How Bacteria Influence Food Cravings and Weight.
By Renata Trister DO
Literature Review
Studies on the gut-brain axis suggest that the bacteria in your gut could strongly influence your food choices.
97 percent of women and 68 percent of men report having cravings for foods they are trying to avoid. Cravings are thought to be a combination of psychological and physiological factors and are a major barrier to weight loss and health.
Recent evidence suggests that gut microbes might play a significant role in influencing cravings. Given that microbes evolved with us and depend on the foods we eat for survival, it follows that these organisms influence our eating preferences to improve their own chances of survival.
The enteric nervous system (found in the gut) is connected to the central nervous system (the brain and spinal cord) via the gut-brain axis. This term is more of a description of the interrelationship between the intestines and the brain. The two are connected by the circulatory system and the lymphatic system.
The enteric nervous system is also connected directly to the brainstem via the vagus nerve. The vagus nerve acts as a superhighway for communication between the gut and the brain and is the longest nerve cell in the autonomic (unconsciously controlled) nervous system. Studies on the vagus nerve found that vagal blockade can lead to marked weight loss, while vagal stimulation triggers excessive eating in rats.
Different microbes have different food preferences. Bacteroidetes have a preference for particular fats; Prevotella likes carbohydrates; Bifidobacteria prefer dietary fiber.
All of these microbes require these foods to grow and reproduce. Studies have shown that a low concentration of nutrients triggers increased virulence in many microbes as a survival mechanism. Virulence is the ability of a particular microbe to cause damage to the host. For many human-associated microbes, the production of virulence toxins is altered by the detection of simple sugars and other nutrients.
When bacteria metabolize foods, they produce various metabolites. Microbial metabolites include many neuroactive agents that are small enough to penetrate the blood-brain barrier. Studies on chocolate cravings have found that even when eating identical diets, people who crave chocolate have different microbial breakdown products in their urine than people who do not crave chocolate.
Short-chain fatty acids (SCFAs), metabolites produced from the fermentation of dietary fiber in the GI tract, are able to modify the expression of genes in cells throughout the body, including brain cells.
Other microbially derived molecules are able to mimic hunger or satiety hormones. Your body normally secretes hormones like ghrelin (to stimulate your appetite) and peptide YY (to signal that you are full). Many gut bacteria are able to manufacture small peptides that mimic these hormones. Helicobacter pylori is a great example. Eradication of Helicobacter pylori is accompanied by an array of metabolic and hormonal changes in the host. Weight gain following H. pylori eradication is a poorly understood phenomenon and probably results from an interaction between multiple factors. Ghrelin, a peptide hormone secreted by the stomach, is involved in the regulation of food intake and appetite and may account for some of these changes. Studies have demonstrated that H. pylori infection suppresses circulating ghrelin levels. Gastric expression of ghrelin, also suppressed by H. pylori, clearly increases following eradication. Weight gain following H. pylori eradication may be attributable to changes in plasma and gastric ghrelin. As wide use of antibiotics continues, many people now no longer have Helicobacter pylori present in their microbiome.
Microbes therefore can interfere with human appetite by either directly mimicking satiety and hunger hormones or indirectly inducing this autoimmune response.
Bacteria also produce neurotransmitters. More than 50 percent of your body’s dopamine and 90 percent of your body’s serotonin are produced in your gut, along with about 30 other neurotransmitters. These molecules are critical for signaling between cells of the nervous system. Dopamine and serotonin are involved in the regulation of eating behaviors.
An increasing number of studies are showing connections between the gut microbiota with stress, depression and anxiety. In 2004, an experiment showed that mice raised in sterile conditions with no gut microbes had an exaggerated hypothalamic–pituitary–adrenal (HPA) axis response to stress. The effect was reversed by colonization with Bifidobacterium species. Furthermore, a study published in 2012 found that germ-free mice prefer sweets and have a greater number of sweet taste receptors.
Microbial diversity may determine how easily host behavior can be changed. Obese individuals tend to have lower microbial diversity than individuals of a healthy weight. This may partially explain why people who are overweight tend to have difficulty with cravings.
To support your microbiome you may try the following:
Probiotics
Several strains of Bifidobacterium and Lactobacillus have been shown to improve anxiety- and depression-like eating behaviors.
Probiotics
Prebiotics are foods that selectively feed certain beneficial microbes. Try fermentable fiber found in foods like plantains, onions, garlic, and sweet potatoes. Supplementing with inulin or resistant starch is also an option.
Nutrient density
Eating a clean diet rich in green vegetables, healthy proteins and fats supports the health of both your body and the microbiome.
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Vitamin D and Inflammatory Bowel Disease
By Renata Trister DO
Literature Review
A relationship between vitamin D and Inflammatory Bowel Diseases (IBD) has recently been proposed. Vitamin D has several important actions beyond the bone maintenance. Vitamin D also exerts various effects on the immune system. Vitamin D deficiency has been implicated in the development of IBD such as Crohn’s Disease (CD). Current research also suggests a role for vitamin D in modulating some IBD complications, including osteopenia, colorectal neoplasia, and depression.
Vitamin D is well established as a regulator of calcium homeostasis. Recently, literature has linked vitamin D to a number of other conditions, including cancer, cardiovascular disease, and autoimmune diseases such as multiple sclerosis, diabetes mellitus, and
Crohn’s disease (CD). The incidence of Crohn’s disease, in general, appears to rise with increasing distance from the equator. Those residing in temperate climates have less exposure to sunlight, which is responsible for up to 95% of vitamin D production in humans. Vitamin D deficiency is found in 22 to 70% of patients with CD and has been proposed to play a key role in its pathogenesis.
Vitamin D deficiencies are common in patients with IBD. Normal levels of vitamin D are approximately 30 ng/mL. Levels between 20 and 30 ng/mL are considered insufficient, and anything below 20 ng/mL is considered deficient. The prevalence of vitamin D deficiency in inflammatory bowel disease (IBD) varies in different studies.
Laboratory experiments in various mice models have also shown that animals are more susceptible to colitis and that such colitis can be treated by vitamin D supplementation. These findings suggest, that there is at least a significant component of vitamin D level perhaps contributing to the development of IBD; vitamin D deficiency is not purely a consequence of prolonged, undertreated IBD or bowel damage, but is rather an artifact of immune dysregulation.
