The benefits of milk are substantial especially in cultures where malnutrition contributes to unfavorable outcomes in common co-morbidities like diarrhea.
This article highlights the slippery slope at which one risk factor contributes to another, namely the combined risk factors of poor sanitation compounded by malnutrition and acceptance of formula or feeding replacements (cereal) in lieu of mammal milk. This leads to further food intolerances, allergies, bone deformation and other later in life consequences that begin to appear as the result of compound interest so to speak. Asian countries come to mind, namely Japan.
I would invite you to read critical info below regarding immune function of mammals and the importance of galactose as an essential contributor to immune health and development as mammals are the only producers of lactose and there is no such thing as a genetic predisposition toward the rejection of being a mammal despite chromosomal mutations in some populations as milk helps restore critical immune function even in the elderly. In other words you never outgrow the biological significance of the benefits of milk sugars, namely lactose.
By the way…. The Genome Project has established that the Ashkenazi Jews are a Turkic race so they’re not Semitic, therefore there is no such thing as anti semitism toward this particular ‘genetic’ group. Similar to ‘mammalian rejection’ or other forms of ‘genetic or biological determinism’… a non starter. People assign far too much weight or importance to genetics. This has been shown repeatedly when specific or unique environmental factors produced similar impact on worldwide populations.
Malnutrition Contributes To Lactose Intolerance
More than 10 million cases and more than 1000 deaths are reported every year due to diarrhea in India. There are many risk factors behind this large number of cases, but almost 90% are attributed to unsafe drinking water, poor sanitation and poor hygiene. In developing countries, mortality rates are further exacerbated by the vicious cycle between malnutrition and infection, the lack of adequate health care and transport facilities and other factors like lactose intolerance.
Diarrhea is the one of the leading cause of childhood morbidity and mortality in India. Diarrhea damages the intestinal mucosa which consequently causes transient lactase deficiency and causes lactose intolerance.
Some of the factors influencing lactose intolerance were studied. Lactose intolerance was more common in cases with malnutrition. The results were statistically significant and correlated with the severity of malnutrition. Lactose intolerance is positively correlated with nutritional status.
Severe malnutrition can lead to intestinal atrophy and subsequently lactose intolerance. In a systematic review and meta-analysis Matilda A. Kvissberg et al., reviewed 20 studies relating to nutritional status and carbohydrate intolerance. They concluded that carbohydrate malabsorption including lactose intolerance was prevalent in cases with acute malnutrition.
The majority of infants and babies with malnutrition related malabsorption can continue to tolerate dietary carbohydrates, including lactose.
Lactose intolerance may be a clinical syndrome of 1 or more than 1 of the following symptoms: abdominal pain, diarrhea, nausea, flatulence, and/or bloating when lactose or lactose-containing food substances are taken. Lactose malabsorption: Lactose malabsorption is the physiological problem manifested as lactose intolerance due to an imbalance between the amount of lactose absorbed and the potential of lactase to hydrolyse the disaccharide.
Lactose malabsorption is the physiological problem manifested as lactose intolerance due to an imbalance between the amount of lactose absorbed and the potential of lactase to hydrolyse the disaccharide. Primary lactase deficiency It is due to the relative or absolute absence of lactase, developing in different age groups of childhood and in different race groups and is the most common cause of malabsorption and lactose intolerance. Primary lactase deficiency is also referred to as adult type hypolactasia, lactase non-persistence or hereditary lactase deficiency.
Lactose is a disaccharide only found in mammalian milk. If lactose is ingested, it cannot be used as such, it must first be hydrolyzed into the sugar glucose and galactose.
During digestion, it is hydrolysed into monosaccharide’s glucose and galactose by the enzyme lactase. Lactase is formed in the brush border of enterocytes on the villous tip of small intestine. Affected expression of lactase producing gene or affected intestinal mucosa form the major patho-physiological processes causing lactose intolerance.
Lactose intolerance is a form of carbohydrate malabsorption caused by lactase deficiency. Lactase is one of the b –galactosidases seen in the small bowel, it is most active in jejunum. During digestion lactose is hydrolysed into 2 monosaccharides: glucose and galactose. After hydrolysis, galactose and glucose are actively absorbed from the gut, but they have separate mechanisms in the mucosa. Galactose is absorbed somewhat more efficiently than glucose. Galactose is metabolized mainly in the liver via the Leloir pathway to glucose. This route is very efficient because half of the galactose administered reaches the body’s glucose pool within 30 minutes.
