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April 22, 2019

Hypertension (Part 1)

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

Hypertension or high blood pressure: Blood pressure is the pressure against blood vessels and arteries created by the heart pumping blood around the body.  The force of this pressure against the arteries is blood pressure. It increases and decreases throughout the day. If it remains too high, then it is high blood pressure or hypertension. If blood pressure stays too high, it puts a strain on the heart and arteries, possibly resulting in cardiovascular disease, a heart attack or a stroke.

According to the CDC:

  • 32% of Americans or 1 in every 3 adults has high blood pressure (1)
  • About 1 in 3 American adults has prehypertension; blood pressure numbers that are higher than normal but is not yet hypertension (1)
  • This means 2 out of 3 Americans has an issue with blood pressure – either prehypertension or hypertension (1)
  • Only about half (54%) of people with high blood pressure have their condition under control (2)

How is BP calculated?

Two numbers are used to calculate blood pressure. First, systolic blood pressure is the pressure in blood vessels when the heart beats. The second number is diastolic blood pressure and is the pressure in blood vessels when the heart rests between beats (3). See the chart below (3) to identify if a BP reading is high, low or normal:

Blood Pressure Levels
Normal systolic: less than 120 mmHg
diastolic: less than 80mmHg
At risk (prehypertension) systolic: 120–139 mmHg
diastolic: 80–89 mmHg
High systolic: 140 mmHg or higher
diastolic: 90 mmHg or higher

 

Types of hypertension:

There are different types of hypertension.  Primary or essential hypertension is when the cause is unknown. Secondary hypertension is caused by another disease and is a symptom of that disease. If the root cause of that disease can be addressed, then often blood pressure is reduced or even becomes normal. Less common types of hypertension are:

  • Malignant hypertension has very obvious symptoms like changes in vision, chest pain, anxiety, nausea, numbness or weakness in arms or legs, shortness of breath, headache or reduced urination (4).
  • Resistant hypertension is persistent even after dietary & lifestyle changes have been made and/or the person is taking blood pressure medication (4). It is difficult to treat and may have an underlying cause that has yet to be identified.
  • Pulmonary hypertension is often indicated by a shortness of breath during routine activity, fatigue, chest pain, racing heartbeat, pain in the abdomen near the liver or decreased appetite (4).
  • White coat hypertension is when a person’s blood pressure measures high in the doctor’s office but is normal when the reading is taken at home (4).
  • Isolated systolic hypertension is when the systolic number is too high while the diastolic number is normal (4). It typically affects older people and is normally due to a condition or issue elsewhere in the body.

The exact cause of hypertension is currently unknown. Certain factors are believed to contribute to high blood pressure (3):

  • Stress
  • Smoking
  • Being overweight or obese
  • Excessive alcohol consumption
  • Too much salt or too little salt in the diet
  • Insufficient intake of potassium, calcium, and magnesium
  • Lack of physical activity
  • Age
  • Genetics
  • Kidney disease, Diabetes, Sleep apnea, Hormone disorders

One study has found that high blood pressure is associated with gut microbiota dysbiosis, both in animal and human hypertension (5). Dysbiosis is when there are too few health-promoting, good bacteria and too many harmful or pathogenic bacteria in the gut.

So what can you do about hypertension?

Fortunately there are numerous action steps you can take to manage hypertension which include diet, supplements and lifestyle factors. Hypertension is part of metabolic syndrome which is very much a lifestyle disease. Thus diet has a strong impact on the incidence and management of hypertension.  We will concentrate on diet changes that can help lower BP (blood pressure) in this article. We will run a second article to cover supplements and lifestyle factors that can help reduce blood pressure.

What Diet Changes can you make to reduce and manage your BP?

  • Reduce Sugar and Refined Carbohydrates: Multiple studies have found that reducing sugar intake in all forms leads to lower blood pressure (6, 7, 8).
  • Sodium and Potassium: Despite conventional wisdom, studies have found that too much or too little sodium can increase blood pressure in some individuals (9). For most healthy individuals, we recommend consuming between 3’000 and 6’000 mg of sodium per day (9). Below 3’000 mg of sodium per day was associated with a 27% increase in cardiovascular disease and death (9). Consuming more than 6’000 mg per day was associated with a 15% increase in cardiovascular disease and mortality (9). It appears that there are a subset of sodium-sensitive individuals whose BP increases from excessive sodium intake. However, this is not everyone. We recommend that those with high blood pressure do an experiment with salt and measuring BP (see action steps at the end of this article). In addition to sodium, other minerals like potassium have a significant influence on BP as well. Another study found diets rich in potassium to be more effective than an aggressive salt reduction to prevent hypertension (10).  Recommended potassium intake per day is 4’000-5’000 mg but the average person only gets 2’800 mg daily (11). Increase your potassium by eating high potassium foods like banana, sweet potato, white potato, orange, winter squash, white beans, beets, parsnip and spinach.  It may be necessary to supplement potassium in addition to adding potassium to the diet.

(Note: One teaspoon of salt is approximately 2’300 mg sodium. One medium banana has 422 mg of potassium.)

  • Magnesium and Calcium: Consuming a healthy diet that provides the recommended amount of the mineral magnesium can be help control BP (12). The RDA (Recommended Daily Allowance) for magnesium is 310–420 mg for adults and can be found in these foods high in magnesium: nuts, spinach & other greens, seeds, avocados, dark chocolate. Calcium, along with potassium and magnesium, may improve blood pressure levels and reduce coronary heart disease and stroke (13). It is recommended to get these minerals through increased consumption of fruits and vegetables (13). Calcium-containing foods include seeds, cheese, yogurt, bone-in fish like sardines, legumes, almonds and whey protein. The RDA for calcium varies depending on age and gender. Adults between 51 and 70 years are recommended to get 1’000- 1’200 mg per day.
  • Reduce Alcohol: It is well established that excessive alcohol consumption is a significant predictor of the development of hypertension and that alcohol reduction in patients with high BP can significantly lower systolic and diastolic blood pressure (14).
  • The DASH Diet: DASH or Dietary Approaches to Stop Hypertension is often regarded as the diet to follow for hypertension. In research, it has a reducing effect on both systolic and diastolic blood pressure but there is variation in the extent of the fall in blood pressure in different subgroups of patients (15). We think a generally healthy diet would be equally effective, as long as the sodium potassium balance is well managed and there are sufficient levels of other minerals.
  • Specific Foods can help to reduce blood pressure include: hibiscus tea (16), beets (17), fatty fish such as salmon (18), olive oil (19) and nuts (20).
  • Improve Gut Health: One study indicates that diet changes to re-balance gut microbiota could be a new strategy using nutrition to help reduce hypertension (5). This study goes on to say that probiotics affect BP. Trials showed a significant decrease in both systolic and diastolic BP in patients who took a daily dose of probiotics (21).

In Part 2 on Hypertension, we will discuss the supplements and some lifestyle factors that will significantly work to reduce hypertension. Please stay tuned for these tips.

Here are the abbreviated action steps you can take based on the information in this article:

  • Significantly reduce sugar and refined carbohydrates by skipping dessert, avoiding pastries, cookies, cakes, and anything made with white flour. You can take it a step further if you like and avoid all gluten and sugar, choosing a moderate amount of fresh fruit and a small amount of raw, unfiltered local honey to satisfy any sweet needs. You could even try avoiding all grains for a period of time and use stevia as an alternative to sweeteners. Allow sweet potatoes, squash, beets, plantains, and carrots to become satisfying sweets. Possibly add a square or two of dark chocolate (75% and higher cocoa content) as this can help with nutrients that can regulate BP.
  • Increase potassium intake by having plenty of starchy tubers like potatoes and sweet potatoes, plantains, avocados, bananas (eat them on the green side to have less blood sugar impact and get more resistant starch for good gut bacteria to feed on), and lots of leafy greens and some fresh fruits. Track with an app like MyFitnessPal for a few days and make sure you are getting at least 4’700mg/day. If BP is high, you may want to shoot for 6’000mg daily (some hunter-gatherer cultures have been reported to get as high as over 10’000mg daily on average).
  • Do a salt experiment by taking precisely 1.5 teaspoons sea salt (just over 3’000mg on the low end of intake that was found to be in the healthy range for cardiovascular disease prevention) and putting it into a small dish. Make this your salt for the day. Cook all your meals at home and consume only food that has no added salt (nothing packaged that has any sodium content to it). Add salt from the dish to food you are cooking and to food on your plate that day. Make sure you have finished the salt in the dish by the end of the day (you will have to adjust things if you are cooking for more than just yourself so that you are getting the full dish worth of salt that day). Take your blood pressure first thing in the morning on this day and 2-3 times throughout the day. Notice if it is higher, lower, or the same as usual. Also keep a note on how it felt. Did that seem like a lot of salt? A small amount? Or about usual for you? Then do the experiment again another day but this time use 2.5 teaspoons of sea salt (just under the 6’000mg high end for healthy salt intake). How did your blood pressure do that day?
  • Consume magnesium and calcium-rich foods and/or supplement to get adequate intake of both of these minerals. Be sure to have some nuts, seeds, plenty of greens including spinach, avocado, and some dark chocolate (1-2 squares at 75%+ cocoa content). Also get a couple of servings of grass-fed full fat dairy if you tolerate dairy (yogurt, kefir, cheese, etc.) and/or bone-in canned fish (canned wild salmon with the bone or canned sardines with the bones – the canning process makes the bones soft enough to eat – of course do not eat bones from fresh fish that are hard and brittle).
  • Limit alcohol consumption to 3 drinks per week (men) or 2 drinks per week (women) or less. And make sure a drink is actually a single drink (i.e. 4 oz pour for wine and not 6 or 8 oz). If it has been a while since you’ve gone a month without alcohol, try stopping entirely for 30-60 days.
  • Drink 2-3 cups of hibiscus tea daily by brewing a gallon of tea using loose leaf hibiscus flowers. Brew it strong and store in the fridge to drink over a few days.
  • Eat fermented foods and/or take probiotics daily. For example you can eat sauerkraut, kimchi, fermented beets, make beet kvass and drink it, unsweetened grass-fed kefir, etc. Or get professional-grade probiotics to take. Also consume prebiotic rich foods like lentils, green bananas, green plantains, potatoes that have been cooked then cooled 24-hours, onions that are still a bit crunchy (not fully caramelized), leeks, and dandelion greens.