A growing body of literature has linked disease severity to low vitamin D levels. For example, a comparison of 3000 people with Crohn’s disease or ulcerative colitis and examined vitamin D levels showed that there is a gradation in the risk of surgery in people who had normal, insufficient, and deficient levels of vitamin D. People who had insufficient levels of vitamin D (20-30 ng/mL) had a higher risk of surgery and hospitalization, and people with levels lower than 20 ng/mL had an even higher risk of surgery and hospitalization.
Vitamin D can be considered a hormone with a number of effects on the immune system that are responsible for mediating susceptibility to infections and perhaps malignancy. Studies have suggested that vitamin D levels may be important in how patients respond to pathogens. Studies have linked low vitamin D levels with an increased risk of cancer, particularly colon cancer, in people with IBD. Low vitamin D levels are also linked to a higher risk of Clostridium difficile infection.
It is important to further evaluate the relationship of vitamin D deficiency and IBD to determine which one comes first. Prolonged bowel damage can cause IBD, with growing evidence and laboratory data suggesting that vitamin D is a potential mediator of several immune responses, the connection between Vitamin D levels and subsequent development of autoimmune conditions should not be disregarded. It is important to understand the role of vitamin D in the treatment of IBD itself, and not just for the treatment of vitamin D deficiency. We also need to better understand the optimal dose of vitamin D supplementation, and whether there are factors such as genetics that influence response to such supplementation. It is also important to define what the optimal vitamin D level should be in patients with IBD, and whether there should be a different adequate level when looking at inflammation. There is also growing evidence supporting the relationship between the gut microbiome and Vitamin D axis in autoimmunity. Bacterial induced modifications in Vitamin D metabolism can have vast effects on Vitamin D levels and Vitamin D Receptor signaling. Probiotics promote Vitamin D Receptor expression and its antimicrobial effects. This can be beneficial in treating colonic inflammation. Proper Vitamin D balance may restore healthy gut microbiome and decrease inflammation.
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VITAMIN D FACTS. BRIEF REVIEW.
The sequential metabolic processes which convert inactive pro-hormone (Vitamin D) to Active form called Vitamin D endocrine system. The key elements of this system are photo-conversion, the liver, the kidney as an endocrine gland, the vitamin D receptor (VDR) and the vitamin D binding protein (VDBP).
Vitamin D is then transported to the liver where it’s hydroxylated by an enzyme (CYP2R1) to produce 25(OH)D (25-hydroxyvitamin-D). 25(OH)D is then transported to the kidneys where it’s hydroxylated by another enzyme (CYP27B1) to produce 1,25OH2D (1,25- dihydroxyvitamin-D). Many cells outside the kidneys contain VDR and express CYP27B1 (the enzyme that catalyzes 25(OH)D to 1,25(OH)2D).
The vitamin D receptor (VDR), nuclear receptors, transduce hormonal signals from the immediate environment and transactivate genes in response to these signals .VDR has been identified in 37 different tissues throughout the body (including the nucleus of phagocytic cells of the immune system)
The most important function of 1,25(OH)2D is to bind to the VDR nuclear receptor and mediate the transcription of DNA, triggered by signaling proteins
The effects of 1,25(OH)2D are pleiotropic;
Most dividing cell types, normal and malignant, can express VDR and respond to 1,25(OH)2D.
VDR- activated genomic expression mediates many tissue-specific biological effects. Classical effects (e.g., calcium transport and bone health, etc.) and Non-classical, extra-skeletal effects (cell differentiation, central nervous system, skin/hair, immune regulation, hormone secretion, etc.).
In addition to the classical VDR-mediated genomic pathway, 1,25(OH)2D also has been shown to elicit rapid responses that occur within a few minutes after hormone treatment and are considered too rapid to be explained by a VDR-mediated genomic pathway. These rapid responses are mediated by a direct action of 1,25(OH)2D on the plasma membrane of target cells stimulating a signal transduction pathway involving the rapid opening of voltage- sensitive Ca2+ channels and activation of protein kinases.
VDR are present in most cell types of the immune system, particularly in antigen- presenting cells (APCs) such as monocyte, macrophages and dendritic cells. The influence of 1,25(OH)2D on the immune system is one of its most important roles. In general, the innate system is enhanced and the adaptive system is inhibited by 1,25(OH)2D. The innate system is suppressed by 25-OH and the adaptive system is stimulated by 1,25(OH)2D.
1,25(OH)2D activates the VDR to express antimicrobial peptides (AMPs) such as cathelicidin and beta defensins which attack pathogens. Recently, 1,25(OH)2D-induced autophagy has been reported (autophagy contributes to anti-aging, antimicrobial defense, and tumor suppression). VDR immune system regulation also involves cell proliferation, differentiation and apoptosis. The VDR is also expressed in both B and T white blood cells (lymphocytes)
In monocytes and macrophages (innate immune system), synthesis of 1,25(OH)2D from 25(OH)D promotes an antibacterial response to infection. Monocytes sense pathogen-associated molecular patterns (PAMPs) by utilizing pattern-recognition receptors (PRR), such as toll-like receptors (TLRs). Induction of CYP27B1 occurs following PAMP-sensing by TLR2/1. The inflammatory cytokine interferon γ (IFNγ) also stimulates expression of CYP27B1 by macrophages. As a result, 1,25(OH)2D production is increased in response to a pathogen immune challenge.
1,25(OH)2D modulates the adaptive immune system by inhibiting dendritic cell maturation, reducing T helper (Th) cells, and shifting Th1/Th17 cells to the Th2 and T regulatory pathways. In addition, 1,25(OH)2D inhibits Th1 cytokines that support cell-mediated immunity and promotes Th2 cytokines that support humoral immunity (antibodies circulating in bodily fluids). The immune response is heavily dependent on the vitamin D endocrine system, performing a balancing act of inflammation/anti-inflammation.
There is no consensus on the definition of vitamin D deficiency or insufficiency and authorities haven’t agreed on the significance of low 25(OH)D.
The Institute of Medicine (IOM) report emphasized that the current measurements, or cut-off points, of sufficiency and deficiency of 25(OH) D in use by laboratories have not been set using rigorous scientific studies. The IOM report emphasized that the current measurements, or cut-off points, of sufficiency and deficiency of 25(OH) D in use by laboratories have not been set using rigorous scientific studies. They suggest that since no central authority has determined which cut-off points to use, reports of deficiency and lab ranges may be skewed and numbers overestimated. Most importantly, 25(OH)D may not always reflect the level of 1,25(OH)2D (the active metabolite).
