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Sugar Fuels Lymphedema
How sugar increases pain and swelling, what you can change to feel better
Sugar, salt, and fat make foods tasty. Many people know salt and fat can make lymphedema worse. Few understand that sugar is both damaging and addictive. Eating less sugar is an achievable first step in improving lymphedema symptoms and reducing lymphedema risk. Reducing sugar consumption also helps improve other health conditions.
By sugar we mean much more than just table sugar. All foods containing carbohydrates, including baked goods and dairy products, contain sugars. Refined carbohydrates contain smaller sugar molecules that are absorbed more rapidly than the larger molecules found in starches or complex carbohydrates.
Sugar contributes to all the major lymphedema and lipedema symptoms including systemic inflammation (which causes and amplifies pain), swelling (which can also cause pain), and damaging tissue changes. Sugar-related changes in gut microbes and liver disease also contribute to other health issues.
Systemic inflammation results from endotoxins circulating in the bloodstream and triggering an immune system response. Inflammation contributes to lymphedema swelling, damaging tissue changes, and infections because endotoxins stop the normal pumping action of lymphatic vessels, interfering with the normal flow of lymph, and cause lymphatic vessels to leak. Stopping lymph flow interferes with the action of the immune system, prolongs inflammation, and increases the risk of infections and disease.
Leaky lymphatic vessels increase swelling and trapped fluid causes damaging tissue changes including the accumulation of abnormal fat in affected areas. Abdominal fat accumulation and swelling affects many people who are obese or have metabolic syndrome, as well as people with lymphedema. Over time, swelling and accumulated fat can form a hanging abdominal panniculus.
Endotoxins (or lipopolysaccharides) are sturdy molecules made from fat and hundreds of sugar molecules. Gram-negative bacteria make endotoxins as part of their protective outer shell. These bacteria shed endotoxins as they grow and endotoxins remain after the bacteria die or are killed by cooking. Endotoxins are non-living and can resist being boiled for 30 minutes.
Gram-negative bacteria and endotoxins are commonly found in the large intestines of humans and other animals, and in feces. There are many varieties of gram-negative bacteria, most of which are harmless or beneficial, however a few varieties are harmful.
In healthy people, the small intestine does not contain many bacteria or endotoxins. Two factors can increase endotoxin levels in the small intestine: foods containing bacteria or endotoxins, or gut dysbiosis.
Bacteria and Endotoxins in Foods
Gram-negative bacteria and endotoxins are common in many food ingredients, especially foods that may have been exposed to intestinal contents or feces. Most bacteria are killed by cooking or other food preparation techniques before foods are eaten. Harmful bacteria, such as toxic E. coli, can remain in uncooked or under-cooked foods, such as hamburger.
Endotoxins however, are tougher than bacteria and not living, so they remain in foods after cooking. Meats and some processed foods contain significant quantities of endotoxins. Vegetables and fruits do not contain many endotoxins.
Our digestive tract extends from the mouth to rectum and contains a large community of gut microbes including bacteria, yeast or fungi, and viruses. We have a mutually beneficial relationship with these organisms and they provide many important functions including digesting foods, synthesizing vitamins, regulating levels of estrogen and other hormones, and helping to control appetite and mood.
The mix of gut microbes varies over time in terms of the number of different microbe varieties (microbial diversity) and the relative numbers of microbes of each type. Food choices, medications, infections, exercise, and other factors influence the mix of gut microbes. Changes gut microbes affect our physical and mental health via multiple pathways.
Western diets high in sugar, fats, and protein but low in fiber cause a series of unhealthy changes in intestinal microbes that result in gut dysbiosis. Gut dysbiosis is both a symptom of obesity and a cause of obesity and related disorders.
Early stage gut dysbiosis affects many people, including obese children and adults. Symptoms of gastrointestinal distress from early stage gut dysbiosis are not common or may not be consistent. Lab tests may show markers of inflammation.
More advanced gut dysbiosis can cause a range of digestive symptoms including pain, constipation, and diarrhea. Dysbiosis is associated with digestive system disorders such as irritable bowel syndrome, small intestine bacterial overgrowth (SIBO), ulcerative colitis, Crohn’s disease, and inflammatory bowel disease, as well as other diseases.
Most gut microbes live in the large intestine. A healthy small intestine contains relatively few microbes that are passing through as part of intestinal contents. Only a fraction of these microbes are gram-negative bacteria.
Changes associated with gut dysbiosis include larger numbers of gram-negative bacteria colonizing in the small intestine, fewer beneficial gram-positive bacteria, lower overall microbial diversity. Damage to the protective mucus lining in the small intestine leads to gut leakage or increased intestinal permeability. Dysbiosis also slows down the movement of food through the digestive tract and contributes to obesity by extracting nutrients from foods more effectively.
Gram-negative bacteria are the source of endotoxins and gut dysbiosis increases endotoxin levels in several ways. Gram-negative bacteria colonizing in the small intestine create more bacteria and as well as more endotoxins. Since bacteria reproduce by dividing, the population of gram-negative bacteria can double every 20-30 minutes when sugar is available. Even if these bacteria die quickly, their endotoxins remain in the small intestine.