 

References

  1. Nwankwo T, Yoon SS, Burt V, Gu Q. Hypertension among adults in the US: National Health and Nutrition Examination Survey, 2011-2012. NCHS Data Brief, No. 133. Hyattsville, MD: National Center for Health Statistics, Centers for Disease Control and Prevention, US Dept of Health and Human Services; 2013.
  2. Farley TA, Dalal MA, Mostashari F, Frieden TR. Deaths preventable in the U.S. by improvements in the use of clinical preventive services. Am J Prev Med. 2010;38(6):600–9.
  3. Centers for Disease Control and Prevention. Division for Heart Disease and Stroke Prevention. 2016. High Blood Pressure Fact Sheet. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_bloodpressure.htm. Accessed March 12, 2019.
  4. 2018. Types of Hypertension – Understanding the Differences. https://www.resperate.com/blog/hypertension/facts/definition-symptoms/types-of-hypertension. Accessed March 12, 2019
  5. Yang T, Santisteban MM, Rodriguez V, Li E, Ahmari N, Carvajal JM, Zadeh M, Gong M, Qi Y, Zubcevic J, Sahay B, Pepine CJ, Raizada MK, Mohamadzadeh M. 2015. Gut dysbiosis is linked to hypertension. Hypertension. 2015 Jun ;65(6):1331-40.
  6. Chen L, Caballero B, Mitchell DC, Loria C, Lin PH, Champagne CM, Elmer PJ, Ard JD, Batch BC, Anderson CA, Appel LJ. 2010. Reducing consumption of sugar sweetened beverages is associated with reduced blood pressure: a prospective study among United States adults. Circulation. 2010 Jun 8;121(22):2398-406. doi: 10.1161/CIRCULATIONAHA.109.911164.
  7. Malik AH, Akram Y, Shetty S, Malik SS, Yanchou Njike V. 2014. Impact of sugar sweetened beverages on blood pressure. Am J Cardiol. 2014 May 1;113(9):1574-80. doi: 10.1016/j.amjcard.2014.01.437.
  8. Brown IJ, Stamler J, Van Horn L, Robertson CE, Chan Q, Dyer AR, Huang CC, Rodriguez BL, Zhao L, Daviglus ML, Ueshima H, Elliott P. 2011. Sugar sweetened beverage, sugar intake of individuals, and their blood pressure: international study of macro/micronutrients and blood pressure. Hypertension. 2011 Apr;57(4):695-701. doi: 10.1161/HYPERTENSIONAHA.110.165456.9.
  9. O’Donnell M, Mente A, Rangarajan S, McQueen MJ, Wang X, Liu L, Yan H, Lee SF, Mony P, Devanath A, Rosengren A, Lopez-Jaramillo P, et al. 2014. Urinary Sodium and Potassium Excretion, Mortality, and Cardiovascular Events. N Engl J Med. 2014; 371:612-623. DOI: 10.1056/NEJMoa1311889.
  10. Lelong H, Blacher J, Baudry J, Adriouch S, Galan P, Fezeu L, Hercberg S, Kesse-Guyot E. 2017. Individual and Combined Effects of Dietary Factors on Risk of Incident Hypertension. Hypertension. 2017;70:712–720. org/10.1161/HYPERTENSIONAHA.117.09622.
  11. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. 2005. Origins and evolution of the Western diet: health implications for the 21st Am J Clin Nutr. 2005 Feb;81(2):341-54.
  12. Kostov K, Halacheva L. 2018. Role of Magnesium Deficiency in Promoting Atherosclerosis, Endothelial Dysfunction, and Arterial Stiffening as Risk Factors for Hypertension. Int J Mol Sci. 2018 Jun 11 ;19(6).
  13. Houston MC, Harper KJ.2008. Potassium, magnesium and calcium: their role in both the cause and treatment of hypertension. J Clin Hypertens (Greenwich).2008 Jul;10(7 Suppl 2):3-11.
  14. Collart F, de Timary P, Dom G, Dor BD, Duprez D, Lengelé JP, Matthys F, Peuskens H, Rehm J, Stärkel P. 2015. Alcohol-induced hypertension: an important healthcare target in Belgium. Acta Clin Belg. 2015 Dec;70(6):389-95. doi: 10.1179/2295333715Y.0000000039.
  15. Saneei P, Salehi-Abargouei A, Esmaillzadeh A, Azadbakht L. 2014. Influence of Dietary Approaches to Stop Hypertension (DASH) diet on blood pressure: a systematic review and meta-analysis on randomized controlled trials. Nutr Metab Cardiovasc Dis. 2014 Dec;24(12):1253-61. doi: 10.1016/j.numecd.2014.06.008.
  16. McKay DL, Chen CY, Saltzman E, Blumberg JB. 2010. Hibiscus sabdariffa L. tea (tisane) lowers blood pressure in prehypertensive and mildly hypertensive adults. J Nutr. 2010 Feb;140(2):298-303. doi: 10.3945/jn.109.115097.
  17. Coles LT, Clifton PM. 2012. Effect of beetroot juice on lowering blood pressure in free-living, disease-free adults: a randomized, placebo-controlled trial. Nutr J. 2012; 11: 106. doi: 1186/1475-2891-11-106.
  18. Ramel A, Martinez JA, Kiely M, Bandarra NM, Thorsdottir I. 2010. Moderate consumption of fatty fish reduces diastolic blood pressure in overweight and obese European young adults during energy restriction. 2010 Feb;26(2):168-74. doi: 10.1016/j.nut.2009.04.002.
  19. Moreno-Luna R, Muñoz-Hernandez R, Miranda ML, Alzenira F, Jimenez-Jimenez CL, Vallejo-Vaz AJ, Muriana FJG, Villar J, Stiefel P. 2012. Olive Oil Polyphenols Decrease Blood Pressure and Improve Endothelial Function in Young Women with Mild Hypertension. J.of Hypertension, Volume 25, Issue 12, 1 December 2012, Pages 1299–1304, https://doi.org/10.1038/ajh.2012.128.
  20. Mohammadifard N, Salehi-Abargouei A,  Salas-Salvadó J, Guasch-Ferré M, Humphries K, Sarrafzadegan 2015. The effect of tree nut, peanut, and soy nut consumption on blood pressure: a systematic review and meta-analysis of randomized controlled clinical trials. The Amer. J. of Clncl Nutr., Volume 101, Issue 5, 1 May 2015, Pages 966–982, https://doi.org/10.3945/ajcn.114.091595.
  21. Khalesi S, Sun J, Buys N, Jayasinghe R. Effect of probiotics on blood pressure: A systematic review and meta-analysis of randomized, controlled trials. 2014;64:897–903.
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April 9, 2019

To Supplement or Not to Supplement?

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

Nutritional or dietary supplements have become popular. Should you be taking them or not?

There are many reasons why, in our modern lives, we do not get adequate nutrition from the food we eat. Given that this applies to just about everyone in modern society, it is often necessary to use supplements.

Why We Need Supplements:

  • Poor diet: About 75% of the US population does not consume the recommended intake of fruit, and more than 80% do not consume the recommended intake of vegetables (1). In fact, 95% of Americans are deficient in vitamin D, 94% in vitamin E, 61% in magnesium, 51% in vitamin A, 49% in calcium, 43% in vitamin C, 15% in B6, 13% in folate, 12% in zinc, 8% in iron, 5% in copper and 4% in B12 (2). This is due to our modern diet of inadequate vegetables and fruits coupled with excessive amounts of processed foods. Processed and refined foods have been shown to be so devoid of nutrients that governments have mandated fortification of foods like processed grains with certain vitamins and minerals such as folic acid, riboflavin, vitamin D, iron, calcium, and others. Iodized salt has iodine added because goiter used to be more common due to iodine deficiencies from poor dietary choices.

 

  • Less diverse diet: We do not eat, nor do we even really have access to, the diversity of food types that our ancestors ate. Additionally, many of the foods we do have access to have been bred for taste and flavor, not nutritional content. Many wild ancestors of modern plants had far more nutrition and phytonutrients as compared to the modern varietals that we eat today.

 

  • Poor soil quality: Current modern farming practices, such as over-cropping and overgrazing, have depleted the soil of vitamins and minerals. This has led to a lower nutrient content in the foods grown in the soil. One study found “reliable declines” in the amount of protein, calcium, phosphorus, iron, vitamin B2 and vitamin C in vegetables and fruits grown in depleted soil over the past half century (3). In addition, once harvested, the nutritional content of vegetables and fruits declines over time. Produce is stored and shipped for weeks and is unfortunately not very fresh by the time it arrives on our supermarket shelves.

 

  • Toxic load due to chemicals exposure: Our food supply today is contaminated. There are many chemicals found in our food due to farming practices and chemicals in the environment. These include heavy metals, pesticides, industrial chemicals, pharmaceuticals, radioactive elements, electronic waste pollutants, plastics, nanoparticles and others (4). Furthermore, we are exposed to countless industrial chemicals. “In reality,” Lynn R. Goldman, Former Assistant Administrator for Toxic Substances at the U.S. Environmental Protection Agency (EPA) said, “we really don’t know how many chemicals are currently in commerce in the United States” (5). It is estimated that there are somewhere between 25,000 and 84,000 industrial chemicals in the United States (5).  Our bodies’ toxic loads are therefore increased by this unprecedented exposure to all sorts of chemicals. When subjected to this level of chemicals and toxin exposure, the body requires more nutrients to detoxify and cope.

 

  • Chronic stress: The American Psychological Association’s 2010 Stress in America survey found that “most Americans are suffering from moderate to high stress, with 44% reporting that their stress levels have increased over the past five years” (6). Stress has many negative effects on health and requires more nutrients to combat these damaging effects. It depletes many important vitamins and minerals, namely B vitamins, C, E and magnesium, which can lead to nutrient deficiencies, fatigue, weakened immunity and possibly other illnesses if not addressed.

 

  • Widespread use of medications (birth control, antibiotics, antidepressants, painkillers, NSAIDs, etc.): Nearly 70% of Americans are on at least one prescription drug, and over 50% take two (7). 20% of patients are on five or more prescription medications, according to Mayo Clinic and Olmsted Medical Center researchers (7). Most medications, including OTC ones, cause a depletion of important vitamins and minerals. The result is that most Americans, on medication, are depleted in some essential nutrients. For a tool to find out researched nutrient depletions associated with particular medications or combinations of medications, visit: https://mytavin.com

 

  • Poor gut health impairs absorption: One function of a healthy gut is nutrient absorption from the food we eat. If gut function is not strong, then nutrients will not be well absorbed from the diet. We have a near epidemic of gut issues today due to all of the reasons mentioned above; poor diet, less diverse diet, exposure to toxins, stress, medications. This reduces our ability to absorb nutrition from our food. The overuse of antibiotics together with excessive hygiene practices and increases in procedures which are elected and not medically necessary, like Caesarean section birth, have all contributed to gut microbiome changes. The bacterial populations in the gut are important for absorbing and even creating certain nutrients in the body. For these and many other reasons, gut health is a critically important variable for nutrient delivery and absorption.

 

Vitamin and mineral deficiencies are often common as a result of these factors. Deficiencies often lead to symptoms and physical problems that are difficult to identify. For example, these deficiencies could lead to symptoms of fatigue, reduced ability to fight infections, or impaired cognitive function (concentration, focus or memory issues), mood issues such as depression or anxiety and other problems. Micronutrient inadequacies can also have longer term consequences for health and increase the risk of chronic disease like cancer, cardiovascular disease, type 2 diabetes, osteoporosis and others.  This is why it can be important to use supplementation for certain health conditions as part of the therapeutic approach.