Lactose metabolism in normolactasia
In normolactasia, the activity of lactase remains until adulthood and enables people to consume large quantities of milk without abdominal discomfort.
Lactose metabolism in hypolactasia
In primary adult type hypolactasia, lactase activity has decreased to about 10 percent of normal levels in infants. The age at which this decline occurs varies between two years in Thais and 10 to 20 years in Finns. The low enzymatic activity is caused by a reduced amount of lactase protein, not because the enzyme in the mucosa changes into an inactive form.
The speed and efficiency of lactose metabolism in the intestine is not only determined by lactase activity on a small intestinal mucosa, but also by a number of other factors:
• the amount of lactose in the intestine
• the speed of emptying the stomach and intestinal passage
• the ability of the intestinal microflora to ferment lactose
• the reaction of the large intestine to the osmotic stress
Microbial decomposition of lactose Micro flora contributes to the absorption of lactose in malabsorbers. Only some of the intestinal microflora, but not all, can ferment lactose.
Primary lactase deficiency It is due to the relative or absolute absence of lactase, developing in different age groups of childhood and in different race groups and is the most common cause of malabsorption and lactose intolerance. Primary lactase deficiency is also referred to as adult type hypolactasia, lactase non-persistence or hereditary lactase deficiency.
Secondary lactase deficiency
Secondary lactase deficiency is a lactase deficiency that results due to small intestine injury, caused by diseases such as acute gastroenteritis, persistent diarrhea, small intestine overgrowth, cancer chemotherapy or other causes of damage to the small intestine mucosa and may be present at any age, but more is common in infancy.
Secondary lactase deficiency can be found in celiac disease, crohns disease and other enteropathies.
Causes of secondary lactate deficiency:
• Acute gastroenteritis
• Celiac disease
• Intestinal irradiation
• Antimetabolite therapy
• Intestinal resection
• Inflammatory bowel disease
• Cow’s milk allergy
Congenital lactase deficiency
Congenital lactase deficiency is extremely rare. Before the 20th century, children with congenital lactase deficiency cannot be expected to be able to survive when no easily accessible and nutritionally sufficient lactose – free breast milk substitute was available.
Developmental lactase deficiency
Developmental lactase deficiency is now defined as the relative lactase deficiency observed among pre-term infants of less than 34 weeks’ gestation. Although some studies noted that feeding preterm infants with lactase supplemented or lactose free feeds may be beneficial no long term deleterious effects were documented in those fed with lactose containing feeds or breast milk. Bacterial lactose metabolism reduces fecal pH, and now has a beneficial effect, favoring certain organisms (e.g. Bifidobacterium and Lactobacillus species) in young infants instead of potential pathogens (Proteus species, Escherichia coli and Klebsiella species).
About 70% of the world’s population has a primary deficiency of lactase. The percentage varies with ethnicity and is related to the use of dairy products in the diet, causing the genetic selection of persons with the ability to digest lactose.
In populations with dominance of milky foods in the diet, the mostly northern European population has a primary lactase deficiency of only 2 percent of the population. Contrast to this, the prevalence of primary lactase deficiency in Hispanic people is between 50% and 80%, in black and Ashkenazi Jews 60% to 80% and in Asian and American Indians nearly 100%.
The age and prevalence of the onset differentiate between different populations. Approximately 20 percent of Hispanic, Asian and black children under 5 years of age have lactase deficiency and lactose malabsorption, while white children do not typically develop lactose intolerance symptoms until after 4 or 5 years of age. However, most of the individuals show clinical symptoms in late adolescence or adulthood.
Limiting the lactose to a level that is tolerated is the main strategy of management and is tailored to each individual because lactase deficient individuals vary in the amount of lactose that is tolerated. However, those having primary lactase deficiency and no small intestine injury can consume at least 12 grams of lactose per sitting without symptoms, or with only mild symptoms. It is tolerated even better if consumed throughout day in divided portion.
Severe malnutrition can lead to intestinal atrophy and lactose intolerance. Research concludes that carbohydrate malabsorption including lactose intolerance is prevalent in cases with acute malnutrition. In developing countries diarrhea mortality rates are exacerbated by the cycle of malnutrition and lactose intolerance.
• Acute diarrhea is one of most common cause of admission in children with varied causations and outcomes.
• Lactose intolerance is very common in cases with acute diarrhea and is often underemphasized.
• Treatment of lactose intolerance with low lactose feeds has the potential for speedier recovery and improved outcomes in cases with diarrhea.
• By improving the nutritional status, the morbidity associated with diarrhea can be curtailed.