Researchers in Denmark measured the baseline serum 25(OH)D and total cholesterol levels of 182 fair-skinned and dark-skinned subjects; and studied the effect of UV radiation on their serum 25(OH)D levels. They found the amount of serum 25(OH)D produced was determined by the amount of cholesterol in the skin, not on skin pigmentation. Most importantly, skin pigmentation doesn’t negatively affect vitamin D status. Persons with dark skin compensate for low 25(OH)D by rapidly converting it to the active 1,25(OH)2D metabolite, thus allowing them to maintain adequate vitamin D status. Matsuoka et al concluded that while racial pigmentation has a photo-protective effect, it does not prevent the generation of normal levels of active vitamin D metabolites. The concern about dark skin and vitamin D deficiency appears to be misplaced. ample opportunities exist to form vitamin D (and store it in the liver and fat) from exposure to sunlight during the spring, summer, and fall months even in the far north latitudes.
Our bodies have mechanisms for preserving the vitamin D we acquire during the summer; which have evolved to stabilize and maintain serum levels of vitamin D in environments with variable vitamin D availability. The Vitamin D Binding Protein (DBR) optimizes and stores 25(OH)D for later use; it also binds 1,25(OH)2D, as well as the parental vitamin D itself. DBP sequesters vitamin D sterols in the serum, prolongs their serum half-lives, and provides a circulating store of vitamin D to meet transient periods of deficiency. In so doing, DBP helps to prevent the development of severe vitamin D deficiency.
Clothing is a barrier to ultraviolet radiation but this is an issue only for people who cover themselves from head to toe (e.g., woman who wear a burka may not be exposed to sufficient sunlight). It takes relatively little sunlight exposure to acquire adequate stores of vitamin D and few people wear enough clothes to prevent that from happening. Ten to 15 minutes of sunlight or daylight exposure to a small area of skin (e.g., the forearm or face, etc.) twice a week (without sunscreen) supplies all the vitamin D necessary for health. Evidence for a beneficial effect of vitamin D supplementation in cancer is lacking. The findings of a large prospective study in 2008 do not support the claim that vitamin D is associated with decreased risk of prostate cancer; in fact, higher circulating 25(OH)D concentrations may be associated with increased risk of aggressive disease. The Women’s Health Initiative (WHI) Calcium plus Vitamin D Supplementation Trial, published in November 2013, concluded that after an average of 11 years, calcium and vitamin D supplementation did not decrease colorectal cancer incidence.
Adequate vitamin D is essential to prevent rickets, but adequate calcium is equally important; if either calcium or vitamin D is deficient, bone health suffers. Rickets is rare in the developed world; however, children in developing countries, who usually photosynthesize enough vitamin D from sunlight, develop rickets if poverty prevents them from eating enough calcium rich food. Studies found rickets occurs in sunny countries due to poor calcium intake and is cured with increased calcium ingestion.
Osteoporosis is a bone disease characterized by a decrease in bone mineral density and the appearance of small holes in bones due to loss of minerals. Vitamin D is an important factor in maintaining bone health to avoid osteoporosis. Precise maintenance of the physiologic levels of both extracellular and intracellular ionized calcium is essential to life; 1,25(OH)2D maintains calcium homeostasis between blood, cells and bones by stimulating calcium absorption from the intestines, reabsorption in the kidneys, and resorption in bones. 1,25(OH)2D up-regulates VDR in the small intestine, which then transcribes genes that shuttle calcium and phosphorus through the intestinal epithelium. However, mucosal response and calcium/phosphorus absorption is dependent on a competent VDR and elevated 1,25(OH)2D reduces VDR competence. Thus, calcium and phosphorus absorption may be inhibited if VDR function is impaired by elevated 1,25(OH)2D. This is illustrated by a study of Crohn’s patients with elevated 1,25(OH)2D and low bone mineral density which concluded that treatment of the underlying inflammation would improve metabolic bone disease.
Vitamin D supplementation is ill- advised above a threshold of 30ng/ml 25-D. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D, which would explain why low vitamin-D status is reported in a wide range of disorders. It would be wiser to seek reasons underlying the low vitamin-D level, such as inflammatory processes. Elevated 1,25(OH)2D leads to bone loss. When levels are above 42 pg/ml 1,25(OH)2D stimulates bone osteoclasts. This leads to osteoporosis, dental fractures and calcium deposition into the soft tissues: lungs, breasts, muscle bundles, kidneys. An earlier study warned, “Vitamin D is a toxic compound, and excessive amounts can cause soft-tissue calcification. There is a narrow leeway between the amount required and that initiating tissue damage.” Combination of high 1,25(OH)2D and low 25(OH)D is associated with the poorest bone health. This significant evidence regarding bone loss should motivate medical practitioners and researchers to measure both 25(OH)D and 1,25(OH)2D to determine vitamin D status.
Autoimmune diseases: An alternate hypothesis posits a bacterial etiology in which a persistent intracellular infection causes a cytokine release that induces signals to T cells and B cells, and the antibodies they produce (to the intracellular invader) include some that attack human proteins, as well as target the pathogens. In other words, when an innate immune system is forced to respond to a persistent infection, the resulting cascade of chemokines and cytokines will also stimulate an adaptive response. Vitamin D has a positive effect on autoimmune disease because it reduces symptoms via immune system suppression. For example, abnormal T cell reactivities in MS patients were reduced with vitamin D supplementation; serum 25(OH)D levels after 12 months were increased to 71.7 ng/ml ± 39 ng/ml. Vitamin D inhibits pro-inflammatory processes by suppressing the enhanced activity of immune cells that take part in the autoimmune reaction.
Exposure to ultraviolet light, especially UV-B wavelengths, can impair immune responses in animals and humans. Thus, seasonal variation can have an impact on the immune response; in the summer, when vitamin D3 is highest, 1,25(OH)2D down-regulates the immune system. Reduced immunity following exposure of skin to UV radiation may explain the positive latitude gradient measured for a number of autoimmune diseases (decreased incidence of disease with residence at lower latitudes). Unfortunately, some researchers believe immunosuppression is the best form of treatment for autoimmune disease. Vitamin D proponents have failed to recognize the immunosuppressive effect of elevated 25(OH)D and to acknowledge that immunosuppression is contraindicated in the presence of infection. As a result of vitamin D immunosuppression inflammation, clinical disease markers and symptoms of autoimmune disease are reduced but this doesn’t treat the underlying cause and relapse is common.