Even a healthy person can become depleted due to all of the reasons above, so supplements are often helpful for the maintenance of good health. The supplements that are often required for simple maintenance of good health are:

  • B vitamins: Especially if you don’t eat liver, nutritional yeast, and lots of vegetables. Supplemental B12 is very important for vegetarians and vegans who often don’t get enough.
  • Omega 3: Especially if you don’t eat at least 1 pound of cold water fatty fish per week. We typically recommend Cod Liver Oil because it also contains pre-formed vitamin A that is often deficient in people who do not eat liver.
  • Magnesium: We like Magnesium Glycinate as a preferred form.
  • Probiotics: Especially if you don’t eat fermented foods daily like sauerkraut, kim chi, kvass, plain unsweetened yogurt or kefir preferably full-fat and from grass-fed cows.
  • Vitamin D: Especially if you don’t get at least 15 minutes of sun exposure on arms and/or legs without sunscreen between the hours of 11am – 3pm at least 5 days per week. When supplementing with Vitamin D, make sure you add Vitamin K2 as well.
  • Multi vitamin & mineral: Most are not shown to be helpful in the research. This is likely due to a quality issue. Professional supplement brands use better forms and ratios of vitamins and minerals as compared to most products found on the supermarket shelves. For this reason, we have put together a ‘sustain and maintain’ supplement pack that covers the most important vitamins, minerals, probiotics, magnesium, fish oil, and liver detoxification support all in one simple AM and PM packet. For details and ordering, email service@livinglovecommunity.com
  • Collagen protein: Glycine is an amino acid found in collagen. It is generally consumed in insufficient quantities for optimal connective tissue and collagen formation. You can take collagen or you can take straight glycine. It is even more important to do so if there are joint issues, methylation defects like MTHFR genetic mutation or sleep issues.
  • Choline: Especially if you do not eat many eggs or liver, which are the top sources of choline in the diet. Adding sunflower lecithin or phosphatidylcholine as a supplement can help.
  • NAC, ALA, Carnitine, and CoQ10 (as ubiquinol): For people focused on longevity and enhanced energy, mitochondrial support with these supplements can be very helpful.

In addition to the importance of taking supplements, it is also critical to take high-quality supplements. There are a number of retail supplements available that have fillers, additives, synthetic compounds and poorly absorbable ingredients. It is best to consult a professional to ensure that you take the supplements that are right for you and are of the best quality. In order to help you choose professional brands that are third-party lab tested, we’ve set up an online store with access to all the supplements mentioned on this page and more. Only high-quality brands vetted by us make the cut. View our store here: http://refill.livinglovecommunity.com

Whether you have a medical condition, want to maintain good health or don’t know which brands are the best and safest quality, don’t struggle with trying to decide on a supplement plan yourself. Come in to see us. We will work with you to develop a personalized supplement program to address your individual health needs. To find out more schedule a discovery call (free 15-minute call with one of our staff). If you just want to get a supplement pack for general wellness without a consultation, email us at service@livinglovecommunity.com for more details on how to get started with supplement packs shipped direct to your door each month.

 

References

  1. US Department of Health and Human Services and US Department of Agriculture. 2015-2020 Dietary Guidelines for Americans December 2015. Available at: https://health.gov/dietaryguidelines/2015/. Accessed 2/27/19.
  2. Fulgoni VL, 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr. 2011;141(10):1847-1854.
  3. Davis DR, Epp MD, Riordan HD. Changes in USDA food composition data for 43 garden crops, 1950 to 1999. J Am Coll Nutr. 2004; Dec. 23 (6).
  4. Thompson LA,Darwish WS. Environmental Chemical Contaminants in Food: Review of a Global Problem. J Toxicol. 2019; doi: 10.1155/2019/2345283.
  5. Identifying and Reducing Environmental Health Risks of Chemicals in Our Society. Roundtable on Environmental Health Sciences, Research, and Medicine; Board on Population Health and Public Health Practice; Institute of Medicine. Washington (DC): National Academies Press (US); 2014 Oct.
  6. American Psychological Association. 2011. Stressed in America. January 2011, Vol 42, No. 1. https://www.apa.org/monitor/2011/01/stressed-america. Accessed Feb. 27, 2019.
  7. Mayo Clinic. 2013. Nearly 7 in 10 Americans Take Prescription Drugs, Mayo Clinic, Olmsted Medical Center Find. https://newsnetwork.mayoclinic.org/discussion/nearly-7-in-10-americanse-prescription-drugs-mayo-clinic-olm-taksted-medical-center-find/. Accessed Feb. 27, 2019.
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April 2, 2019

What is Functional Medicine? Should you Consider it over Conventional Medicine?

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

What is Functional Medicine and Should you Consider it over Conventional Medicine?

There is a lot of frustration with conventional medicine these days. Obesity, diabetes, cancer, heart disease, autoimmune diseases and other chronic conditions are all on the rise.

6 in 10 Americans have at least 1 chronic disease (defined by the CDC as cancer, heart disease, lung disease, stroke, Alzheimer’s, diabetes, kidney disease) (1).

4 in 10 Americans have 2 or more chronic diseases (1).

Trends show an overall increase in chronic diseases: Chronic diseases are responsible for seven out of 10 deaths in the US, killing more than 1.7 million Americans each year; and more than 75% of the $2 trillion spent on public and private healthcare in 2005 went toward chronic diseases (2).

90% of the 3.3 $ trillion annual health care expenditures are for chronic and mental health conditions (3).

A recent Milken Institute analysis determined that treatment of the seven most common chronic diseases coupled with productivity losses will cost the U.S. economy more than $1 trillion dollars annually (2).

Heart disease and stroke are the leading killer: One third of all deaths are due to heart disease or stroke every year. These diseases cost the health care system $199 billion per year and cause $131 billion in lost productivity on the job (3). 

Cancer is the second leading cause of death: Each year more than 1.6 million people are diagnosed with cancer, and almost 600,000 die from it. The cost of cancer care continues to rise and is expected to reach almost $174 billion by 2020 (3).

Diabetes is the seventh leading cause of death in the U.S. in 2015 (4): Diagnoses of type 2 diabetes increased from 0.93% in 1958 (5) to 9.4% of the U.S. population in 2015 (4). More than 30 million Americans have diabetes, and another 84 million adults in the United States have pre-diabetes, which puts them at risk for type 2 diabetes (3). Diabetes can cause heart disease, kidney failure, and blindness, and costs the US health care system and employers $237 billion every year (3).  

The overall prevalence of obesity was 39.8% of the population in 2015-2016 (6). Obesity affects 1 in 3 adults and almost 1 in 5 children (3). Over 25% of all Americans aged 17 to 24 years are too heavy to join the military (3). Obesity-related conditions include heart disease, stroke, type 2 diabetes and certain types of cancer. These are some of the leading causes of preventable, premature death (6). The estimated annual medical cost of obesity in the United States is $147 billion per year (3).

Arthritis is a leading cause of work disability in the United States (3): Arthritis affects 1 in 4 adults or 54.4 million adults in the United States (3).  It one of the most common chronic conditions and is a common cause of chronic pain. The total cost of arthritis and related conditions was about $304 billion in 2013. Of this amount, nearly $140 billion was for direct medical costs and $164 billion was for indirect costs associated with lost earnings (3).

Alzheimer’s disease is the sixth leading cause of death among all adults and the fifth leading cause for those aged 65 or older (3). It is an irreversible, progressive brain disease that affects about 5.7 million Americans (3). In 2010, the costs of treating Alzheimer’s disease were estimated to fall between $159 billion and $215 billion (3). By 2040, these costs are projected to jump to between $379 billion and $500 billion annually (3).

About 20% of Americans suffer from autoimmune diseases (7) and the incidence of autoimmune conditions are rising.

Common autoimmune diseases are rheumatoid arthritis, Hashimoto’s, Grave’s, lupus, celiac disease, MS, IBD (Crohn’s disease or ulcerative colitis), Type 1 diabetes and approx. 100 others.  Autoimmune diseases are among the top ten causes of death in girls and women under 65 years (8). 

Between 2001 and 2009, the incidence of type 1 diabetes increased by 23%, according to The American Diabetes Association (9).

The incidence of celiac disease is on the rise. Until the 1970s the estimated prevalence of celiac disease was 0.03%. The current estimated prevalence is 1% in the USA (10).

The incidence of RA appears to be rising: This rise in RA followed a period of 4 decades of declining incidence and appears to be limited to women (11).

Diagnoses of IBD (Crohn’s disease or ulcerative colitis) has risen to 1.3% of US adults in 2015, up from 0.9% in 1999 (12).  IBD seems to be increasing in children, according to a 12-year study showing the incidence rate doubling in the period 1991–2002 (8). 

Most of these chronic health problems have been getting dramatically worse over the past couple of decades and are only going to continue to get worse if effective treatment is not found…and soon. As most of these chronic diseases can be prevented and/or resolved through lifestyle and targeted natural supplements, they are primarily caused by diet and the way Americans live. Many chronic diseases are not inevitable and can be prevented with better diet & lifestyle. They can possibly be reversed with a more appropriate approach to treatment.

Conventional medicine is great at treating acute and crisis issues. For example, in 1900 the top causes of death were from infectious disease (typhoid, tuberculosis, and pneumonia). Today none of those are even in the top 10 causes of death. However, when it comes to treating chronic diseases, Conventional Medicine tends to only offer drugs to manage symptoms, but nothing to resolve root causes. Conventional medicine uses medicine designed for acute conditions for these chronic diseases.

In the midst of this depressing scenario, Functional Medicine emerges as a solution. Functional Medicine truly shines in its ability to work with chronic disease. The rest of this article defines what Functional Medicine is and how it strives for optimal health.

Functional Medicine defined:

Functional Medicine or FM aims to look for and address the root causes of disease. The body is one integrated system. Segregating specialties by organs / systems misses the boat on the researched interconnected impacts between different systems in the body. FM treats the whole system at the root cause level, not just the symptoms at the single organ / system level.

In FM, your doctor or practitioner will spend time with you to assess your case. This is often very difficult to do in the 10-15 minute consultation conventional doctors provide.

FM is not attempting to match your symptoms to a pharmaceutical drug. Rather, it aims to find the underlying root causes and address these causes. For example, a conventional medicine doctor may diagnose hypertension (high blood pressure) and prescribe an anti-hypertensive drug (to lower blood pressure). In most cases there will be little discussed around the root causes of high blood pressure. Perhaps in some cases there will be a vague mention of exercise and possibly a comment about lowering salt intake, but no thorough testing for specific root issues.

In FM, a thorough investigation into the root cause for high blood pressure will ensue. There may be testing around cortisol levels (an adrenal hormone related to stress), gut issues, toxic burden, a thorough dietary assessment, and an investigation into nutrients like potassium (potassium deficiency is one commonly missed root cause of high blood pressure). After the comprehensive assessment, the functional medicine doctor will typically meet with the client for 30-60 minutes and review the findings of the lab work and other assessments about possible root causes. The FM doctor will then prescribe a thorough treatment plan including a prescription of natural supplements like vitamins, minerals, and herbs, plus some specific nutrition and lifestyle changes. In the Living Love clinic, this is then followed up by support from a functional health coach to implement the plan in a step-by-step process with thorough explanations and answers to questions. This allows for the client to understand why they are doing what they are doing, how to overcome challenges that present themselves along the way, and support for tweaking / honing / refining the plan along the way as needed to keep moving towards desired results.

