The information contained in this groundbreaking article applies to at least 75 percent of people who are struggling to lose weight. It is a major factor contributing to the fatigue associated with being overweight and having symptoms of hypothyroid. It involves new discoveries regarding iron metabolism and explains why even if you eat foods containing plenty of iron you may still have rather dramatic iron deficiency issues, which handicap your metabolism and thyroid function.
Traditional thinking about iron is that either you get enough in your diet or you don’t. People who don’t eat red meat, menstruating women, those who exercise a lot, and those with digestive bleeding or other blood loss issues are at risk for iron deficiency and either functional or blatant anemia. In general, iron deficiency is thought to be associated with undernutrition or malnourishment.
Ironically, in the past few years it has become clear that at least half the people who are overweight have impaired iron metabolism detectable on blood tests. In many of these cases dietary iron intake was adequate, perplexing researchers. It now appears that inflammation associated with excess body weight elevates a hormone in your liver called hepcidin, which has the net effect of reducing iron absorption into your body from your digestive tract. The result is a metabolic nightmare of weight gain, fatigue, and poor thyroid function.
It is now clear that hepcidin levels elevate in response to inflammation. This could be from inflammation of any type: infection, toxin exposure, excess alcohol, medications, injury, excess exercise, lack of sleep, too much stress, etc. In this regard, being overweight is an ongoing inflammatory problem wherein your extra pounds of white adipose tissue crank out inflammatory signals 24 hours a day, seven days a week, as if someone will not stop yelling at you. The more excess weight you have, the higher the inflammation (in addition to all other potential sources of inflammation).
Iron is utterly indispensable to your metabolism and survival. For example, mice that are genetically bred to have high levels of hepcidin die within a few days from iron deficiency. Iron is need for growth, repair, assembly of proteins into your body structures, nerve function, and much more.
On the other hand, iron is highly reactive. Your body literally keeps it in cages like ferritin, similar to a lion at the zoo. When needed, the lion is let out at the proper place and time so that it can do something useful. If the cage is opened at the wrong time or place, iron can jump out and set off damaging free radical chain reactions. It appears that hepcidin intentionally reduces iron intake during times of inflammatory stress to prevent the inflammation from damaging iron transport and storage systems (causing inappropriate iron release). In other words, if your body is in a state of inflammatory wear and tear it may be difficult to use iron in a healthy way.
This offers excellent survival features for short-term inflammatory distress. However, a chronically inflamed person, as from obesity, can develop a real catch-22 wherein hepcidin is elevated for too long, creating a scenario of ongoing iron deficiency, either functional (meaning not enough iron for metabolism to function well) or blatant (meaning anemia).
Rampant overuse of antibiotics and high-sugar diets have created an epidemic of candida albicans overgrowth in overweight people. This is especially common in overweight people with thyroid problems, as I have observed first hand since 1985. Interestingly, hepcidin is a powerful antifungal. This means that your body may raise hepcidin levels as part of its natural defense against candida overgrowth. Again, this has survival advantages, especially in olden times. However, in a population of overweight people with antibiotic-induced candida overgrowth, it is a double whammy against functional metabolism.
The consequence to thyroid metabolism is twofold. First, the inactive thyroid hormone, T4, is converted to the biologically active hormone, T3, mostly on cell membranes of liver cells. Hepcidin is made in your liver and is produced excessively in response to high inflammation. Such inflammation will also damage liver cell membranes, thus reducing the conversion of T4 to T3. This is one main reason why inflammation of any type disturbs thyroid function.
Second, when biologically active thyroid, T3, binds to cell membranes and communicates to the nucleus of your cells how fast their metabolic pace should be set, it is like a hormone manager giving an order to a cell factory. The worker bees in the cell factory then need iron for the genes that will implement the thyroid order. In fact, the next 80 metabolic genes responding to a thyroid order all need iron. If iron is lacking, metabolism simply cannot run at an optimal pace, resulting in all the symptoms of hypothyroid—even in the presence of normal T4 and normal T3.
Even if iron is normal on a blood test, a person can still have all the problems above, though levels tend to be toward the lower end of the normal range. Hemoglobin (Hgb) and hematocrit (Hct) are also on the low side of the normal with this problem. One or another being out of range or on the low side signifies a major problem. Serum ferritin is typically low or low normal, unless inflammation is very high, which can actually drive up ferritin scores. Lab tests can help; however, fatigue along with trouble losing weight despite eating better and exercising are general indicators of a potential problem.