Verway et al. wonder, “Is a specific pathogen responsible for disease or rather is a dysregulated immune response generated against a complex microbial population? Why would immune-suppressive drugs be efficacious if the primary defect is an immune deficiency?”
The suppressed immune system enables chronic infection and inflammation. Intracellular bacteria are able to persist and proliferate in host phagocytes, successfully compete for nutritional resources and displace commensal organisms from their niche. The result is chronic illness.
There is a positive role for vitamin D in bone health but not in other health outcomes. Genetic findings in those predisposed to longevity cast doubt on whether low levels of vitamin D cause age-related diseases and mortality. A study concluded that vitamin D supplementation did not reduce knee pain or cartilage volume loss in patients with symptomatic knee osteoarthritis. Subjects supplemented with high doses of vitamin D saw no improvement in serum lipids, HbA1c, or HS-CRP. Supplementation did not significantly reduce the incidence or duration of upper respiratory tract infections. In a study of older adults, the decline in physical performance and strength was not associated with 25(OH)D.
Vitamin D deficiency or insufficiency can occur in certain situations. Genetic defects in the VDR may result in vitamin D deficiency; a number of mutations have been identified that lead to hereditary vitamin D resistance. Disorders that limit vitamin D absorption and conditions that impair conversion of vitamin D into active metabolites may cause deficiency. Sick or elderly people who rarely go outdoors and have poor diets are also at risk.
Decreases in vitamin D levels are a marker of deteriorating health. Inflammation is the common factor between most non-skeletal health disorders and low 25(OH)D concentrations.
Increases in 25(OH)D have no effect on inflammatory processes or on disorders at the origin of these processes.
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The Immune System, brief review.
To defend as form invaders body has two immune systems:
The first defense system is an innate immune system we are born with. This is a first defense against any foreigners-microbes, viruses, funguses. This is antigen non-specific defense mechanisms which respond to invaders immediately or within several hours after exposure to every foreigner. Cells associated with innate immune system are Macrophages, Dendritic cells and B-lymphocytes.
The second defense system is an adaptive immune system (acquired) immunity refers to antigen-specific defense and require several days to become protective and are designed to react with and remove a specific antigen. Adaptive immunity is the immunity one develops throughout life. Cells associated with adaptive immune system are T- and B-Lymphocytes
One of the function of the innate immune system is an APC ( antigen presentation cells)-is an identification, isolation of the antigen-specific protein -epitope-actual portions or fragments of an antigen that react with receptors on B-lymphocytes and T-lymphocytes, as well as with free antibody molecules) and presentation it in the from of complex : MHC I/epitope or MHC ii/epitope on the surface of the APC ( Macrophages, Dendritic cells, B-Lymphocytes).Epitope is a fragment of the antigen which will provide adaptive immune system a specific information about invader ( antigen).Without ability to perform this function as an APC innate immune system will be unable to “educate” adaptive immune system about structure of the antigen.
Polysaccharides antigens( 3-4 sugar residuals) usually have many epitopes but all of the same specificity.
Proteins antigens (5-15 amino acids )usually have many epitopes of different specificities.
Immune responses are directed against many different epitopes of many different antigens of the same microbe.
The body recognizes an antigen as foreign when epitopes of that antigen bind to B-lymphocytes and T-lymphocytes by means of epitope-specific receptor molecules having a shape complementary to that of the epitope.
MHC molecules
MHC-I molecules are made by all nucleated cells in the body
MHC-I presents epitopes to T8-lymphocytes; MHC-II presents epitopes to T4-lymphocytes.
MHC-I molecules are designed to enable the body to recognize infected cells and tumor cells and destroy them with cytotoxic T-lymphocytes or CTLs.
CTLs are effector defense cells derived from naïve T8-lymphocytes.
MHC-I molecules are made by all nucleated cells in the body; bind peptide epitopes typically from endogenous antigens; present MHC-I/peptide complexes to naive T8-lymphocytes and cytotoxic T-lymphocytes CTL.
MHC-II molecules are made by antigen-presenting cells or APCs, such as dendritic cells, macrophages, and B-lymphocytes; bind peptide epitopes typically from exogenous antigens; and present MHC-II/peptide complexes to naive T4-lymphocytes or effector T8-lymphocytes that have a complementary shaped T-cell receptor or TCR
Exogenous antigens enter antigen-presenting macrophages, dendritic cells, and B-lymphocytes through phagocytosis, and are engulfed and placed in a phagosome where protein antigens from the microbe are degraded by proteases into a series of peptides. These peptides are then attached to MHC-II molecules that are then put on the surface of the APC.
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By Renata Trister DO
Artificial Sweeteners
Literature Review
The health risks surrounding high sugar foods are well known. As a result many health conscious people are turning to artificial sweeteners as a healthy alternative. The benefits of artificial sweeteners have been controversial ever since saccharin, the first no calorie artificial sweetener, was discovered in 1878. Even then, many questioned whether these man made sweeteners were actually safe. Saccharin (sweet & low) was discovered by a chemist working with coal tar, a carcinogenic material. Nearly 150 years—and an infinite number of conflicting studies—later, the issue still debated. Saccharin has been shown to cause cancer in laboratory animals.
Cancer concerns aside, researchers are finding new reasons that these no calorie sweeteners are causing undue health risks without fulfilling the promise of helping you lose weight.
TASTE BUDS
Artificial sweeteners, even natural ones like stevia, which comes from an herb, are hundreds, sometimes thousands, of times sweeter than sugar. Sucralose, sold under the brand name Splenda, is 600 times sweeter than table sugar. Evidence suggests that exposing your taste buds to these high-intensity sweeteners makes them less receptive to natural sources of sweetness. This dulls the taste buds making one more likely to seek out sweeter and sweeter foods.
THE GUT
The gut gets confused when exposed to zero-calorie-but-super-sweet artificial sweeteners. The sweet taste sends a signal to your gut that something high calorie is on its way, so your gut anticipates foods that are sweet and high in calories. When these foods never actually arrive, your gut doesn’t utilize the foods efficiently, and that causes a cascading effect that interferes with your body’s hunger signals.
HORMONES
Part of that cascading effect has to do with the hormone insulin. When you taste sweet foods, even if they have zero calories, your body still releases insulin as if you’d eaten sugar. Insulin leads to blood sugar spikes, which increase cravings.
OVEREATING
It’s not just a biochemical reaction that leads artificial sweeteners to pack on the pounds. Artificially sweetened foods trick people into eating more because of the way they feel in your mouth. The taste and feel of food in our mouth influences our learned ability to match our caloric intake with our caloric need.