There is more than one root cause in most cases. Addressing the root causes are typically done through natural modalities such as supplement prescriptions including vitamins, minerals, and herbs, diet and nutrition, and lifestyle modifications using exercise, meditation, stress management and other tools. FM may use pharmaceutical drugs but this is not the first reflex. Drugs are typically used in the lowest dose for the shortest time while getting to the root causes and resolving them.

Dr. Mark Hyman, MD, calls FM ‘the future of conventional medicine’.

Principles of FM:

  • Find the root causes. There can be a variety of issues in a complex case. Why is someone suffering from a particular symptom? Get to the underlying reasons for why the symptom or symptoms exist and address those underlying root causes. This may be due to:
    • Chronic inflammation (but what is causing the chronic inflammation?)
    • Nutritional deficiencies (B12, iron, folate, zinc, glycine, potassium, etc.)
    • Toxicity (mold, toxins from Lyme, other biotoxins, metals, chemicals, etc.)
    • Chronic infections (Lyme, Epstein-Barr Virus, or other viral, bacterial, fungal, etc.)
    • A poor diet of inflammatory foods
    • Stress and/ or psychological or emotional issues that can be improved with lifestyle changes
    • A lack of movement or even excessive or the wrong types of exercise for the individual
    • Gut issues like infection, overgrowth, dysbiosis or other, etc.
    • These issues or root causes need to be untangled to really get to the crux of the problem. Then an approach to resolve the root causes can be taken to make the patient well again.

 

  • Test don’t guess. FM uses extensive advanced lab testing to find out what the root causes are. In FM, specific lab testing is used looking at blood, stool, urine and occasionally breath samples. Many of these tests are not used in conventional medicine. Using advanced lab testing helps your FM practitioner to get the full picture to assess what the root causes are. Without testing, a practitioner is forced to make guesses about your health that may or may not be correct.

 

  • Prevention is key. FM seeks to be preventative. There are often signs of a problem lurking years before a person is diagnosed with a disease. We can see antibodies in blood tests years before an autoimmune condition is diagnosed. We can see type 2 diabetes coming if the right blood glucose and insulin tests are examined. Rather than focusing on disease, functional medicine focuses on optimal function. This means that in addition to getting well when chronic disease is present, there is also a focus on longevity, increasing vitality and energy, and not just feeling okay but instead feeling great. There is also a focus on sustaining and maintaining wellness once achieved. Strategies are implemented to help prevent recurrence of issues that had been present in the past.

 

  • FM is very science-based. It draws upon the latest research to understand how the body functions. This is why lab testing is frequently used so that your FM practitioner can see what is happening rather than making assumptions. Peer-reviewed studies are regularly reviewed by the greater functional medicine community and it does not take the 15-20 years that it sometimes takes for research to become integrated in conventional medicine. Instead, research is applied to clinical practice shortly after being published and that means innovative and new interventions are being utilized quickly.

 

  • Health is not just a lack of disease but is rather, a state of optimal vitality. Many of the conditions that society thinks are due to aging can actually be improved or eradicated with a FM approach. Declining health in later years is not a given. A preventative FM approach can improve how a person ages. The last 10 years of a person’s life are important to the functional medicine practitioner. The FM doctor will be thinking about not only how to feel good now, but also how to stay well enough into old age to play with grandchildren, travel the world, and enjoy retirement to its fullest.

 

When to turn to FM:

  • FM is ideal for complex cases in which people have seen many doctors but are still ill
  • FM is great when there are unexplained or unresolved issues that conventional medicine has been unable to identify and/or resolve
  • FM can help to improve and even reverse chronic lifestyle diseases like diabetes and pre-diabetes, and obesity
  • FM can help reverse root causes for immune dysfunction (autoimmune diseases), gut issues (IBS, Crohn’s, Ulcerative Colitis, Small Intestinal Bacterial Overgrowth [SIBO], etc.), hormone imbalance (without the need to take hormone replacement in many cases), chronic infections like Lyme disease, toxic burden like mold toxin illness (also call Chronic Inflammatory Response Syndrome or CIRS), and many more because the root causes of nearly every chronic illness are similar.
  • FM is for anyone who wants to prevent health problems before they become debilitating, or even appear
  • FM is for everyone who wants to experience optimal health and enjoy life to the fullest! Just because some people feel good now doesn’t mean you can’t feel even better. Longevity, vibrant vitality, unshakeable happiness, and an inspired sense of purpose are all areas of focus for a more holistic kind of functional medicine.

If you or someone you know is interested in learning more about functional medicine, please click here to schedule a complimentary 15-minute phone consultation and/or call or text 720-722-1143 and/or email service@livinglovecommunity.com . We will help you learn more about taking the next steps in a more functional and holistic care model. We work with people who do not live locally so feel free to contact us regardless of where you live. We look forward to playing a part in your health and happiness!

 

References

  1. Centers for Disease Control and Prevention. National Center for Chronic Disease Prevention and Health Promotion. November 19, 2018. About Chronic Diseases. https://www.cdc.gov/chronicdisease/about/index.htm. Accessed February 12, 2019.
  2. Raghupathi, W.  and Raghupath, Vi. 2018. An Empirical Study of Chronic Diseases in the United States: A Visual Analytics Approach to Public Health. Int J Environ Res Public Health. doi: 10.3390/ijerph15030431
  3. Centers for Disease Control and Prevention. National  Center for Chronic Disease Prevention and Health Promotion. February 11, 2019. Health and Economic Costs of Chronic Diseases. https://www.cdc.gov/chronicdisease/about/costs/index.htm. Accessed February 12, 2019.
  4. Centers for Disease Control and Prevention. CDC Newsroom. July 18, 2017. New CDC report: More than 100 million Americans have diabetes or prediabetes. https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html. Accessed February 12, 2019.
  5. Centers for Disease Control and Prevention.  CDC’s Division of Diabetes Translation. April 2017. Long-term Trends in Diabetes. https://www.cdc.gov/diabetes/statistics/slides/long_term_trends.pdf. Accessed February 12, 2019.
  6. Centers for Disease Control and Prevention. August 13, 2018. Adult Obesity Facts. https://www.cdc.gov/obesity/data/adult.html. Accessed February 12, 2019.
  7. American Autoimmune Related Diseases Association Inc. April 29, 2017. How many Americans have an autoimmune disease? https://www.aarda.org/knowledge-base/many-americans-autoimmune-disease/. Accessed February 12, 2019
  8. Tincture. Jan 29, 2016.  An Invisible Epidemic –  When your body attacks itself –  Autoimmune Disease. https://tincture.io/an-invisible-epidemic-when-your-body-attacks-itself-autoimmune-disease-5738b699de12. Accessed February 11, 2019.
  9. Medical News Today. June 22, 2012. Autoimmune Disease Rates Increasing. https://www.medicalnewstoday.com/articles/246960.php. Accessed Feb 10, 2019.
  10. Medical News Today. February 2019. The Spectrum of Celiac Disease: Epidemiology, Clinical Aspects and Treatment. https://www.medscape.com/viewarticle/720681_2. Accessed February 12, 2019.
  11. Myasoedova E, MD PhD, Crowson C. S., MS, Kremers H. M., MD MSc, Therneau T. M., PhD, and Gabriel S.E., MD MSc. 2011. Is the incidence of rheumatoid arthritis rising? Results from Olmsted County, Minnesota, 1955-2007. Arthritis Rheum. doi: 10.1002/art.27425
  12. Centers for Disease Control and Prevention. November 14, 2018. Inflammatory Bowel Disease (IBD). Data and Statistics. https://www.cdc.gov/ibd/data-statistics.htm. Accessed February 11, 2019.
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March 27, 2019

Cold & Flu Season Isn’t Quite Over Yet…

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

 

We’re not quite out of the cold & flu season just yet.

  • Each year, children suffer up to 5 colds and adults have 2-3 infections, leading to time off school or work and considerable discomfort. Most symptoms resolve within 1 week, but coughs often can last longer (1).
  • Figures show that direct medical costs due to the flu and cold averaged $10.4 billion annually (2). Projected lost earnings due to illness and loss of life amounted to $16.3 billion annually (2). The total economic burden of annual influenza epidemics is $87.1 billion (2).

 

Here are a few ideas for you in case you do get a late cold or flu.

Wash your hands:

The transmission of common cold infections is mostly through hand-to-hand contact rather than spread by droplets (1). Furthermore, cold viruses can survive on surfaces for several hours. Hands can readily become contaminated after contact with such surfaces. This makes hand washing “crucial in preventing the spread of colds” (3).

Zinc Lozenges:

Studies using high doses of zinc (>75 mg/day, as zinc acetate lozenges) consistently found that colds were shortened by 42% as a result of the zinc lozenges (4). Specifically, zinc acetate lozenges improved multiple symptoms of a cold. They shortened the duration of nasal discharge by 34%, nasal congestion by 37%, sneezing by 22%, scratchy throat by 33%, sore throat by 18%, hoarseness by 43%, and cough by 46% (5). Zinc lozenges shortened the duration of muscle ache by 54%, but there was no difference in the duration of headache and fever (5).  These studies started zinc treatment within 24 hours of the onset of a cold so it is best to use zinc lozenges at the earliest sign of a cold (5).

Zinc acetate has been proven to be most effective. A high dose of 80-90 mg is recommended in divided doses. Lozenges should have at least 18 mg zinc each and take at least 30 minutes to dissolve. Taking one lozenge every 2 hours and, in total 5 per day, for no more than 3 days in a row can dramatically lessen time with a cold. Try to avoid products with citric acid as this binds to the zinc and makes it less effective (4). Try Life Extension Enhanced Zinc Lozenges. We have found this product to be one of the few available that uses zinc acetate, avoids citric acid, takes at least 30 minutes to dissolve, and has at least 18 mg per lozenge.

Elderberry syrup:

Elderberry enhances and activates immune cell behavior, has antioxidant properties and is antiviral in that it can stop a virus from entering cells (6). These protective qualities enable it to inhibit the potential damage of a virus, particularly when given in the first 48 hours of a viral infection (6). Studies show that elderberry improves cold symptoms within 2-4 days instead of 7-8 days without elderberry (6).

There are a couple of elderberry syrup products to try such as Wise Woman Herbals Elderberry Syrup and Planetary Herbals Elderberry Syrup.

Alternatively, you can make your own elderberry syrup. We like this recipe from www.juicing-for-health.com (7):

Elderberry syrup recipe:

  1. 16 ounces of elderberry juice
  2. 4 tablespoons of lemon juice
  3. 1 tablespoon of raw honey

Instructions:

  • Prepare the elderberry juice. Place elderberries in a saucepan, cover them with water, and heat until the mixture starts to boil. Then, remove from heat, but leave the elderberries in the liquid for a few hours. Afterward, strain the liquid, discard the berries, and store it in the fridge.
  • Next, in a saucepan, mix the elderberry juice with lemon juice, and heat over medium heat. Bring the mixture to boil, allow to simmer for 20 minutes then remove from heat.
  • Add the honey, and drink the syrup while warm.

