By Renata Trister DO
IDEAS FOR NATURAL LIVER SUPPORT
Your liver is one of the largest organs in your body, and it
performs a vast array of metabolic functions.
Additionally, the liver plays a role in regulating blood sugar,
breaking down damaged blood cells, and removing toxins from our
bodies. Because of these important functions, a sluggish or
diseased liver can take its toll on your overall health.
SUPPORTING THE LIVER
There are many steps you can take to support your liver and ensure
its proper function. One of the simplest things you can do is to
avoid or limit toxins. This includes alcohol, processed sugar and
sweets and over-the-counter pain relievers. Diet also plays a huge
role in the health of our liver. The following is a list of natural
remedies that can be used for liver support.
ACIDIC DRINK IN THE MORNING
In Chinese medicine, Qi is your vital life force and is responsible
for the harmonious “flow” of energy in our bodies. Because of its
role in healthy circulation, the liver is largely responsible for
maintaining Qi. Additionally, Chinese medicine believes that the
best time to support your liver is first thing in the morning.
There are studies that show the benefit of consuming acidic
substances for the liver. Apple cider vinegar has been shown to
have a protective effect on the liver and lower oxidative stress.
Citrus juices, like lemon, also have benefits, including anti-
inflammatory and antioxidant capabilities.
Drinking these acidic drinks early in the morning may increase the
beneficial effects. Wake up your liver in the morning by adding a
couple TBSP of apple cider vinegar and a squeeze of lemon to a
cup of warm water.
HERBS TO SUPPORT THE LIVER
Milk thistle benefits work by drawing toxins out of the body
and protecting the liver from damage. This herb is used for
liver support, milk thistle is a powerful liver cleanser. It helps
rebuild liver cells while removing toxins from the body that
are processed through the liver. Silymarin, which is derived
from the milk thistle plant, has been used in traditional
medicine as a natural remedy for diseases of the liver because
of its potent antioxidant activity.
Oregon Grape Root for its ability to stimulate liver function
and relieve congestion. This herb also helps improve the flow
of bile through our bodies, which promotes efficient blood
Beet Root is shown to have protective and anti-carcinogenic
benefits for the liver. Beets are widely available at the
grocery store and can also be juiced. Supplements containing
beet root powder are also available.
Dandelion is an herb that has been noted for purifying and
protecting the liver from oxidative stress and injury.
Dandelion is available in tea, tincture and can be eaten fresh
Alfalfa Sprouts are vitamin-rich shoots that help to reduce
the accumulation of cholesterol in the liver.
Cichoric acid, found in the herb Echinacea purpurea, has
demonstrated promise for its preventive effects liver lipid
metabolism disorders in obesity.
CASTOR OIL PACKS
Castor oil packs have been used to promote circulation of the
blood and lymphatic drainage.
Historical textbooks list castor oil as one of the oldest ways to
support health with citations dating back to 1550 BC in Egypt,
thousands of years in India and China, and Europe.
WHAT IS CASTOR OIL?
Castor oil and its major constituent ricinoleic acid, an unsaturated
omega-9 fatty acid, has been researched for analgesic, anti-
inflammatory, laxative, and uterine relaxation effects. Specifically
castor oil has been shown to increase the levels of T-11
lymphocytes in the top layers of the skin, increase prostaglandin
E2, and activate the EP3 prostanoid receptor. Increase in T-11
lymphocytes is hypothesized to support immunity.
The heat from a castor oil packs increases blood flow and may
improve oxygenation to target tissues. Castor oil also activates the
VR1 receptor similarly to capsaicin, and this may account for its
Castor oil has a lipid structure that easily passes through the skin’s
surface. As castor oil moves through the lymph system, it
stimulates a healthy flow of lymph fluid. This flow is essential to
removing waste materials from the body. Castor oil contains
ricinoleic acid, which is easily absorbed into the liver. Ricinoleic
acid is a powerful anti-inflammatory agent that also provides
significant pain relief.
Castor oils packs are typically placed on top of the liver or on top
the uterus. The former supports liver health, while the latter
supports reproductive health. Castor oil packs should be avoided
while trying to become pregnant, and during pregnancy.