High fat, high sugar foods taste both sweet and dense, signaling to your brain that they’re high calories. But artificially sweetened foods often have a thinner consistency and texture than sugar-sweetened foods and thus, aren’t as satisfying.
DIABETES RISK
Diet soda drinkers have an increased risk of developing type 2 diabetes. It is not fully clear why this is so. A study from the University of Texas found that people who drank diet soda were 65 percent more likely to be overweight than people who drank no soda and they were more likely to be overweight than people who drank regular soda. There is a possibility that gut bacteria are able to make medium chain fatty acids from artificial sweeteners, contributing to calorie count and disruption of gut flora.
WATER POLLUTION
In a 2009 study published in the journal Environmental Science & Technology, Swedish researchers detected sucralose and acesulfame K in treated wastewater, including samples that were pulled from a municipal water-supply source. They also noted that the artificial sweeteners hadn’t degraded in wastewater sludge after a period of seven hours. These sweeteners are now showing up in our rivers and streams.
MOST OF THESE SWEETENERS ARE GENETICALLY MODIFIED
Sucralose, aspartame, neotame, and erythritol can all be made from corn, soy, or sugar beets. In the United States, the vast majority of those three crops have been genetically altered to resist or produce harmful pesticides.
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By Renata Trister DO
The Standard American diet and the Immune System
Review current literature
The Standard American or Western diet has been gaining attention as a potential contributor to the increase in immune-mediated diseases. The Western diet is characterized by an over consumption of refined sugars, salt, and saturated fat. In addition to many illnesses, this diet has an impact on the gut microbiome, these dietary choices are encoded into our gut, our genes, and are passed to our children. Although the modern diet has successfully prevented many macronutrient deficiencies, our over abundance of calories and the macronutrients that compose our diet may all lead to increased inflammation, reduced control of infection, increased rates of cancer, and increased risk for allergic and auto-inflammatory disease.
The Western diet is characterized by a high intake of saturated and omega-6 fatty acids, reduced omega-3 fat intake, an overuse of salt, and too much refined sugar. This type of eating can damage the heart, kidneys, and cause obesity/metabolic disorders. Increasingly, it has become apparent that this diet damages the immune system also. The modern lifestyle, reduced exposure to microorganisms, increased exposure to pollutions, heightened levels of stress, and a host of other exceptionally well reviewed variables that likely contribute to immune dysfunction.
Intake of adequate calories and micronutrients is vital for optimal immune function. Deficiency in total calories and/or protein, with starvation, severely reduces the immune system’s ability to respond. The Western diet is plagued with obesity. Adipocytes release inflammatory substances including interleukin (IL-) 1, IL-6, and tumor necrosis factor (TNF). These act as signals in infection, but when they are released without an actual infection, the system wears out. When an actual infection comes along, the response may be delayed.
Obese individuals have fewer white blood cells to fight infection and those cells they do possess have reduced phagocytosis capability. While a complex interplay of hormonal, metabolic, and immunologic processes contribute to the biologic responses in the obese the resultant immune dysfunction increases the risk of infections of the gums, respiratory system, and post op infections.
Sugar
Processed, simple sugars reduce white blood cell phagocytosis and possibly increase inflammatory cytokine markers in the blood. The impacts of artificial sweeteners are less clear; provocative, yet highly limited, evidence implicates saccharin and sucralose as contributors to Crohn’s and Ulcerative Colitis via interference with homeostatic inactivation of digestive proteases. More studies are being conducted to investigate this.
Saturated fatty acids
One potentially harmful effect of fat is enhancement of the prostaglandin system as it feeds into the arachadonic and prostaglandin E2 (PGE2) pathways. PGE2 is pro-inflammatory, increasing IL-17 production and macrophage activation. Additionally, dietary fats alter the lipids of the membranes of immune cells, disrupting the immune functions. Modern produced dietary fat can also directly trigger the inflammatory process. This is most troubling.
One of the first-line weapons the immune system deploys against infection are molecules called Toll-like receptors (TLR). This is a very complex aspect of the immune system; when these receptors come across a potential pathogen, they are designed to evaluate if it is bacterial, viral, or fungal. If the body finds evidence of any of these organisms, the immune system can begin its attack immediately while the adaptive immune system assesses what specific pathogen it is facing. One of the TLR weapons, TLR4, is designed to sense bacteria. Unfortunately the part of the bacteria TLR4 binds, lipopolysaccharide (LPS), contains mostly saturated palmitic and steric fatty acids. Meaning that TLR4 can generate inappropriate signaling when exposed to certain saturated fats if in too great of frequency, amount, or homogeneity rather than in a more biological balance and dosage. Any resultant, abnormal signaling may lead to a misguided attack upon saturated fat when it is perceived as a bacterial invader. The resulting inflammation in the gut can lead to a break down of barriers, allowing harmful substance to leak from the gut into the blood stream and contribute to immune dysfunction that worsens infection control.
Omega-6 fatty acids
While saturated fats are the most inflammatory, overabundance of omega-6 (n-6) poly-unsaturated fats, such as those found in most cooking oils, have also been implicated in immune response through several mechanisms including effects on TLR4 [53] and serving as precursors for inflammatory mediators
Omega-3 fatty acids
The immune impact of trans unsaturated fatty acids (trans fats) have gone under investigated whilst researchers focus on their deleterious cardiovascular effects, Another possible contributor to modern diet-induced immune dysfunction may be the increased consumption of omega-6 in lieu of omega-3 fatty acids.
Gluten
Recent animal and cell-culture models have found that elements in gluten can stimulate inflammation through TLR4. This is a possible explanation of the current gluten-free dietary trend.
The microbiome and inheritance
Diet, stress, and environment can have a big effect on the gastrointestinal system. Recent studies have determined some of the mechanisms by which our lifestyle impacts our microbiome and leads to dysbiosis. In the gut (and on the skin), there is an optimal balance of bacterial species. Some strains of bacteria are needed to digest fiber while others produce valuable nutrients like vitamin K. Beneficial bacteria also competitively in habit the microenvironment thus preventing harmful bacteria from taking over. The current understanding on how dietary fats alter the microbiome include TLR4-dependent induction of local inflammation leading to altered host environment, shifts in immune cell membrane functions, and changes in nutrient availability favoring some organisms over others. Dietary simple sugars can to lead to dysbiosis directly through changes in local nutrient concentrations. Interesting some preliminary research has shown the gut microbiome to possess the ability to metabolize the artificial sweeteners considered otherwise non-caloric for humans. While results must be interpreted cautiously, gut bacteria can process sweeteners into various short-chain fatty acids (SCFA) that hold a wide array of potential consequences; while some SCFA may be beneficial, their production may shift the bacterial balance, may be processed into absorbable byproducts that provide calories, and may activate the TLR4 pathway.