Echinacea:

Studies have shown that Echinacea decreased the odds of developing the common cold by 58% and the duration of a cold by 1-4 days (8). In another study, Echinacea reduced the total number of cold episodes and the number of days people suffered from the cold (9). Cold prevention increased when people followed the protocol of taking the Echinacea over a 4-month period (9).  Another study indicated that symptoms of the cold were 23.1% less severe in people taking Echinacea vs. those who did not take Echinacea (10).

Andrographis:

A combination of two herbs, Andrographis (Andrographis paniculata) and Eleuthero (Eleutherococcus senticosus), were shown to be an effective therapy “superior to conventional antiviral medications for reducing severity and duration of influenza infections” (6). Andrographis alone has been found to prevent the cold (11). In one study, it was found that there was a significant decrease in the incidence of colds when people took andrographis for a period of 3 months and that the relative risk of catching a cold was 2.1 times lower for the people taking andrographis vs. those who did not take it (11). The protective effect was 33%, suggesting that andrographis has a preventive effect against common colds during the winter period (11).

Garlic:

Garlic, when taken in supplemental form throughout the winter season, has been shown to result in a lower number of colds and a shorter duration of the cold (6).  You can cook with garlic and get the active anti-microbial constituent, but only if you handle it properly. The allin and a heat sensitive enzyme that reacts with allin to create allicin are stored in separate areas of the clove. If you simply crush or cut the garlic and cook with it right away, you destroy the heat sensitive enzyme and will not get much allicin. Instead crush or finely chop the garlic and let it sit on a cutting board in a condensed pile for 10 minutes. The enzyme will react with allin to make allicin. Allicin is heat stable so now you can cook with garlic and get the anti-microbial constituent.

Ginseng:

North American Ginseng has reduced the incidence, duration and severity of colds in studies. In one study, the number of reported colds declined by 9.2%, the risk of getting a cold decreased by 12.8%, the severity of symptoms was rated to be 31% lower and the duration of symptoms was 34.5% less (6).

Ginger:

Ginger was found to inhibit some types of influenza (virus) and also exhibits anti-viral properties against other viruses (13, 14). Make fresh ginger juice with a juicer or fine grater and mix it with lemon and hot water to help slow viral replication. Add cayenne for a little spice and honey to soothe the throat.

Propolis:

Tincture or capsules of propolis can help reduce influenza virus (15). Sometimes you can get propolis mixed with honey and make a soothing hot beverage. This is great to have around for cold and flu season.

Meditation and Exercise:

Lifestyle modifications such as mediation and exercise can also be effective in reducing the cold and flu illness burden. One study found that sufficient evidence exists to justify testing the hypothesis that training in meditation or exercise can reduce susceptibility to colds and flus (12). Furthermore, studies have demonstrated that psychological stress influences susceptibility to infection (6). Given that meditation and exercise help to reduce psychological stress, they can also help to reduce susceptibility to infection.

 

In conclusion, try these ideas if you are unlucky enough to catch a late season cold or flu. These natural approaches can support the body’s immune system, potentially decreasing the incidence of colds and flu, shortening the duration, decreasing the intensity of symptoms and preventing possible complications.

 

 

 

References

1. Arroll B. 2011. Common Cold. BMJ Clin Evid. 1510.

2. Molinari NA, Ortega-Sanchez IR, Messonnier ML, Thompson WW, Wortley PM, Weintraub E, Bridges CB. 2007. The annual impact of seasonal influenza in the US: measuring disease burden and costs. Vaccine.  27: 5086-96.

3. Sattar SA, Jacobsen H, Springthorpe VS, Cusack TM, and Rubino JR. 1993. Chemical disinfection to interrupt transfer of rhinovirus type 14 from environmental surfaces to hands. Appl Environ Microbiol. 59(5): 1579–1585.

4. Hemila H. 2011. Zinc lozenges may shorten the duration of colds: a systematic review. Open Respir Med. 5:51-8. doi: 10.2174/1874306401105010051.

5. Hemila H, Chalker E. 2015. The effectiveness of high dose zinc acetate lozenges on various common cold symptoms: a meta-analysis. BMC Fam Pract.  16:24. doi: 10.1186/s12875-015-0237-6.

6. Roxas M and Jurenka J. 2007. Colds and Influenza: A Review of Diagnosis and Conventional, Botanical, and Nutritional Considerations. Alternative Medicine Review Volume 12, Number 1.

7. Ding S. 2018. Elderberry Syrup Recipe to Beat Cold and Flu at any Season. https://juicing-for-health.com/elderberry-syrup-recipe. Accessed March 3, 2019.

8. Shah SA, Sander S, White MC, Rinaldi M, Coleman CI. 2007. Evaluation of echinacea for the prevention and treatment of the common cold: a meta-analysis. The Lancet. 7: 473-480. Doi: 10.1016/s1473-3099(07)70160-3.

9. Jawad M, Schoop R,  Suter A, Klein P, and Eccles R. 2012. Safety and Efficacy Profile of Echinacea purpurea to Prevent Common Cold Episodes: A Randomized, Double-Blind, Placebo-Controlled Trial. Hindawi. doi:10.1155/2012/841315.

10. Goel V, Lovlin R, Barton R, Lyon MR, Bauer R, Lee TD, Basu TK. 2004. Efficacy of a standardized echinacea preparation (Echinilin) for the treatment of the common cold: a randomized, double-blind, placebo-controlled trial. J Clin Pharm Ther. 1:75-83.

11. Caceres DD, Hancke JL, Burgos RA, Wikman GK. 1997. Prevention of common colds with Andrographis paniculata dried extract. A Pilot double blind trial. Phytomedicine. 2:101-4. doi: 10.1016/S0944-7113(97)80051-7.

12. Barrett B, Hayney MS, Muller D, Rakel D,Ward A,  Obasi CN, Brown R, Zhang Z, Zgierska A, Gern J, West R, Ewers T, Barlow S, BA, Gassman M, Coe CL. 2012. Meditation or Exercise for Preventing Acute Respiratory Infection: A Randomized Controlled Trial. Ann Fam Med. 4: 337–346. doi: 1370/afm.1376

13. Mudyiwa, R, et al. “Anti-Alternaria Solani Activity of Onion (Allium Cepa), Ginger (Zingiber Officinale) and Garlic (Allium Sativum) In Vitro.” International Journal of Plant & Soil Science, vol. 10, no. 4, 2016, pp. 1–8., doi:10.9734/ijpss/2016/24488.

14. Chang, Jung San, et al. “Fresh Ginger (Zingiber Officinale) Has Anti-Viral Activity against Human Respiratory Syncytial Virus in Human Respiratory Tract Cell Lines.” Journal of Ethnopharmacology, vol. 145, no. 1, 2013, pp. 146–151., doi:10.1016/j.jep.2012.10.043.

15. Shimizu, Tomomi, et al. “Anti-Influenza Virus Activity of Propolis in Vitro and Its Efficacy against Influenza Infection in Mice.” Antiviral Chemistry and Chemotherapy, vol. 19, no. 1, 2008, pp. 7–13., doi:10.1177/095632020801900102.

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January 8, 2019

FIBROMYALGIA Part 3

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

In Part 2, we covered the gut as a root cause, the triggers and risk factors for FM. Now in Part 3, we will cover the specific action steps to take if you have FM. We first take a look at the various dietary issues that play a role in FM, starting with excitotoxins. A general anti-inflammatory diet is a great place to start, and then it would be beneficial to trial some of these other dietary ideas, along with finding a good Functional Medicine practitioner to help work through the possible root causes of your FM.

What is the role of excitotoxins?

Excitotoxins are molecules, such as glutamate and aspartate, which are involved in pain occurrence (10). They are excitatory neurotransmitters, whose role is to maintain and extend action potentials, which are electrical signals, in the brain. This is how brain cells communicate with each other. When these neuron receptors are exposed to excitotoxins, they fire impulses at such a rapid rate that they become exhausted, damaged or die. This is excitotoxicity.

Through a chemical process in the brain, the excitatory amino acid glutamate can cause chronic pain (10). In addition to glutamate’s role in central sensitization of pain, abnormal glutamatergic neurotransmission has also been implicated in other common pain conditions such as migraine, TMJ disorder, IBS and depression (10). Furthermore, substance P is a compound in the brain thought to be involved in the transmission of pain and other nerve impulses. It is co-released with glutamate and increases the permeability of the blood brain barrier (BBB) (10). If this barrier becomes permeable, then more glutamate can enter the brain and have further influence on the sensation of pain in FM.

In the diet, glutamate and aspartate are found in foods such as MSG, hydrolyzed protein, protein isolates/concentrates, yeast extract, aspartame, as well as in specific food items such as soy sauce, fish sauces and aged cheeses like sharp cheddar and parmesan cheese. People who eat more of these foods, or who are more sensitive to excitotoxins, could have higher blood concentrations which could lead to abnormal central sensitization of pain, which could be negatively compounded in people with an impaired BBB (10).

One study looked at 4 patients and found that all 4 had complete, or nearly complete, resolution of their symptoms within months after eliminating MSG plus aspartame from their diet (11). Further studies have shown a decrease in FM symptoms after the removal of excitotoxins (10).

It is certainly worth trialing a diet free of excitotoxins to see how it may help FM symptoms as dietary excitotoxins may be leading to increased symptoms in FM. This would involve focusing on a whole foods diet and removing MSG, aspartame and altered proteins (like gelatin, hydrolyzed protein, autolyzed yeast extract, protein concentrates and protein isolates). Certain ingredients on food labels like spices, seasoning, flavoring and natural flavoring should also be avoided since these terms are not specific and could hide these additives. Seasoning packets commonly contain flavor enhancers like MSG.  Additionally, foods naturally high in free glutamate including soy sauce, fish sauces, Worcestershire sauce, Bragg’s amino acids and cheeses like parmesan should also be avoided. To avoid aspartame, it is important to avoid diet soda, gum and breath mints. Yogurt, cereal and bread often have aspartame added. 

A 1-month testing period (without eating out) is ideal, though in prior research most subjects started to feel an improvement by the end of the first week (10).

Are micronutrient deficiencies involved?

Another dietary avenue found in research involves correcting particular micronutrient deficiencies. Micronutrients play an important role in optimal neuronal function, and a few nutrients in particular may relate to glutamatergic neurotransmission (10).

  • Magnesium and zinc are two minerals in the diet with a key role in regulating excitotoxicity. It is thought that low magnesium and zinc levels could support excitotoxicity (10).
  • Another micronutrient of importance to glutamatergic neurotransmission is vitamin B6. Deficiency in B6 can lead to higher levels of glutamate which would enhance excitotoxicity in the central nervous system (10).
  • Deficiency in omega-3 fatty acids has been shown to increase excitotoxicity (10). Omega-3 fatty acids to can potentially clear excess glutamate and prevent excitotoxicity.
  • Finally, excessive glutamatergic neurotransmission leads to increased need for antioxidants in the diet (10). The two main vitamin antioxidants in the diet are vitamin C and vitamin E.