The most basic approach is to follow The Leptin Diet®, which is anti-inflammatory. As you begin to lose weight, you reduce inflammation, hepcidin levels should come down, and the iron in your diet will work better. If you have little iron in your diet, you should take a high-quality iron supplement. I like iron glycinate, a true protein chelate of iron. I would stay away from all cheap iron salts such as ferrous sulfate (these cause free radical damage).
There are many basic supplements that are fundamental to metabolism along with a good diet, as I have outlined in The Leptin Diet Weight Loss Challenge #1 – Overview and Basic Needs. All of these are significantly contribute to anti-inflammatory basic nutrition. Based on the new information in this article, it is accurate to say that ensuring you have adequate iron intake should be added to this basic list of nutrient needs for weight loss, especially in conjunction with basic anti-inflammatory nutrition.
A more comprehensive approach to this specific issue is to take an iron supplement as a trial to see if it helps your energy. Additionally, fat-soluble antioxidants that are targeted to improve liver function would be top choices. My top recommendations would be acetyl-l-carnitine, coenzyme Q10, tocotrienol E, r-alpha lipoic acid, and silymarin. Many other anti-inflammatory nutrients may also be of value. Your bottom line is to get enough support to engage the process of weight loss, maintain steady progress, improve your energy level, and direct your hemoglobin and hematocrit levels to the middle of the normal range on a blood test.
Some individuals may need to employ a more targeted anti-candida program to fully solve this problem. I discuss these topics more fully in my series of comprehensive articles on the Leptin Diet Weight Loss Challenge. It is important to know the direction you are heading. If you are doing well and making progress, you are most likely doing enough – at least as long as you are getting somewhere. If you hit a plateau or fail to get out of the starting block, you certainly need to become an active problem solver for your metabolic issues. Hepcidin issues are far more common than not in any person who struggles with weight.
Traditional thinking about iron is that either you get enough in your diet or you don’t. People who don’t eat red meat, menstruating women, those who exercise a lot, and those with digestive bleeding or other blood loss issues are at risk for iron deficiency and either functional or blatant anemia. In general, iron deficiency is thought to be associated with undernutrition or malnourishment.
Ironically, in the past few years it has become clear that at least half the people who are overweight have impaired iron metabolism detectable on blood tests. In many of these cases dietary iron intake was adequate, perplexing researchers. It now appears that inflammation associated with excess body weight elevates a hormone in your liver called hepcidin, which has the net effect of reducing iron absorption into your body from your digestive tract. The result is a metabolic nightmare of weight gain, fatigue, and poor thyroid function.
Hepcidin 101
Hepcidin is a hormone produced in your liver, discovered in 2000. Scientists discovered that it regulates iron use throughout your body (iron homeostasis). One of the ways in which hepcidin regulates iron status is by deciding how much iron to let into your body. In essence, it communicates directly to the cells of your digestive tract, either allowing them to let iron in or not. High levels of hepcidin reduce or prevent dietary iron intake, regardless of the iron content of your food.It is now clear that hepcidin levels elevate in response to inflammation. This could be from inflammation of any type: infection, toxin exposure, excess alcohol, medications, injury, excess exercise, lack of sleep, too much stress, etc. In this regard, being overweight is an ongoing inflammatory problem wherein your extra pounds of white adipose tissue crank out inflammatory signals 24 hours a day, seven days a week, as if someone will not stop yelling at you. The more excess weight you have, the higher the inflammation (in addition to all other potential sources of inflammation).
Iron is utterly indispensable to your metabolism and survival. For example, mice that are genetically bred to have high levels of hepcidin die within a few days from iron deficiency. Iron is need for growth, repair, assembly of proteins into your body structures, nerve function, and much more.
On the other hand, iron is highly reactive. Your body literally keeps it in cages like ferritin, similar to a lion at the zoo. When needed, the lion is let out at the proper place and time so that it can do something useful. If the cage is opened at the wrong time or place, iron can jump out and set off damaging free radical chain reactions. It appears that hepcidin intentionally reduces iron intake during times of inflammatory stress to prevent the inflammation from damaging iron transport and storage systems (causing inappropriate iron release). In other words, if your body is in a state of inflammatory wear and tear it may be difficult to use iron in a healthy way.