Another concern is that the harmful effects of diet can actually stretch across generations. A mother’s diet may potentially shape her child’s flavor preferences even before birth, potentially skewing their palette towards anything from vegetables to sugary sweets in ways that could influence subsequent propensity for obesity and/or unhealthy dieting. Children inherit their microbiome from their mother mostly through parturition but also during breast-feeding and development until the bacterial balance matures around two to four years of age. However, recent evidence suggests that the microbiome may also be seeded into the unborn fetus while still in the womb. When the mother’s diet causes a harmful imbalance of her bacteria, she can pass this imbalance on to her child. This developmental dysbiosis may have an impact on the baby’s immune system.
In addition to altering TLR-mediated inflammation and potentially DNA epigenetics, a mechanism by which alteration in microflora may drive immune-mediated disease involves the gut bacteria’s effect on regulatory T-cells (Tregs), the cell tasked with keeping the immune system in balance during both inflammation and homeostasis. Alterations in the microbiome have been shown in both mice and (to a less extensive degree) humans to affect Treg development, and reduction in Treg signal is associated with worse outcomes in infection control, autoimmunity, and allergic sensitization Therefore, dietary choices that alter gut microbiome likely alter systemic responses through changes in the number and function of regulatory T cells.
Determining which specific bacterial strains are either the protectors or pathogens is not yet fully clear. The desire to foster a healthy microbiome is the driving force behind the therapeutic use of probiotics. Supplementation with various Lactobacillus, Lactococcus, and Bifidobacterium has proved to be beneficial but they are not a cure –all. Our microbiome is far more complex than what is found in a supplement bottle. Simply taking supplements creates a very homogeneous microflora that lacks diversity.
Palmitic acid (found is certain processed fats) may potentiate iron-mediated toxicities and increase the rates of DNA mutations. Dietary intake of the saturated palmitic and steric fatty acids as well as the omega-9 oleic acid, may be independent risk factors for the development of colon cancer. Simple sugars were thought to heighten cancer risk through several well-reviewed in vitro mechanisms.
The exact mechanism of how any individual dietary element impacts cancer development is far from fully understood. Many of the reportedly protective vitamins and minerals share anti-oxidant properties, suggesting a mechanism more related to protection of DNA from damage than altered immune function.
In summary, there is enough quality, direct human evidence to conclude that many of the dietary choices in today’s modern society appear to have harmful impacts on our immune system and likely on the immune system of our children. Although promise remains, it also appears unlikely that synthetic supplements or probiotics will be able to fully heal the damage of our diet. Lifestyle modifications are a must. The greatest negative consequence of our poor diets can be encoded into our DNA and gut microbiome. These harmful immune modifications are passed to our offspring during the time of critical development. This can affect the health of many generations to come.
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Babesiosis
By Renata Trister DO
Babesia are parasitic protozoans that reproduce in the red blood cells of mammals. The various forms of Babesia complex life cycle live in exchange between ticks (Ixodes) and mammals. Babesia species was first described in 1888 by Victor Babes, a Hungarian pathologist in whose honor the organisms were named.
Babesiosis has long been recognized as a disease of cattle and other domesticated animals, but the first human case was not described until 1957, when a young Croatian farmer contracted the illness and died some days later of renal insufficiency. In the late 1960s, the first North American cases appeared on Nantucket Island, and the disease is now recognized as an emerging and occasionally serious zoonosis in the United States.Adapted over hundreds of millions of years: stealthy”cryptic inhabitants” within vertebrate and invertebrate hosts. Co-infection with Borrelia thought to increase impact.
Babesiosis has been reported in North and South America, Europe, and southern and eastern Asia. In the United States, the primary agent of human babesiosis is Babesia microti, which is transmitted by the bite of Ixodes scapularis, the same tick species that is a vector for Lyme disease. Cases of babesiosis caused by B. microti occur in southern New England and the northern Midwest. Additional cases of babesiosis caused by other species of Babesia occur primarily in the western U.S.; cases from Missouri and Kentucky have also been reported. It is a frequent co infection with Lyme disease.
Babesiosis has a wide spectrum of disease severity. It varies from patient to patient. Most patients experience a viral-like illness lasting anywhere from a few weeks to a few months. A small segment of patients are completely symptom free. In patients with a complicating condition, however – such as underlying immunosuppression – the disease course can be severe and potentially fatal. Primarily transmitted by tick bite, babesiosis can also be transmitted via blood transfusion and maternal-fetal transmission.
Signs and Symptoms
If you think lyme disease is bad-meet Babesia!
Symptoms of babesiosis usually begin 1-6 weeks after infection and are non-specific. Typical early manifestations include: day sweats, night sweats ( occasionally drenching) intermittent fevers, fatigue, headache, chills ,flashing ,air hunger, cough and myalgias. Nausea, vomiting, poor appetite and depression can also occur. Some patients will develop enlarged livers or spleens. The usual disease course lasts weeks to several months, but some patients take even longer to fully recover. Co-infection with Lyme disease or anaplasmosis may complicate the clinical presentation and predispose the patient to more severe disease.
Different strains of Babesia may cause different set of symptoms, yet all can significantly exacerbate a Lyme disease infection.
Babesia and Malaria share the same set of symptoms, and the infections may look the same to a laboratory technician viewing parasites under the microscope.
At the greatest risk for severe babesiosis are the elderly, asplenetic patients, patients with HIV or malignancies, and patients on immunosuppressive medications. In these populations, the disease course is longer and the fatality rate is in the neighborhood of 20%, even with proper antibabesial therapy. The most common serious complication of babesiosis is acute respiratory failure, but heart failure, liver and renal failure, disseminated intravascular coagulation and coma are also well-recognized severe manifestations of babesiosis.
Diagnosis
Early symptoms of babesiosis are non-specific making the diagnosis difficult. A simple blood panel can be indicative of an infection. Babesia causes lysis of red blood cells, patients can develop hemolytic anemia, as well as lymphopenia and thrombocytopenia. Elevated serum lactate dehydrogenase levels, hyperbilirubinemia and an elevated erythrocyte sedimentation rate may also be present.