What about supporting serotonin?

Another study focused on relieving FM symptoms through supporting serotonin synthesis through proper absorption of tryptophan in food, while avoiding food components such as fructose and sorbitol that may interfere with the absorption of tryptophan (12). The study was done on 1 FM patient. Encouragingly, this diet resulted in a rapid improvement of symptoms after only few days on the diet, up to the remission of most symptoms in 2 months (12). The patient periodically challenged herself by breaking the diet which resulted in a recurrence of the symptoms.

The patient’s diet included eggs, meat, fish, clams, potatoes, carrots, celery, spinaches, beets, chards, dark chocolates (at least 70 + % cacao), rice, millet, carob powder, walnuts, extra virgin oil, grape seed oil, thyme, sage, rosemary, coffee, green tea, and small amount of almonds. Foods that were avoided were processed food containing artificial sweeteners, high fructose corn syrup, sorbitol, glutamate, and aspartame such as soft drinks, fruit juices and confectionery, any food containing free fructose such as honey and fruits, most legumes, wheat and cereals, and many vegetables that contain fructans and inulins (12). Whilst very encouraging, this study involves one person so it is unclear how applicable it may be to other FM sufferers.

Also, natural supplements can help. We like 5-HTP for serotonin support. 50-100mg per day is a good place to start. If there are sleep issues, taking it before bed can help improve melatonin status because after 5-HTP converts to serotonin, it then converts to melatonin.

What about raw food?

A small study involving 30 patients was done trialling a mostly raw, pure vegetarian diet (13). Participants ate raw fruits, salads, carrot juice, tubers, grain products, nuts, seeds, and a dehydrated barley grass juice product. 19 of the 30 participants experienced significant improvement in all symptoms (13). At 7 months, these people were no longer statistically different from norms for women ages 45–54, apart from the symptom of bodily pain (13). This was the symptom that responded least well to the raw diet.

What about going gluten-free?

One study looked at people suffering from FM, as well as IBS. Amongst their study sample, 7 were women who also had (previously undiagnosed) celiac disease. After 1 year on a gluten-free diet, these participants experienced significant improvement in FM symptoms. The authors of the study believe that this indicates an underlying food hypersensitivity-related mechanism (14).

 

Would healing the gut help?

If a gluten-free diet can lead to significant improvement in symptoms and we know that there may be a connection between FM and gut conditions like IBS, SIBO, dyspepsia, leaky gut, celiac disease and possibly others, then we can surmise that healing the gut will help in the case of FM. We could take that one step further and embark on a specific and targeted gut healing protocol, which would focus on healing the specific gut condition, be it IBS, SIBO, celiac, etc., in order to alleviate FM symptoms.

Conclusion

Although conventional medicine has focused on managing symptoms of FM, there are a number of dietary treatment ideas that can lead to a complete or partial improvement in FM symptoms, according to the studies that exist.

Gut healing is an obvious place to start with the possibility of also focusing on excitotoxins, micronutrient levels and/ or serotonin support.

Things that you can do for FM:

  • Find a functional medicine doctor to do root cause lab testing (call us at 720-722-1143 if you want to find out more about how to set up an appointment in our office)
  • Get functional lab tests to identify root causes (a list of these are included below)
  • Dietary change (trial different diets and include elimination of excitotoxins, removal or minimization of gluten and sugar, and increase micronutrients discussed in this article)
  • Support serotonin through diet and/or take 5-HTP 50-100mg daily (before bed if you have sleep issues) – you can order through our online supplement store here: https://us.fullscript.com//welcome/livinglove
  • Some of the micronutrients that could be supplemented (and/or you can get them from diet) include: Vitamin B6 (P-5-P 50mg per day), Zinc (15-30mg daily), Omega 3 (Cod Liver Oil or other quality fish oil), Vitamin C (600-1200mg per day), Vitamin E (we don’t like alpha tocopherol, but Annatto Tocotrienols that are high Gamma can help at about 125mg daily with dinner).
  • Magnesium is often helpful for FM: Magnesium Glycinate 400-600mg per day
  • If you’d like a supplement pack auto-shipped to you monthly with a specially formulated combination including the above plus some other supplements we have found helpful, email drmiles@livinglovecommunity.com with the subject line “Fibromyalgia Supplement Packs” to find out more information about how to get started.

Labs to find root causes associated with FM:

  • Small Intestinal Bacterial Overgrowth (SIBO) breath test
  • Comprehensive Data Stool Analysis (CDS) with Parasitology x3
  • HLA-DR panel for genetics associated with mold toxin accumulation
  • Blood sugar panel including fasting glucose, HgA1c, and fasting insulin
  • Blood hormone panel including Estradiol, Progesterone, Testosterone, Cortisol, and DHEA-S (for menstruating women not on a hormonal birth control, getting this on days 18-22 is best)
  • Toxic metals panel
  • Organic Acids panel
  • NOTE: not all of these labs are needed for everyone with FM. A skilled functional medicine doctor can prioritize which are most necessary based on a comprehensive case history to assess for which root causes are more likely. The functional medicine doctor can then prioritize the most likely root causes and start testing just for some of the main issues that would be most likely. Follow-up testing can be done if findings are not as expected on the initial lab order. If you would like to find out more about getting started with a functional medicine doctor in our clinic, click on “Schedule a Discovery Call” now.

REFERENCES

10. Holton The role of diet in the treatment of fibromyalgia. Pain Management. 2016; 6.

11. Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001; 35:702-6.

12. Lattanzio SM, Imbesi F. Fibromyalgia Syndrome: A Case Report on Controlled Remission of Symptoms by a Dietary Strategy. Front. Med. 2018 | https://doi.org/10.3389/fmed.2018.00094

13. Donaldson MS, Speight N, Loomis Fibromyalgia syndrome improved using a mostly raw vegetarian diet: An observational study. BMC Complement Altern Med. 2001; 1: 7.

14. Rodrigo L, Blanco I, Bobes J, and de Serres Clinical impact of a gluten-free diet on health-related quality of life in seven fibromyalgia syndrome patients with associated celiac disease. BMC Gastroenterol. 2013; 13: 157.

15. Curtis K, Osadchuk A, Katz J. An eight-week yoga intervention is associated with improvements in pain, psychological functioning and mindfulness, and changes in cortisol levels in women with fibromyalgia. J Pain Res. 2011 ;4:189-201.

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December 7, 2018

FIBROMYALGIA BLOG SERIES PART 2

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

In Part 1 of this 3-part series on FM, we looked at what FM is and what the root causes are thought to be, according to both the research and Functional Medicine. These include abnormalities in the central nervous system, genetic factors, psychological variables, and environmental factors (1). In Functional Medicine, we will also look at gut issues, toxic burden, chronic infections, insulin resistance and hormone and/or neurotransmitter imbalances.

Here, In Part 2 we cover the gut as a root cause, the triggers and risk factors for FM. We will also touch on the treatment of FM, which we will then explore in much greater depth in Part 3 of this series on FM.

 

 

Could FM be related to the gut?

One environmental (or epigenetic) factor that has been looked at is gut health. It is possible that gut health is a contributing cause of FM, although this has not yet been proven. However a number of studies have linked FM to gut dysbiosis, infections and other gut conditions. Many of the studies correlate FM with GI symptoms, Irritable Bowel Syndrome (IBS) and dyspepsia (7). Other studies have associated FM with Small Intestinal Bacterial Overgrowth (SIBO) and leaky gut (8). Finally one study found that FM symptoms improved in fibromyalgia patients who treated and resolved their SIBO condition with antibiotics. In this same study, no improvement was seen in the patients who took a placebo or who still tested positive for SIBO after the antibiotics. (7). This suggests that SIBO plays a causal role in fibromyalgia for at least some patients.

Although gut health is not a defined known cause of FM, we mention it here because it is a distinct possibility and there are indications that this may be an avenue for further research. It is also worth highlighting because improving gut health is something that everyone can work on, whether they have FM or not. If FM is in a person’s family history, then it may be even more relevant to work on gut health.

We suggest finding a good functional medicine doctor and testing for gut issues like SIBO (lactulose breath test) and other bacterial / parasite / fungal issues (comprehensive stool test).

 

What are the triggers of FM?

There is often a trigger of the onset of FM. It can be triggered by various factors such as:

  • stress and/or a major life event such as divorce or the death of a spouse
  • trauma, whether it is emotional, physical or in the form of an accident
  • an infection or virus of some sort
  • surgery
  • repeated injuries
  • childbirth

 

What are the risk factors for FM?

There are certain risk factors that contribute to the likelihood of developing fibromyalgia. These include:

  • Gender: 80-90% of patients with FM are women between 30 and 50 years of age (9). The reason for this isn’t known.
  • Family history: As mentioned above, a family history of the condition may increase the risk of developing FM
  • Disease: Although fibromyalgia isn’t a form of arthritis, having a rheumatic disease like lupus or rheumatoid arthritis or osteoarthritis may also increase risk.
  • Inflammation (from one or more of the causes we discussed and/or inflammation from poor diet)

 

How is FM diagnosed?

FM is difficult to diagnose. There is currently no available imaging technologies or analytical tests for an objective diagnosis (1). FM is now defined as chronic widespread pain, persisting for more than 3 months, without any obvious wound or lesion. FM is commonly accompanied by additional symptoms, as mentioned above, such as joint stiffness, fatigue, sleep disturbance, cognitive dysfunction, and depression. Diagnosis tends to be subjective based on the symptoms and how the patient describes them to their doctor. Diagnosis also includes ruling out other possible diseases such as Rheumatoid Arthritis, depression, Multiple Sclerosis or other autoimmune conditions. Although debate on the concept of FM has continued ever since the classification criteria for diagnosis were first published, FM is now better understood and is generally recognized as a disorder.

 

How is FM treated?

There is no clear-cut treatment plan for FM and no one treatment alone gives strong relief of symptoms. The current conventional medicine approaches seek to manage the condition and manage the pain. Conventional medicine typically uses analgesic medications (OTC pain relievers like ibuprofen, or prescription drugs like tramadol), antidepressants, and anti-seizure drugs (which are sometimes helpful in reducing certain types of pain).There are, however, a number of things that can be done that have shown promise or that have worked in specific studies. We will mention a few natural dietary approaches for which there is promising research.

Functional medicine doctors will look for root causes of inflammation and resolve those root issues. We have seen many people with FM have complete recovery in our clinic from working out inflammatory root causes.

 

What are specific treatment ideas for FM?

Diet is increasingly thought to be a factor in FM. There is growing evidence that diet may contribute to symptoms, with strong evidence for how specific foods may lead to abnormal neurotransmission and continue the process of central sensitization (of pain) (10).