This offers excellent survival features for short-term inflammatory distress. However, a chronically inflamed person, as from obesity, can develop a real catch-22 wherein hepcidin is elevated for too long, creating a scenario of ongoing iron deficiency, either functional (meaning not enough iron for metabolism to function well) or blatant (meaning anemia).
Rampant overuse of antibiotics and high-sugar diets have created an epidemic of candida albicans overgrowth in overweight people. This is especially common in overweight people with thyroid problems, as I have observed first hand since 1985. Interestingly, hepcidin is a powerful antifungal. This means that your body may raise hepcidin levels as part of its natural defense against candida overgrowth. Again, this has survival advantages, especially in olden times. However, in a population of overweight people with antibiotic-induced candida overgrowth, it is a double whammy against functional metabolism.
The Impact of Low Iron on Metabolism
A new study details the dire metabolic consequences of low iron status. It shows that low iron turns on genes in your liver and muscles that promote fat storage and cause abnormal blood sugar elevation – precisely what goes wrong with metabolism that leads to the metabolic syndrome.The consequence to thyroid metabolism is twofold. First, the inactive thyroid hormone, T4, is converted to the biologically active hormone, T3, mostly on cell membranes of liver cells. Hepcidin is made in your liver and is produced excessively in response to high inflammation. Such inflammation will also damage liver cell membranes, thus reducing the conversion of T4 to T3. This is one main reason why inflammation of any type disturbs thyroid function.
Second, when biologically active thyroid, T3, binds to cell membranes and communicates to the nucleus of your cells how fast their metabolic pace should be set, it is like a hormone manager giving an order to a cell factory. The worker bees in the cell factory then need iron for the genes that will implement the thyroid order. In fact, the next 80 metabolic genes responding to a thyroid order all need iron. If iron is lacking, metabolism simply cannot run at an optimal pace, resulting in all the symptoms of hypothyroid—even in the presence of normal T4 and normal T3.
Even if iron is normal on a blood test, a person can still have all the problems above, though levels tend to be toward the lower end of the normal range. Hemoglobin (Hgb) and hematocrit (Hct) are also on the low side of the normal with this problem. One or another being out of range or on the low side signifies a major problem. Serum ferritin is typically low or low normal, unless inflammation is very high, which can actually drive up ferritin scores. Lab tests can help; however, fatigue along with trouble losing weight despite eating better and exercising are general indicators of a potential problem.
Solving Iron Deficiency Relating to Stubborn Weight
Adequate iron intake (red meat) compared to obvious iron loss (menstrual cycles, etc.) is still important to understand. However, this new data says that a condition of less inflammation must exist in order for iron to work properly in your body.The most basic approach is to follow The Leptin Diet®, which is anti-inflammatory. As you begin to lose weight, you reduce inflammation, hepcidin levels should come down, and the iron in your diet will work better. If you have little iron in your diet, you should take a high-quality iron supplement. I like iron glycinate, a true protein chelate of iron. I would stay away from all cheap iron salts such as ferrous sulfate (these cause free radical damage).
There are many basic supplements that are fundamental to metabolism along with a good diet, as I have outlined in The Leptin Diet Weight Loss Challenge #1 – Overview and Basic Needs. All of these are significantly contribute to anti-inflammatory basic nutrition. Based on the new information in this article, it is accurate to say that ensuring you have adequate iron intake should be added to this basic list of nutrient needs for weight loss, especially in conjunction with basic anti-inflammatory nutrition.
A more comprehensive approach to this specific issue is to take an iron supplement as a trial to see if it helps your energy. Additionally, fat-soluble antioxidants that are targeted to improve liver function would be top choices. My top recommendations would be acetyl-l-carnitine, coenzyme Q10, tocotrienol E, r-alpha lipoic acid, and silymarin. Many other anti-inflammatory nutrients may also be of value. Your bottom line is to get enough support to engage the process of weight loss, maintain steady progress, improve your energy level, and direct your hemoglobin and hematocrit levels to the middle of the normal range on a blood test.
Some individuals may need to employ a more targeted anti-candida program to fully solve this problem. I discuss these topics more fully in my series of comprehensive articles on the Leptin Diet Weight Loss Challenge. It is important to know the direction you are heading. If you are doing well and making progress, you are most likely doing enough – at least as long as you are getting somewhere. If you hit a plateau or fail to get out of the starting block, you certainly need to become an active problem solver for your metabolic issues. Hepcidin issues are far more common than not in any person who struggles with weight.
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