CASTOR OIL PACK SUPPLIES:
Wool flannel large enough to cover the liver.
Organic, cold pressed castor oil.
Hot water bottle.
Towel that you don’t mind getting dirty.
Storage container for wool flannel once finished with pack (a
mason jar or plastic bag).
Warm water on the stove until almost boiling. Lay towel on bed or
Stretch plastic wrap over towel and lay out piece of wool flannel.
Saturate the flannel in castor oil (you want it fully saturated, but
Once water is warm, fill water bottle.
Place wool flannel and plastic wrap on top of liver or abdomen.
Cover as much of the flannel as possible with plastic wrap.
Lie down on towel and place warm water bottle on top of liver.
Relax for 20-30 minutes or longer. Repeat this procedure as often
You may also enhance your castor oil pack with essential oils for a
relaxing, aromatic experience.
By Renata Trister DO
The Low FODMAPs DIET for IBS
The low FODMAPs diet is an elimination type diet that has become first line of dietary therapy recommended for patients suffering with IBS.
This plan was developed by Australian dietitian Sue Shepherd and the researchers at Monash University in the late 1990s. Much research was done on this subject and in the early 2000s the Monash university team developed a well-defined and structured diet plan specifically formulated for patients with IBS.
What is FODMAPs?
The acronym FODMAPs stands for Fermentable Oligosaccharides Disaccharides Monosaccahrides and Polyols. These are complex names for different short chain sugars found in foods. The F in Fermentable means that intestinal bacteria can consume these sugars producing gas through their digestive processes. The rest of the acronym just lists the names of the different types of short chain sugars. These fermentable sugars are found in various carbohydrate rich foods, such as starchy foods (certain grains, breads and cereals) as well as in some fruits, vegetables and dairy. These short chain sugars are not very well absorbed by the body. Rather than being absorbed in the small intestine, these small chain sugars travel to the large intestine. The large intestine contains trillions of bacteria that use these undigested sugars for food. When these bacteria consume these sugars, they produce gas. Patients with IBS have sensitive intestinal lining and experience this with bloating and pain. Furthermore, the presence of undigested FODMAP sugars in your colon attracts water, causing loose stools and diarrhea. Reducing the number of FODMAPs in the diet, can decrease gas, pain and fluid in the large intestine of patients with IBS. A low FODMAPs diet has also been shown to reduce the amount the amount of histamine. Histamine is a natural substance, a biogenic (resulting from the activity of living organisms such as, fermentation) amine that is present in many foods and is produced by human cells with a wide array of functions. Histamine is a neurotransmitter, it has a role in allergic reactions, often associated with causing itching, redness, swelling, cough or rash. Histamine regulates sleep and aids in digestion by playing a role in stomach acid secretion. The accumulation of histamine and the inability of the body to completely degrade it may play a role in the pain symptoms many IBS sufferers experience. Studies have shown that following a low FODMAPs diet plan can have an 8-fold decrease in histamine levels in some IBS patients.
Where are FODMAPs found?
Examples of foods high in each of the FODMAPs.
Oligosacchrides/ Fructans: Artichokes, Garlic, Leek, Onions, Green Onions, Shallots, Wheat, Rye, Barley, Fructo-oligosaccharides (FOS) found in Agave Syrup and Asparagus. Galacto-Oligosaccharides (GOS) found in Beans, Lentils, Chickpeas.
Disaccharides/ Lactose: Dairy products such as Milk, Ice Cream, Yogurt, Soft Cheeses (such as cream cheese ricotta, cottage, brie).
Monosacchrides/ Fructose: Apples, Mangos, Pears, Watermelon, Honey, High-Fructose Corn Syrup.
Polyols: Found in stone fruits such as Apricots, Nectarines, Pears, Plums, Prunes, as well as in sugar alcohols sorbitol, mannitol, xylitol, maltitol and isomalt. These sugar alcohols are often found on ingredient labels of many prepackaged and processed foods.