In our clinic, we use a variety of dietary approaches that are specifically tailored to the root causes we find on lab testing. Unfortunately, there is not one diet that works best for everyone with FM. Many times we have patients do one diet for a period of time and then switch diets if we’re not getting results. We also are combining diet with specific supplement and herbal protocols all based on root cause. All this to say that we cannot give one diet that will work for everyone. What we can do is give some general principles that can be helpful guides to consider as part of your dietary plan.

Many with FM do well avoiding gluten and sometimes even all grains. Avoiding refined sugar is also often helpful. Some have success with Paleo diets, others do well with Autoimmune Paleo, others do well with Ketogenic diets, and still others do well with Mediterranean diets (usually gluten-free). There are a few more specifics that can be helpful that will be covered in the next sections.

Please stay with us and read Part 3 of our FM series. In Part 3 we will cover the specific dietary and other action steps to take if you have FM.

 

References

1. Park DJ, Lee SS. New insights into the genetics of fibromyalgia. Korean J Intern Med. 2017; 32:984-995.
2. Abeles AM, Pillinger MH, Solitar BM, Abeles M. Narrative Review: The Pathophysiology of Fibromyalgia. Ann Intern Med. 2007; 146:726-734.
3. Flodin P, Martinsen S, Löfgren M, Bileviciute-Ljungar I, Kosek E, Fransson P. Fibromyalgia is associated with decreased connectivity between pain- and sensorimotor brain areas. Brain Connect. 2014; 4:587-94.
4. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol. 2004; 31:364-78.
5. Kwiatek R, Barnden L, Tedman R, Jarrett R, Chew J, Rowe C, et al. Regional cerebral blood flow in fibromyalgia: single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis Rheum. 2000; 43:2823-33.
6. Mogil JS. Pain genetics: past, present and future. Trends Genet 2012; 28:258–266.
7. Wallace DJ, Hallegua DS. Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep. 2004; 8:364-8.
8. Goebel A, Buhner S, Schedel R, Lochs H, Sprotte G. Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome. Rheumatology (Oxford). 2008; 47:1223-7.
9. Carranza-Lira S, Villalobos Hernandez IB. Prevalence of fibromyalgia in premenopausal and postmenopausal women and its relation to climacteric symptoms. Prz Menopauzalny. 2014; 13: 169–173.
10. Holton K. The role of diet in the treatment of fibromyalgia. Pain Management. 2016; 6.
11. Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001; 35:702-6.
12. Lattanzio SM, Imbesi F. Fibromyalgia Syndrome: A Case Report on Controlled Remission of Symptoms by a Dietary Strategy. Front. Med. 2018 | https://doi.org/10.3389/fmed.2018.00094
13. Donaldson MS, Speight N, Loomis S. Fibromyalgia syndrome improved using a mostly raw vegetarian diet: An observational study. BMC Complement Altern Med. 2001; 1: 7.
14. Rodrigo L, Blanco I, Bobes J, and de Serres FJ. Clinical impact of a gluten-free diet on health-related quality of life in seven fibromyalgia syndrome patients with associated celiac disease. BMC Gastroenterol. 2013; 13: 157.
15. Curtis K, Osadchuk A, Katz J. An eight-week yoga intervention is associated with improvements in pain, psychological functioning and mindfulness, and changes in cortisol levels in women with fibromyalgia. J Pain Res. 2011 ;4:189-201.

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November 7, 2018

Fibromyalgia | Blog Series Part 1

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

What is Fibromyalgia?

Fibromyalgia (or FM) is a neurological disorder of the central nervous system. It is a syndrome of chronic pain in the absence of an otherwise apparent disease or cause for the pain. Patients with FM experience pain differently than people without FM.

 

Primary symptoms associated with fibromyalgia:

• Widespread pain throughout the body
• Heightened and painful response to pressure resulting in exaggerated tenderness at specific points
• Debilitating exhaustion
• Joint stiffness
• Sleep Issues
• Unrefreshing sleep
• Cognitive decline (problems with brain fog, memory, concentration, etc.)

People with fibromyalgia (or FM) may also have depression or other psychological difficulties, headaches, and an inability to focus or concentrate. FM is only recently recognized as a disorder. It is considered a major health problem, which affects 1% to 5% of the general population (1). It is more common in women than men. Having FM can be challenging and in some cases can lead to a lower quality of life and high medical costs.

The condition is chronic. At this time, conventional medical treatment is focused on managing the condition and the associated pain. The cause or causes are not clear but fortunately significant advances have been made in understanding FM. Fortunately, functional medicine has some insights to offer for those suffering with FM.

What causes FM?

The precise cause of FM has not been identified at this time. Various factors can contribute to or trigger FM.
Currently, FM is considered to involve the interaction of several factors, including abnormalities in the central nervous system, genetic factors, psychological variables, and environmental factors (1).

It is thought that the symptom of pain in FM is related to central sensitization, which is an explanation for chronic pain of FM (2). Central sensitization refers to blunting of inhibitory pain pathways and alterations in neurotransmitter levels, leading to abnormal processing of sensory signals within the central nervous system, eventually lowering the threshold of pain and amplifying the sensations from normal signals, causing chronic pain (2). The details are not fully understood yet.

As the issue lies with the central processing of pain, we know that it is not in the peripheral body areas where FM patients experience the pain. The mechanisms thought to be involved include the central sensitization of pain, a suppression of the descending pathways that inhibit pain, excessive activity of glial cells, and abnormalities of neurotransmitter release or regulatory proteins or both (2). These mechanisms are probably not mutually exclusive.

In studies, FM patients show decreased connectivity between different parts of the brain. Findings suggest that abnormal connectivity patterns between pain-related regions and the remaining brain reflect an impaired central mechanism of pain modulation in FM (3). Weaker coupling between pain regions and other areas of the brain possibly indicate an inefficient control of pain circuits. The findings show that FM primarily is associated with decreased connectivity between regions of the brain, which could reflect a deficiency in pain regulation (3). Essentially the brain is overly sensitive to pain signals or misinterprets pain signals.

Unfortunately, these conventional understandings of the causes of FM leave a lot to be desired. There is not much that is actionable or straightforward in helping people struggling with FM to do something for themselves. Luckily, functional medicine has some strong links and connections with root causes that can be contributing to FM.

From a functional medicine perspective, inflammation is a key element when looking at most kinds of pain. FM pain is certainly one for which it is important to find root causes for inflammation and reverse them.

Functional Medicine Root Causes for FM:

• Gut issues (we will talk about that more in Part 2 of this article)
• Toxic Burden: mold toxin accumulation, toxic metals, and/or excessive chemical exposure
• Chronic Infections: Lyme disease, chronic bacterial or viral infections, or fungal / yeast overgrowths
• Insulin resistance: blood sugar and insulin issues can contribute to inflammation and pain
• Hormone and/or neurotransmitter imbalances

Finding a skilled functional medicine doctor familiar with these root causes can help to do some lab testing for HLA-DR genetics (associated with mold toxin accumulation), Lyme testing (find a Lyme-literate functional medicine doctor), gut testing like SIBO and comprehensive stool testing, comprehensive hormone blood panel, and a blood sugar panel that includes fasting glucose, HgA1c, and fasting insulin.

*NOTE: we DO NOT recommend urine-based neurotransmitter testing (however we do like urine testing for Organic Acids which can give a sense of neurotransmitter levels). It is not accurate in our opinion and research does not support this kind of testing. There are plasma neurotransmitter tests that are decent tests, but because of limitations in testing, we often use organic acids and/or a questionnaire and symptom picture to get a sense for neurotransmitter status.

Is FM genetic?

The other key factor believed to play a role in FM is genetics. There is an observed inherited component to FM. Studies have been conducted looking for family associations in FM and have found that anywhere from 26% to 52% of family members of a person diagnosed with FM also fit the criteria for a FM diagnosis (1).

Interestingly, the genetic aspect ties in with the issue of malfunctioning pain signaling. Researchers have identified pain-related genes and have found that pain-related genes affect the expression or function of specific proteins which influence the pain response (6). Currently, hundreds of pain-regulated genes related to pain perception or analgesia have been identified. These include the genes encoding voltage-gated sodium-channels (Nav), GTP cyclohydrolase 1 (GCH1), mu-opioid receptors, and catechol-O-methyl transferase (COMT); and various genes of the dopaminergic, glutamatergic, and GABAergic pathways (1).

However, we must keep in mind that genes are not destiny. Epigenetic, or environmental factors, affect how a particular gene or genes is expressed. Therefore, having these genes related to pain signaling is not a guarantee that fibromyalgia will follow. It is the genetic expression of these genes that is most relevant and this can be affected by epigenetic factors.

It is thought that hormone imbalances, particularly involving serotonin, dopamine and norepinephrine, can play a part in FM. Recent research has focused on how genes can trigger changes in gene expression in people with FM. Research has shown that genetic SNP’s, or genetic mutations of specific genes, result in an increased sensitivity to pain. These SNP’s are related to certain hormones which help to regulate pain. In fact, associations between FM and certain genetic mutations affecting the serotonergic, dopaminergic, and catecholaminergic pathways have been found (1). These mutations influence symptom severity as well as susceptibility to FM. However, the genetic factors identified to date do not fully explain the cause of FM (1). FM is considered to result from an interaction between genetic factors and environmental factors.

Please read on to Part 2 of this overview of FM. In Part 2 we cover the gut as a root cause, the triggers and risk factors for FM. Part 3 will cover the specific action steps to take if you have FM.

 

References

1. Park DJ, Lee SS. New insights into the genetics of fibromyalgia. Korean J Intern Med. 2017; 32:984-995.
2. Abeles AM, Pillinger MH, Solitar BM, Abeles M. Narrative Review: The Pathophysiology of Fibromyalgia. Ann Intern Med. 2007; 146:726-734.
3. Flodin P, Martinsen S, Löfgren M, Bileviciute-Ljungar I, Kosek E, Fransson P. Fibromyalgia is associated with decreased connectivity between pain- and sensorimotor brain areas. Brain Connect. 2014; 4:587-94.
4. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH. Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol. 2004; 31:364-78.
5. Kwiatek R, Barnden L, Tedman R, Jarrett R, Chew J, Rowe C, et al. Regional cerebral blood flow in fibromyalgia: single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis Rheum. 2000; 43:2823-33.
6. Mogil JS. Pain genetics: past, present and future. Trends Genet 2012; 28:258–266.
7. Wallace DJ, Hallegua DS. Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep. 2004; 8:364-8.
8. Goebel A, Buhner S, Schedel R, Lochs H, Sprotte G. Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain syndrome. Rheumatology (Oxford). 2008; 47:1223-7.
9. Carranza-Lira S, Villalobos Hernandez IB. Prevalence of fibromyalgia in premenopausal and postmenopausal women and its relation to climacteric symptoms. Prz Menopauzalny. 2014; 13: 169–173.
10. Holton K. The role of diet in the treatment of fibromyalgia. Pain Management. 2016; 6.
11. Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001; 35:702-6.
12. Lattanzio SM, Imbesi F. Fibromyalgia Syndrome: A Case Report on Controlled Remission of Symptoms by a Dietary Strategy. Front. Med. 2018 | https://doi.org/10.3389/fmed.2018.00094
13. Donaldson MS, Speight N, Loomis S. Fibromyalgia syndrome improved using a mostly raw vegetarian diet: An observational study. BMC Complement Altern Med. 2001; 1: 7.
14. Rodrigo L, Blanco I, Bobes J, and de Serres FJ. Clinical impact of a gluten-free diet on health-related quality of life in seven fibromyalgia syndrome patients with associated celiac disease. BMC Gastroenterol. 2013; 13: 157.
15. Curtis K, Osadchuk A, Katz J. An eight-week yoga intervention is associated with improvements in pain, psychological functioning and mindfulness, and changes in cortisol levels in women with fibromyalgia. J Pain Res. 2011 ;4:189-201.