If babesiosis is suspected, microscopic examination of blood smears should be pursued. Giemsa or Wright stains are typically used. DNA of Babesia can also be detected by polymerase chain reaction (PCR) in cases where smears are negative but the diagnosis is still suspected.
Treatment
Combination therapy with atovaquone (Mepron) and azithromycin is most commonly recommended for treatment of mild to moderate babesiosis. Treatment is usually continued for 7-10 days.
Doxycycline + Plaquenil ( occasionally with Bactrim DS) with other antimalarian drugs, such as Malarone, and anti-malarian herbs can be effective.
Dapsone : is good for both: Babesia and Lyme disease
A combination regimen of oral clindamycin and quinine has also been proven effective, but the rate of adverse reactions is significantly higher with this combination, so it is not recommended for treatment of uncomplicated disease.
For patients with severe babesiosis, however, intravenous clindamycin and (oral) quinine is considered the preferred treatment, again for 7-10 days. In patients with underlying immunosuppression and persistent signs and symptoms, studies have shown an association between longer treatment duration and a positive outcome; therefore, treatment of these individuals should be continued for weeks or months until blood smears are negative for at least two weeks.
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By Renata Trister DO
Bartonella are gram negative bacteria and are difficult to isolate in the laboratory. These bacteria can live inside cells and in various locations in the body, protected from the immune system and antibiotics.
Generally, three conditions caused by bartonella, cat scratch fever (Bartonella henselae), trench fever (Bartonella quintana), and Carrion’s disease (Bartonella bacilliformis), but research over the past 20 years has shown that bartonella is much more complex.
Bartonella species are widespread in all mammals. Bartonella is typically spread by biting insects (fleas, ticks, mosquitoes, sandflies, lice, chiggers, biting flies, scabies, mites, and even louse-eating spiders), but can also be transmitted by contaminated animal bites and scratches.
The most common bartonella is Bartonella henselae. It is the cause of cat scratch fever. Classically, a scratch from a cat carrying B. henselae develops a rash followed by symptoms including low grade fever, headache, sore throat, and conjunctivitis about 3 to 10 days after the scratch. Swollen lymph nodes are typical and takes weeks to months to subside. Symptoms are not generally debilitating and resolve without treatment in most cases.
When bartonellosis with B. henselae is caused by an insect bite (ticks, fleas, mosquitoes) the symptoms are complex and highly variable.
Bartonella quintana, another common species of bartonella, is the cause of trench fever. The name comes from the trenches of WWI where soldiers lived in desperate and debilitating conditions. B. quintana, spread by body lice, causes symptoms of severe fever, headache, muscle aches, leg and back pain, skin rashes, conjunctivitis, and rarely, heart failure. Today, B. quintana is common in homeless people; again, transmitted by body lice. About 10-20% of homeless populations (3.5 million people in the US) harbor chronic infection with B. quintana.
Bartonellosis
After entering the body (by whatever means), bartonella infects specialized white blood cells called CD 34+. These blood cells are precursors for cells that line blood vessels and other tissues (endothelial cells). The microbe enters the cell and creates a cyst around itself to gain protection. It also turns off the ability of the cell to self-destruct. Chemical messengers stimulated by bartonella cause additional CD 34+ cells to congregate. These messengers simultaneously suppress other parts of the immune response. CD 34+ travel throughout the body and replace damaged endothelial cells. Bartonella becomes established inside blood vessels and uses red blood cells as a nutrient source.
If the person’s immune system is healthy, the cells of the immune system quickly gain the upper hand, and microbe is dispatched within a couple of weeks. In patients with compromised immune systems and other infections, a chronic condition can develop.
Typical Symptoms of Chronic Infection
Skin rash at the site of initial infection, low-grade fever (100-102), and swollen lymph nodes (near the initial infection site) are hallmarks of initial infection. Lymph nodes can be filled with pus and drain in severe cases. Other common symptoms include severe fatigue, muscle pain, body aches, and eye infection (conjunctivitis). Liver and spleen enlargement can occur acutely and with chronic infection. Chronic infection can be associated with relapsing low-grade fever. Chronic eye problems include blurred vision, photophobia and eye irritation. Bartonella commonly infects bone marrow with resulting bone pain. Another symptom of bartonella is pain in the soles of feet upon waking in the morning. This is associated with trauma to blood vessels in the soles of the feet.
Anemia can occur from bartonella scavenging nutrients from red blood cells.
Small vessel disease can affect the brain and nervous system. Headaches and depression may be linked to chronic bartonella infection. Poor stress tolerance and anxiety are also reported.
Small vessel disease can affect function of the autonomic nervous system (sympathetic and parasympathetic systems) resulting in postural orthostatic tachycardia syndrome (POTS).
Chronic bartonella infection affects the entire vascular system. Infection of cells lining the heart (endocarditis) can cause chest pain, shortness of breath, palpitations, and in some cases, damage to heart valves. Respiratory symptoms can include unexplained cough.
Bartonella can affect the urogenital region causing irritable bladder, kidney disease, pelvic pain, and infertility. There is evidence that bartonella can be passed during pregnancy and between partners.
Severely immunocompromised individuals (mainly AIDS) can develop cranberry-like skin lesions from proliferation of infected blood vessels under the skin.
Symptoms are highly variable and often not severely debilitating. The spectrum of symptoms widely overlaps with other low virulence microbes. An average doctor would mark it off as simply aging and offer only prescriptions to control the symptoms, nothing more. For this reason this infection is often overlooked.
Diagnosis and treatment of Bartonella
Indirect fluorescence assay (IFA) tests for antibodies (IgG and IgM) to bartonella. IFA is not very sensitive because antibodies levels tend to be low. Also testing is species specific and generally only tests for the most common species of bartonella. Frye Laboratories (Scottsdale, Az) offers both IFA and standard PCA.
Standard PCR tests for bartonella DNA in the blood. Because concentrations of the microbe are very low with chronic infection, this test is unreliable.
Fluoroquinolones and doxycycline are sometimes successful in treating bartonellosis. However, some doctors report the need to use several antibiotics in combination.
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Auto Brewery Syndrome
By Renata Trister DO
Gut fermentation syndrome or auto-brewery syndrome is a digestive disorder that results in a feeling of being intoxicated. People feel as though they are in a fog, unable to concentrate. In severe cases, people suffering from this condition can actually get a DUI.