The list is not complete. The best way to begin your low FODMAPs protocol is to discuss this with your physician and use the Monash University FODMAPS app.
What does the low FODMAP diet involve?
The Low FODMAP Diet has two phases.
During first phase of the Low FODMAP Diet all high FODMAP foods are strictly eliminated for 4-6 weeks. Using the Monash FODMAPs app is important for this process. The symptom response during this period should be monitored and noted.
During the second phase foods that were restricted in the first phase are reintroduced gradually. This is where the type and amount of FODMAPs that can be tolerated by the individual are identified.
According to a study published in the Journal Gastroenterology, about 3 out of 4 people with IBS had their symptoms ease after starting a low-FODMAP diet and felt the most relief after 7 days or more on the plan. Success rates vary and depend on the type of IBS a patient has.
How Bacteria Influence Food Cravings and Weight.
By Renata Trister DO
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:
Several strains of Bifidobacterium and Lactobacillus have been shown to improve anxiety- and depression-like eating behaviors.
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.
Eating a clean diet rich in green vegetables, healthy proteins and fats supports the health of both your body and the microbiome.
Vitamin D and Inflammatory Bowel Disease
By Renata Trister DO
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.
Nicolai Hartmann and The Four Levels of Reality.
By Renata Trister DO
Nicolai Hartmann (20 February 1882 – 9 October 1950) was a Baltic German philosopher. He was an important Nicolai Hartmann and The Four Levels of Reality.
Nicolai Hartmann (20 February 1882 – 9 October 1950) was a Baltic German philosopher. He was an important philosopher and is regarded as one of the most important twentieth century metaphysicians. Metaphysics is the branch of philosophy concerned with the nature of existence, being and the world. Metaphysics is the foundation of philosophy: Aristotle calls it “first philosophy” (or sometimes just “wisdom”), and says it is the subject that deals with “first causes and the principles of things”.
Hartmann’s major contribution is his concept of the four levels of reality.
Four main levels of reality are distinguished by Hartmann: the inanimate, the biological, the psychological and the spiritual. This includes all historical realities such as history, language, law, art and social customs. The underlying concept is the following: the structure and the laws of history and other spiritual processes are different from the structure and laws of, say, inanimate beings, the former are not in any way less real than the latter. The same intuition applies to the other levels as well: biological and psychological processes are as real as any other process, and they have their own specific groups of categories.
On the other hand, the psychological and spiritual levels are different.
The category of the spirit is divided into personal, objective and objectivated spirit. Personal spirit is the spirit of the individual; objective spirit is the living spirit of communities; and objectivated spirit characterizes the products of spirit. The components of personal spirit are consciousness, will, foresight and, liberty.
There are laws that are valid for all the levels: higher levels rest on lower ones; the lower level is the conditioning one; the higher level is independent from the lower one as to its conformation and its laws.
Each of the four levels of the world contains other levels, organized according to a variety of patterns.
Not all the levels are equally well-known. The group that includes time, space, process, causality and substance, together with the effects that they mutually exert on each other, determines the physical entity.
Hartmann acknowledges that the distinction between the psychological and the spiritual levels is problematic. However, it appears that science provides some help here, especially with the distinction between the objects of psychology and the objects of the sciences of the spirit (linguistics, law, social and historical sciences).
Hartmann assigns language, consciousness, and foresight alternatively to the psychological level or to the personal level of the spirit. He claims that the same acts of consciousness pertain to both psychic and spiritual being.
Hartmann describes the laws that govern the various levels of reality and their connection.
BY RENATA TRISTER DO
Raw milk or milk that is not pasteurized or homogenized is viewed by many as dangerous. A look into claims made by the FDA and CDC related to raw milk being dangerous have been found to be questionable. Although it might have earned a reputation among some for being dangerous raw milk from a safe source is actually beneficial.
What is “raw milk” exactly? It’s milk that comes from grass-fed cows, is unpasteurized and unhomogenized. This means raw milk contains all of its natural enzymes, fatty acids, vitamins and minerals — making it what many refer to as a “complete food.”