As gut dysbiosis progresses, E. coli and other gram-negative bacteria change and become adhesive and invasive. Because the mucus barrier is damaged, these bacteria can adhere to the wall of the small intestine. They can invade and spread throughout the body by living and reproducing inside of macrophages, a type of white blood cell that normally kills bacteria. Invasive bacteria create more inflammatory endotoxins and can infect other body systems. Bacteria block the normal anti-inflammatory and infection fighting functions of the macrophages.
Increased Intestinal Permeability
Endotoxins and other harmful gut contents are able to pass through the wall of the small intestine and enter the bloodstream to cause systemic inflammation when the protective mucus lining of the small intestine is damaged and intestinal permeability is increased. Conditions that increase intestinal permeability include increased levels of bacteria in the small intestine (from gut dysbiosis or infection), liver disease (see below), drinking alcohol, and (in some people) reactions to gluten, a protein found in wheat, barley and rye.
Fats provide another way for endotoxins in the small intestine to enter the bloodstream. The most common type of fat in foods are long-chain fats. Long-chain fats are broken down in the small intestine and converted into a milky liquid called chyle that can also contain endotoxins. Chyle is absorbed through the wall of the small intestine and passed into the bloodstream by the lymphatic system.
Fats are digested and absorbed gradually, raising endotoxin levels in the blood for several hours. For example, a small serving of cream containing fat and sugars increased blood endotoxin levels for more than four hours.
Sugars high in fructose also increase lymphedema swelling by contributing to liver disease, which greatly increases the volume of lymph produced by the liver. Swelling from increased lymph output from the liver can affect the whole body, starting with the trunk and legs.
A normal healthy liver produces half of the total lymph in the body. Lymph output from the liver increases in each stage of liver disease, as liver function declines. Cirrhosis, or late-stage fatty liver disease, increases lymph output from the liver to 6-10 times normal, overloading the lymphatic system with 3-5 times as much total lymph as normal. Liver disease also prolongs inflammation by reducing the liver’s capacity to remove endotoxins and other toxins from the blood.
Risk of liver disease can be increased by obesity, alcohol consumption, infection (hepatitis, Epstein-Barr virus, etc.), genetics, and other factors. Non-alcoholic fatty liver disease (NAFLD) is very common in overweight children and adults. Liver disease often causes malaise, fatigue, and leg swelling but may not be diagnosed until an advanced stage. Liver disease also contributes to other health issues including obesity, gut dysbiosis, and increased intestinal permeability.
Sugar compounds are made of three types of simple sugars: glucose (or dextrose), fructose, and galactose (milk sugar). The mix of simple sugars depends on the source of the food. Table sugar made from sugarcane or sugar beets contains equal parts glucose and fructose.
High fructose sweeteners used in beverages and food products are made from corn, apples, pears, or grapes. These sweeteners contribute to fatty liver disease because fructose gets converted to fat (triglyceride) and stored in the liver when glucose and insulin levels are high. Excessive fat impairs liver function, resulting in disease.
Endotoxins and high-fat diets have each been shown to cause insulin resistance, a pathological condition where cells stop responding to insulin. Insulin resistance results in blood glucose levels remaining elevated for long periods of time and higher than normal blood insulin levels.
Elevated glucose and insulin levels contribute to obesity, metabolic syndrome, type 2 diabetes, liver disease, and other health conditions.
Just like alcohol, frequent sugar intake (specifically fructose) reduces the sensitivity of the dopamine receptors in the reward centers of the brain, resulting in a pattern of addictive behavior. This includes continuous intake with regard for energy need (craving), need for larger quantities or binging (tolerance) and feeling irritable, shaky, anxious, or depressed during withdrawal.
Sugars contribute to damaging tissue changes in lymphedema by rapidly increasing glucose levels. Insulin resistance enables glucose levels to remain high for long periods.
Elevated blood glucose levels promote the formation of advanced glycation end products (AGEs). AGEs are pro-inflammatory pathogens that cause damaging changes in skin tissues, seen in areas affected by lymphedema. They can also trigger nerve damage, blood vessel damage, retinopathy, and other complications of diabetes. AGEs also increase the risk of developing Alzheimer's disease, cardiovascular disease, stroke, and other conditions.
Three Ways to Reduce Sugar
Here are three steps to reduce your sugar intake and improve your health.
If you take insulin or other medication for diabetes, your dosage may need to be adjusted as you change your eating habits to include fewer carbohydrates. Check with your healthcare provider.
Lymphedema and Lipedema Nutrition Guide
Read the Lymphedema and Lipedema Nutrition Guide to learn more about food choices and ‘eating to starve lymphedema.’
The eating plan recommended in the book includes additional ways to reduce inflammation, foods to improve gut dysbiosis and reduce intestinal permeability, and foods that support liver function and fight liver disease.
This guide includes everything you need to change your eating pattern: meal plans, recipes, shopping guide, information on eating away from home, help with the process of change, and more.
© 2017 by Lymph Notes, all rights reserved.
Category: Nutrition and Lymphedema Updated: 2017-02-03
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