• There is a need for considering lactose intolerance in formulating better diarrhea treatment guidelines in India.
Alternavita: All you need to know (critical info in a nutshell)..... by focusing exclusively on these foundational health and immune development issues up to 90% of chronic conditions can be eliminated.
WHO STATEMENTS: 2017 Millennium Goal
- food (security)
- and water security (sanitation)
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.
Researchers found that malnourished children’s microbiota failed to follow the healthy pattern they identified in healthy children. The microbiota of malnourished children is immature, lagging in development behind that of their healthy peers. Supplementing these children’s meals with widely used therapeutic foods that increase calories and nutrient density reduces deaths from malnutrition, but it does not fix their persistent microbiota immaturity.
“Perhaps more insidious than slowing growth is malnutrition’s effect on less visible aspects of health, including impaired brain development and dysfunctional immunity, which follow these children throughout their lives”.
The Father of The Microbiome
Dr. Jeffrey Gordon
SIBO can cause severe malabsorption, serious malnutrition and immune deficiency syndromes in children (non breastfed) and adults.
Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.
The WHO recommends that immunization or treatment be orally administered due to economic, logistical and security reasons. Furthermore, this route offers important advantages over systemic administration, such as reducing side effects, as the molecules are administered locally and have the ability to stimulate the GALT immune responses (Levine and Dougan, 1998; Neutra and Kozlowski, 2006; Bermúdez-Humarán et al., 2011).
For ANY infectious or parasitic disease to start, it is ALWAYS a requisite that the host suffer IMMUNODEFICIENCY. At the same time, infectious and parasitic diseases themselves cause additional IMMUNE SUPPRESSION and more MALNUTRITION. This immune suppression is SECONDARY to the accumulation of free radicals, especially oxidizing species, that occurs during and after infectious and parasitic diseases.
Clinical Aspects of Immunology and Biochem J.
Current IBD Research 2016
Currently available treatments for IBD, which target the systemic immune system, induce immunosuppression, thereby exposing the patient to the risk of infections and malignancy. The interplay between the gut and the systemic immune system determines the final effect on target organs, including the bowel mucosa. Inflammatory bowel diseases (IBD) are associated with an altered systemic immune response leading to inflammation-mediated damage to the gut and other organs.
Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel
Most importantly, the immune modulatory agents used today for IBD do not achieve remission in many patients.
Not all IBD patients benefit from currently available drugs. Young people with IBD do not want to be on long-term drug therapy. Oral immune therapy, while not yet studied in large cohorts of patients, may provide an answer to this unmet need.
Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel
Tolerance is the ability of the immune system to ‘see’ and respond appropriately. Without galactose (a necessary sugar) the immune system can not 'see'. 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. As you will learn the importance of these ‘sugars’ in gut microbiota health is a rapidly expanding field of research, only recently
discovered, including HMO's (human milk oligosaccharides).
Why galactose? 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. 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.
What does immune ‘tolerance’ mean in simple language?
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. The Th1 cytokine profile is vital for clearance of certain organisms and ancillary immune activity, and a limiting effect on this cytokine profile may result in reduced chances for overcoming infections especially intra-cellular organisms residing within macrophages. Effective clearance will depend on appropriate macrophage activation (which occurs through IFN≥ release by Th1 and NK cells) and production of nitric oxide. If this pathway is disrupted IFN≥ secretion is blocked, impairing macrophage activation. Persistent blockade of these inhibitory receptors has lead to the breakdown in immune self tolerance, thereby increasing susceptibility to autoimmune or auto-inflammatory side effects, including rash, colitis, hepatitis and endocrinopathies. Many drugs may cause checkpoint blockade toxicity including pharmaceutical drugs termed ‘immuno therapy’ by pharmaceutical companies, these include Mab drugs and cancer treatments. Checkpoint Inhibitor–Induced Colitis: A New Type of Inflammatory Bowel Disease? Madeline Bertha, MD MS, corresponding author1 Emanuelle Bellaguara, MD, Timothy Kuzel, MD, and Stephen Hanauer, MD ACG Case Rep J. 2017; 4: e112. Published online 2017 Oct 11. doi: 10.14309/crj.2017.112 PMCID: PMC5636906 PMID: 29043290
Mammal milk is required for enhanced phagocytosis as shown by research, especially in the elderly. Whole fat mammal milk can actually restore phagocytosis in senescent cells in the elderly. Phagocytosis, by which immune cells ‘eat’ bacteria or infected cells, is one of the mechanisms that help to resist infections. Lactic acid bacteria strains like acidophilus also increases phagocytosis.