But can’t raw milk cause problems due to the risk of consuming bacteria? The risk of this happening is very, very low. In fact, according to medical researcher Dr. Ted Beals, M.D., you are 35,000 times more likely to get sick from other foods than you are from raw milk. The CDC reports that there are an estimated 48 million foodborne illnesses diagnosed each year. Of these 48 million illnesses, only about 42 each year are due to consumption of fresh, unprocessed (raw) milk.
Studies now suggest that children who drink raw milk are 50 percent less likely to develop allergies and 41 percent less likely to develop asthma compared to children who don’t. A study published in the Journal of Allergy and Clinical Immunology involved 8,000 children with various diets, and one of the conclusions that researchers made was that by drinking raw milk, children experienced “naturally immunizing” effects.
As documented on the Real Milk website, many other studies carried out over the past century have shown that raw milk benefits and supports children’s growth and development in other ways too, including increasing immunity against infections, boosting dental health and supporting skeletal growth, for example.
You might be wondering: How can raw milk reduce allergies, and isn’t dairy tied to high rates of intolerance or sensitivities? Nutrients like probiotics, vitamin D and immunoglobulins (antibodies) found in raw milk naturally boost the immune system and reduce the risk of allergies in both children and adults. Enzymes found in raw milk help with digestion but are often reduced or destroyed during pasteurization, which can contribute to lactose intolerance.
Dairy might have a bad reputation when it comes to causing or worsening acne and skin inflammation, but this is far from the case with raw milk. As we’ve seen, the benefits of raw milk are numerous, but surprisingly one of the most common reasons that people consume it is to benefit their skin. The success stories of people consuming raw milk to improve conditions such as psoriasis, eczema and acne are very widely reported. Raw milk contains large amounts of healthy saturated fats and omega-3 fats, to support skin hydration. Probiotics in raw milk can kill off or balance bad bacteria in your gut, which can dramatically affect the health of your skin.
Fresh raw milk can be used to naturally make Probiotic Foods
Probiotics are microorganisms that line your gut and support nutrient absorption. They also help protect you from foreign invaders like E. coli and parasites. The best way to include probiotics in your diet is to get them in their most natural state, which includes raw milk products, such as cheese, kefir and yogurt. Real, raw and organic probiotic yogurt, cheeses and kefir have been consumed by some of the healthiest populations living around the world for thousands of years. In addition to pasteurization, conventional milk also usually undergoes a homogenization process. Homogenization is a high-pressure process that breaks down fat into tiny particles — however, fat subjected to high heat and pressure becomes oxidized and rancid. Many low-fat dairy products also have thickening agents added to make up for lost texture, and some have even been tied to rising rates of inflammatory diseases like cancer. Raw milk needs no added thickeners or shelf-stabilizers and also doesn’t contain added sugar or flavors.
Nutritional Profile of Raw Milk
Fat-Soluble Vitamins A, D and K2
Because raw milk comes from cows or goats grazing on grass, research studies have shown that it contains a higher level of heart-healthy, cancer-killing, fat-soluble vitamins than milk that comes from factory-farm cows. Studies have shown that one of the most common deficiencies in children is a lack of fat-soluble vitamins. These vitamins support the brain and nervous system and are crucial for development, focus and brain function. Fat-soluble vitamins also support bone density and help naturally balance hormones, however they’re significantly decreased following pasteurization.
Short Chain Fatty Acids, CLA and Omega-3s
In addition to being high in anti-inflammatory omega-3 fatty acids, raw milk from grass-fed animals is a rich source of butyrate, a short chain fatty acid that’s widely known to control health issues related to inflammation, slow metabolism and stress resistance.
Raw Milk vs. Store Bought Milk
Dairy products have gotten a bad rap over the years, but this is actually mostly due to the pasteurization process. When milk is pasteurized, it destroys many of the nutrients that make raw milk beneficial. Why is pasteurization even performed in the first place then? Because it exposes milk to very high temperatures, it can also kill harmful bacteria that are possibly able to make their way into the milk. However, as mentioned above, it’s very rare for these types of bacteria to be found in milk to begin with.
