, vitamin B12, and choline and is essential for synthesis of the purines, pyrimidines, and polyamines required for nuclear development and function, while cysteine is essential for synthesis of taurine and glutathione, which are involved in immune and antioxidant responses. Methionine can be resynthesized from homocysteine by remethylation, but conversion of cystathionine to cysteine is irreversible.

Alpha-lactalbumin is rapidly digested in the small intestine. Bovine Alpha-lactalbumin is found in bovine colostrum, mammal milk and whey.

Why do we want GSH?

GSH is an extremely powerful internal antioxidant that enhances health in numerous ways.

Glutathione (GSH) is a primary endogenous antioxidant.

  • GSH redox imbalance in brain disorders have been well studied and can be considered as a bio marker.  

GSH depletion and GSH-related enzyme deficit are involved in the pathology of brain disorders such as autism, schizophrenia, bipolar disorder, Alzheimer’s disease, and Parkinson’s disease.

Humans with neurodegenerative and neuropsychiatric disorders have altered levels of GSH and oxidized glutathione (GSSG), decreased ratio of GSH/GSSG and impaired expressions of GSH-related enzymes in the blood or brain. GSH depletion can lead to abnormalities in methylation metabolism and mitochondrial function. Some studies have shown that a GSH deficit occurs prior to abnormalities in these diseases.

Alpha-lactalbumin In Acid Whey

Alpha-lactalbumin is a bioactive milk protein found in acid whey, typically containing 20-25% α-LA. This is nearly equal to that found in human breast milk.

When α-LA is broken down (hydrolyzed) by the body it releases cysteine. Cysteine is a precursor to glutathione (GSH), a vital internal antioxidant. Alpha-lactalbumin has a direct effect on the body. It increases production of serotonin and glutathione. Alpha-lactalbumin increases liver glutathione after strenuous exercise.

  • Whey protein increased lymphocyte glutathione (GSH) in humans.
  • Oral administration of substantive amounts of bovine whey protein enhances the glutathione content in the liver, heart and spleen. This change is moderate but sustained over time and biologically significant.

This property is restricted to the undenatured conforma­tion of whey protein.

  • The administration of glutathione itself is of little consequence on tissue glutathione levels, because it  cannot be transported intact across the cell membrane. Some methods of increasing intracellular levels of glutathione concentration are either toxic or dangerous owing to the risks related to the initial phase of glutathione depletion.

  • Undenatured whey protein of bovine origin increases glutathione in various tissues.

Powdered whey bodybuilding supplements are not un-denatured. The word “denatured” is a biochemical process in which proteins lose their structure.

Only Whey Protein Or Diets That Contain This Protein Improve Antioxidant Function

Whey proteins, when compared with other dietary proteins (ie, soy, casein, or wheat), have been shown to enhance antibody production.

When L. lactis ssp. lactis is added to milk, the bacterium uses enzymes to produce energy molecules (ATP), from lactose. The byproduct of ATP energy production is lactic acid.

Microglial Cells

Microglial cells are the resident macrophages of the central nervous system (CNS), including the retina, and play a pivotal role in innate immune responses and regulation of homeostasis in the healthy and degenerating CNS.
Despite being cells of the mononuclear phagocyte lineage, their CNS-specific location and morphology clearly distinguishes them from other macrophage populations.
  • Acid Whey Reverses Neurodegenerative And Retina Inflammation By Activating CNS Macrophages 

Oleic Acid Is Necessary For Proper Brain Function

What is Oleic Acid?

  • One of the most common fats in human breast milk
  • Makes up 25% of fat in cow’s milk
  • Alpha-lactalbumin joins with oleic acid to fight cancer cells (HAMLET)

Myelin is a protective covering or sheath that twists around nerves (neurons), including nerves in the brain. Myelin is made of 70% fat and 30% protein. Oleic acid is one of the most common fats in myelin.

Oleic acid doesn’t just help synthesize myelin, it is also a cell signaling molecule. Oleic acid regulates cholesterol and lipogenesis (making fat) in the brain.

The ability of whey proteins to increase glutathione concentrations and enhance immunity, along with the discovery of the unique antitumor complex called HAMLET (Human Alpha-lactalbumin Made Lethal to Tumor cells).

  • BAMLET is actually shown to be more effective than HAMLET.

Bovine Alpha-lactalbumin is more effective than Human Alpha-lactalbumin.

Bioactive peptides present in milk whey are one of the most studied compounds in different dairy products. Bioactive peptides from dairy sources are majorly classified on the basis of their biological roles as anti-hypertensive, anti-oxidative, immmuno-modulant, anti-mutagenic, anti-microbial, opioid, anti-thrombotic, anti-obesity and mineral-binding agents. These bioactive peptides are produced by enzymatic hydrolysis during fermentation and gastrointestinal digestion. Thus, fermented dairy products like yogurt, cheese and buttermilk are gaining popularity worldwide and are considered as an excellent source of dairy peptides. Furthermore, these dairy products are also associated with lower risks of hypertension, coagulopathy, stroke and cancer.

Note:

Some genetically susceptible individuals may react badly to milk products but this is considered a very rare occurrence and is usually suspected and confirmed while the subject is very young. Intolerance can develop for many reasons later in life not related to severe inherent genetic problems. Galactosemia is one such genetic enzymatic dysfunction that can be investigated before undertaking any mammal milk therapy. Confirmed severe lactose or casein allergy can also prevent undertaking mammal milk therapeutics. Age related decline in tolerance is not a hindrance in most cases as the human body can recover lost digestive capability and humans can naturally eat a variety of foods. Bovine colostrum is generally not included among most milk intolerance problems but one should ensure avoidance of all mammal milk products if there is potential for a severe outcome due to an inherent, irreversible, genetic or other severe clinically confirmed allergic problem.

General widespread food intolerances, malabsorption and chronic malnutrition can become severe due to extensive intestinal damage such as found in SIBO, IBD and Crohn’s, prognosis is poor in these syndromes with current clinical approaches.

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