Gut fermentation syndrome is typically associated with an accumulation of yeast inside the intestines. Yeast can build up to the point to where just having a small amount of sugar can trigger a reaction that is similar to having several alcoholic drinks.
Normally having a small amount of yeast in our bodies is actually a good thing. As part of normal flora, yeasts can help boost the immune system and reduce the chances of developing diarrhea. Saccharomyces cerevisiae, is a yeast normally found in our body. It is also used in the manufacture of alcoholic products and bread.
On occasion, taking antibiotics can cause a major disruption in the normal population of intestinal flora. Antibiotics kill not only bad bacteria, but also beneficial microbes. This can allow yeast to proliferate out of control and cause major problems. Gut fermentation syndrome is one of these problems. If a person with this condition takes in any sugar whatsoever, the body converts it into ethanol. This results in a sudden spike in the body’s blood alcohol content. The Candida yeast, in particular, has been identified as one of the main culprits in causing gut fermentation syndrome.
In severe cases, the body of someone with gut fermentation syndrome produces so much alcohol that he or she can become legally drunk – without having any alcohol. In fact, one woman in New York was actually pulled over because a police officer suspected her of drunk driving, but her case was later thrown out because she was diagnosed with the condition.
Gut fermentation syndrome sufferers will typically complain that they are tired all the time, which is completely understandable, considering they experience mild intoxication on a constant basis.
A diet high in carbohydrates can have a profound effect on triggering a bout of drunkenness due to gut fermentation syndrome. In one study performed in 2010, a 61-year-old man suffering from the condition was given a high-carb meal. His blood was drawn before the meal to establish a baseline blood alcohol content level, and was then checked every two hours. He was also given a Breathalyzer test every four hours – eventually, his blood alcohol level shot up to .12 percent.
Interestingly, researchers also linked this man’s condition to antibiotics he had received six years earlier. It is believed that the antibiotics destroyed so many bacteria in his lower intestine causing a population boom of Saccharomyces cerevisiae yeast. Antifungal medication followed by a course of probiotics seemed to help with his symptoms.
Anything that causes an imbalance between the beneficial and harmful bacteria in the gut can help increase the chance that fermentation in the gut will develop. This can include not only antibiotics, but also overindulgence in sugars and carbohydrates. Watching what you eat could lower the risk of gut fermentation syndrome, and taking probiotics could further protect you by increasing the number of good bacteria in your system.
If you do take antibiotics as well as probiotics, you should take them at different times in order for the probiotic to be able to work. Taking the probiotic at least two hours later will help ensure it will be able to do its job. A good rule is to take the antibiotic after a meal, and then take the probiotic at bedtime.
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Functional Phytotherpy for Ulcerative Colitis:
1.Bowel Flora protocol *.Aim treatment is to resolve dysbiosis
2.Eliminate persistent pathogens:Thuja, Licorice, St.John’d Wort
3.Optimize immune system function: Androghraphis, Echinacea, Myrrh
4.Eliminate Chronic inflammation:Myrrh, Boswellia, Licorice, Meadowsweet, Chamomile
5.Enhance natural barriers: Chamomile,Licorice, Meadowsweet, Golden Seal
6.Protect cells:Green tea, Grape seed, Turmeric, Rosemary, Garlic
7.Optimize digestive system:Wormwood, Gentian, Feverfew, Ginger,Chen Pi
8.Diet:
a.Reduce sugar and refined carbohydrates;Low sulfur diet;Dairy free;Reduce animal protein.
B.Add: Garlic;Soluble fibers; vegetables and spices
Functional Phytotherapy for Crohn’s disease
1.Bowel Flora protocol *.Aim treatment is to resolve dysbiosis
2.Eliminate persistent pathogens: Myrrh
3.Optimize immune system function:Wormwood, Echinacea
4.Eliminate Chronic inflammation:Myrrh, Boswellia, Licorice, Meadowsweet, Wormwood,Chamomile
5.Enhance natural barriers: Chamomile,Licorice, Meadowsweet, Golden Seal
6.Protect cells:Green tea, Grape seed, Turmeric, Rosemary, Garlic
7.Optimize digestive system:Wormwood, Gentian, Feverfew, Ginger,Chen Pi
8.Diet:
a.Reduce sugar, starches and refined carbohydrates;Low sulfur diet;Dairy free;Reduce animal protein.
b.Add:Vegetables and spices
Functional Phytotherapy for SIBO
1.Bowel Flora protocol*.Aim treatment is to resolve dysbiosis: 3-4 cycles ( 8-12 weeks)
2.Add Gentian Wormwood, Feverfew, Ginger (3 times day)
3.Echinacea root twice per day
4.To improve fat absorption & transit time: add Artichoke, Dandelion,Milk Thistle (3 times day)
5. For cramping pain:Cramp Bark, Ginger 2-4 times per day
6.To reduce chronic inflammation: Licorice, Chamomile,Meadowsweet ( 3 times per day)
*Bowel Flora Protocol
Day 1:
Prescribed medicines and supplements are to be taken as normal if the patient is currently on a protocol
Fasting — no food and plenty of water; if the patient cannot fast, recommend to eat light, fresh meals of vegetables and salads only.
No consumption of yeast, sugar or starches is essential. This includes fruits. Vegetable juices and broths are acceptable.
No alcohol or caffeine.
If cravings for carbohydrates are interfering with patient compliance, add Gymnema tablets (3 per day) into the protocol for blood sugar regulation.
Days 2 and 3:
Garlic: 1-2 fresh crushed cloves of garlic twice daily or 2 high quality, enterically-coated garlic tablets. If fresh garlic is used, it should be taken with a copious quantity of water. This has the effect of flushing the fresh garlic quickly into the small intestine.
Goldenseal could be taken here as well: 4 tablets containing at least 500 mg of root per day
Fasting is ideal; if the patient cannot fast, recommend very light, fresh meals of vegetables and salads.
No consumption of yeast, sugar or starches is essential. This includes fruits and fruit juices. Vegetable juices and broths are acceptable.
No alcohol or caffeine.
Days 4-15:
Slippery elm powder: 1-2 heaped teaspoons of slippery elm powder with copious (240 mL) water, to allow it to swell in the GIT.
Herbal antioxidant (green tea, grape seed extract, turmeric, rosemary): 2 tablets at night before bed or on an empty stomach, at least 2 hours away from food
Gradually introduce clean, fresh foods
Daily consumption of green tea
Day 16: Repeat protocol for another 14 days cycle if desireed.
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