Key nutrients and enzymes are greatly reduced during the pasteurization process. If you consider the fact that many of these nutrients are not only reduced, but altered from their original states, you can understand that some of these nutrients are completely unavailable for your body to use and very difficult to digest.
Vitamin B and C levels are decreased as well. In multiple studies, it’s been found low-temperature pasteurization decreases vitamin C content by up to 25 percent, along with the content of B vitamins, iron and calcium. Further reductions in nutritional value takes place when milk sits on supermarket shelves sometimes for weeks where it’s kept until sold. Some have found that following pasteurization, vitamin C (ascorbic acid) is oxidized into dehydroascorbic acid, which is an inactive, degraded form of vitamin C that does not have the same benefits as natural vitamin C. Other studies have found that pasteurization in other food products reduces overall antioxidant activities by about 55 percent to 60 percent and reduces vitamin B2 concentrations by up 48 percent.
Raw milk must be purchased from reputable local farmers in your area.
By Renata Trister DO
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.
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 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.
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.
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.
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.
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.
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.
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  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.
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.
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.
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.
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.
The enthesis organ concept and its relevance to the spondyloarthropathies.
Benjamin M, et al. Adv Exp Med Biol. 2009.
A characteristic feature of the spondyloarthropathies is inflammation at tendon or ligament attachment sites. This has traditionally been viewed as a focal abnormality, even though the inflammatory reaction intrinsic to enthesitis may be quite extensive. We argue that the diffuse nature of the pathology is best understood in the context of an ‘enthesis organ concept’. This highlights the fact that stress concentration at an insertion site involves not only the enthesis itself, but neighbouring tissues as well. The archetypal enthesis organ is that of the Achilles tendon where intermittent contact between tendon and bone immediately proximal to the enthesis leads to the formation of fibrocartilages on the deep surface of the tendon and on the opposing calcaneal tuberosity, but similar functional modifications are widespread throughout the skeleton. Many entheses have bursae and fat near the insertion site and both of these serve to promote frictionless movement. Collectively, the fibrocartilages, bursa, fat pad and the enthesis itself constitute the enthesis organ. However, it also includes both the immediately adjacent trabecular bone networks and in some cases deep fascia. The concept of a synovio-entheseal complex (SEC) and of a ‘functional enthesis’ are complimentary to that of an enthesis organ and also have important implications for understanding spondyloarthropathy. The SEC concept emphasizes the interdependence between synovial membrane and entheses within enthesis organs. It draws attention to the fact that one component (the enthesis) is prone to microdamage and the other (the synovium) to inflammation. If an enthesis is damaged, any ensuing inflammatory reaction is likely to occur in the synovium. The concept of a ‘functional enthesis’ serves to emphasise anatomical, biomechanical and pathological features that are shared between true fibrocartilaginous entheses and regions proximal to the attachment sites themselves where tendons or ligaments wrap around bony pulleys. Such’wrap-around regions’ are well documented sites of pathology in SpA-for tenosynovitis is a recognized feature. Stress concentration at the enthesis itself is dissipated at many sites by fibrous connections between one tendon or ligament and another, close to the insertion site. At a microscopic level, enthesis fibrocartilage is of paramount importance in ensuring that fibre bending of the tendon or ligament is not focused at the hard tissue interface. Normal enthesis organs are avascular in their fibrocartilaginous regions, but tissue microdamage to entheses is common and appears to be associated with tissue repair responses and vessel ingrowth. This makes the enthesis organ a site where adjuvant molecules derived from bacteria may be preferentially deposited. This microdamage and propensity for bacterial molecule deposition in the context of genetic factors such as HLA-B27 appears to lead to the characteristic inflammatory changes of AS. Understanding the enthesis organ concept helps to explain synovitis and osteitis in spondyloarthropathy. An appreciation of the complex anatomy of ‘articular enthesis organs’ (e.g., that associated with the distal interphalangeal joints) is helpful in understanding disease patterns in psoriatic arthritis. In this chapter, we review the extent and types ofenthesis organs and show how a patho-anatomic appreciation of these structures leads to a new platform for understanding the pathogenesis of SpA.