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May 15, 2018

Osteoporosis: Don’t Let it Sneak Up On You!

osteoporosis

In this post we’ll be talking about osteoporosis, which is characterized by bone that has become porous and low density, leading to bone fractures. Osteoporosis is a particularly large problem for post menopausal women, commonly resulting in fractures of the hip, wrist and spine. You may have observed the characteristic “hump back” slumping spine associated with osteoporosis, often seen in older people. In this post we’ll delve into the etiology of osteoporosis and what can be done to prevent and potentially even reverse this condition.

Don’t let it sneak up on you

Osteoporosis can be a “silent killer” that strikes without warning, especially as we get older. It is not uncommon for people to discover they have osteoporosis when a minor impact like a bump or even simply sitting down too quickly results in a fracture. For this reason it is important for people to monitor their bone mineral density as they reach middle age, and especially into older age. Osteoporosis is characterized by low bone density, which makes bone brittle, weak and easily fractured.

We’ll get into bone mineral density testing in more detail later, but first let’s jump into how osteoporosis develops.

Bone remodeling

Bone in the body is constantly being remodeled, which is a process of bone breakdown (resorption) and formation (deposition). Low bone density and osteoporosis occur when the rate of bone resorption exceeds the rate of bone deposition. The early stages of low bone density are called osteopenia, which can later develop into osteoporosis. Whether your bones are still nice and dense, or you have osteopenia, or even osteoporosis, there is a lot you can protect your bones and prevent fractures, so keep reading!

Prevalence of osteoporosis

Osteoporosis causes almost 9 million fractures per year worldwide, many of which happen in western countries like the United States. Overall, women are disproportionately affected, and make up 61% of osteoporotic fractures (1). In women over age 45, osteoporotic fractures account for more time spent in the hospital than many other diseases, including diabetes, myocardial infarction and breast cancer (2). Although women are more commonly affected, the consequences are grim for men as well. Although women suffer fractures more often, men have higher rates of fracture-related mortality. In fact, in the six months following a fracture, the mortality rate was about double that of similarly aged women (3).

Causes of osteoporosis

Many factors can contribute to osteoporosis and it’s often not simply a matter of having enough calcium.

Other contributing factors:

  • Poor nutrient absorption
    • Important bone minerals and fat-soluble nutrients must be absorbed to be utilized
  • Vitamin D deficiency
    • Necessary for the body to absorb and utilize calcium
  • Vitamin K2 deficiency
    • This vitamin found in fermented foods like sauerkraut directs serum calcium to be stored in bone
  • Other important bone mineral deficiencies:
    • Magnesium
    • Boron
    • Phosphorous
  • Sedentary lifestyle
    • Weight-bearing exercise in particular is important to promote bone deposition and adequate bone density
  • Smoking
    • Associated with an increased risk of fracture
  • Certain medications
    • Corticosteroids like prednisone and cortisone
  • Hormone imbalance
    • Estrogen deficiency in women
    • Post menopausal changes in hormones
    • Testosterone deficiency in men
    • Parathyroid hormone
    • Growth hormone
    • Thyroid disease

As we can see, many factors contribute to osteoporosis. It’s important to determine what root cause is underlying low bone density and work from there. In addition, bone density drugs like Fosamax may actually contribute to fractures!

Fosamax

Several drugs like Fosamax (alendronate sodium) are in a category of drugs known as bisphosphonates which appear to increase bone density but may actually contribute to atypical fractures. One such study found that subtrochanteric insufficiency fractures were more common in post-menopausal women taking Fosamax and that the prolonged drug therapy may contribute to these fractures (4). Long-term Fosamax use for ten years or longer is associated with atypical femoral fractures in the shaft of the bone instead of the femoral neck.

Another larger retrospective review found similar increased prevalence of low-energy femoral shaft fractures associated with Fosamax use. They found that Fosamax use was a significant risk factor in the occurance of this type of fracture and that this fracture pattern was 98% specific to Fosamax users. The researchers suggest that this may result from diminished osteoclast activity and a resulting reduction in ability to repair stress fractures (5). Due to suppressed bone turnover, small cracks in the bone are unable to heal and lead to fractures over time as they become more numerous.

As we can see, the current conventional approach to managing bone density and osteoporosis leaves a lot to be desired. Now that we know some of the major players and understand a bit about how osteoporosis develops, let’s switch gears and get into solution mode. Next, we’ll look at natural treatments that can improve bone density, strengthen bone and assist with fracture healing.

Building healthy bones

It’s easy to tell from some of the causes of osteoporosis above some of the ways to prevent bone loss. Ensuring adequate intake and absorption of key nutrients like Vitamin D, Vitamin K2 and minerals like calcium, magnesium and boron is critical. In addition, regular weight-bearing exercise and maintaining hormone balance can be very important. We’ll cover resistance training but let’s first talk about hormone balance in more detail before getting into nutrition and other factors that play a role in osteoporosis.

Hormone balance

The demographics of osteoporosis reveal the importance of hormone balance in osteoporosis, which primarily affects older, post-menopausal women. This risk largely revolves around lower levels of estrogen, a hormone that impacts bone density. After menopause, estrogen levels fall and the rate of bone resorption (breakdown) overtakes the rate of bone formation, leading to bone loss.

Black cohosh

Black cohosh can help to support healthy estrogen levels, and it has a positive impact on BMD as a result. One trial of 62 postmenopausal women found that 40mg of black cohosh per day increased osteoblast activity and had a positive effect on bone remodeling (6). Another study evaluated the effect of black cohosh on rats and found that it has bone sparing properties. Researchers also suggest that black cohosh may prevent osteoporosis in older men, so it may be helpful for both sexes (7).

DHEA

Dehydroepiandrosterone (DHEA) is a precursor to both estrogen and androgen hormones. DHEA levels decline with age and reduced levels are believed to contribute to many age-related changes impacted by sex hormones, including bone density. One trial of 28 men and women in their early to mid 70s with low DHEA levels compared 50mg of DHEA per day to a placebo and found that bone mineral density (BMD) improved in the active group. In addition, fat mass decreased in the DHEA group and they also experience increased serum IGF-1 and testosterone levels (8).

A larger study of 225 healthy adults aged 55 to 85 years found similar results. In this trial, serum IGF-1, testosterone and estradiol all increased in women but not men, and lumbar BMD increased as well. Although there was no increase in BMD for men overall and no increase in hip, femoral neck or total body BMD for women, authors conclude DHEA confers a modest benefit to women. This cohort was made up of healthy (non-osteoporotic) adults, and it would be interesting to see if results might be more impressive in people with low BMD (9).

Next, let’s transition away from hormones and talk about the importance of healthy digestion and nutrient absorption before moving onto the critical nutrients for osteoporosis themselves.

Are you absorbing your nutrients?

One commonly overlooked contributing factor in osteoporosis is impaired digestion that prevents important bone nutrients from being absorbed and utilized to form health, dense bone. The best diet and supplementation will have little impact if the GI tract is not functioning properly. For this reason, it is important to make sure digestion is working properly early on.

As we’ve already begun to see, managing bone density is not as simple as merely consuming calcium, whether from dietary sources, supplements, or a combination of the two. Important bone minerals including calcium, boron, magnesium and phosphorous require strong stomach acid to be absorbed. Hypochlorhydria, or low stomach acid can contribute to low bone mineral density by preventing the absorption of these minerals. Hypochlorhyria, in turn, can result from many different causes.

Hypochlorhydria

One primary cause of low stomach acid, especially as it relates to osteoporosis, is age. Stomach acid production declines with age and results in impaired mineral absorption. Other causes include GI infections like H. pylori and parasitic infections. If stomach acid is low, it is important to correctly identify the upstream cause and work to treat that issue. Consider working with a functional medicine practitioner to be sure you correctly identify and treat your upstream cause, as osteoporosis can result from multiple causes.

SIBO connection

Small intestine bacterial overgrowth is well known to cause hypochlorhydria, and can be an underlying cause of osteoporosis (10). Because SIBO is fairly common and can contribute to so many problems in addition to osteoporosis, consider a SIBO breath test if symptoms warrant. Other common symptoms of SIBO primarily include digestive disturbances like gas, bloating, diarrhea and abdominal pain or cramping. Mood can also be affected, with symptoms of depression or anxiety being common.

Celiac disease

In addition to SIBO, other digestive disorders are commonly implicated as root causes of osteoporosis and low bone mineral density. Celiac disease is another well established root cause which impedes dietary mineral absorption. A systematic review of celiac patients found that adherence to a gluten free diet for five years resulted in normalized bone mineral density. One of the included studies found that a gluten free improved bone mineral density as well as bisphosphonate drugs (11).

Poor fat absorption

Another digestive-related cause of osteoporosis is poor fat absorption. You may have noticed in the earlier section both Vitamin D and Vitamin K2 are critical for bone health. Vitamin A, another fat soluble nutrient, is important as well. Because these are both fat-soluble nutrients, they rely on fat to absorb. And because we must eat fat with fat-soluble nutrients in order to absorb them, people on low-fat diets may become deficient even though they eat many foods rich in these nutrients. Poor fat digestion resulting from gall bladder removal or gallstones is another possible cause of deficiency.

Important nutrients

In this section we’ll discuss the most important nutrients to support increased bone density.

Calcium

Calcium is the most prevalent mineral in the body. Although some studies have shown no benefit to calcium supplementation, many have been poorly designed in light of what we now know about all the nutrients that are required to build bone. Many of these studies used only calcium carbonate, which is very poorly absorbed and has a strong alkalizing effect on stomach pH. In fact, calcium carbonate is the active ingredient of Tums, the popular over the counter heartburn medication, which temporarily relieves symptoms by alkalizing stomach acid.

Because of calcium carbonate’s alkalizing effect on stomach pH, it may actually do more harm that good because very acidic stomach acid is critical to absorbing nutrients. Some studies use calcium carbonate as a control, which may contribute to somewhat misleading data because carbonate may be contributing to worse outcome for the control group.

Another form of calcium that is much more effective is known as MCHA calcium, which stands for microcrystalline hydroxyapitate. The body uses this form to create bone matrix and some research shows supplementary MCHA calcium (also sometimes called MCHC) is an especially beneficial form. Many MCHC supplements are made from whole animal bones and supply a whole complex of necessary nutrients like collagen and trace minerals such as boron, potassium, zinc and copper that are used to construct the bone matrix. They also typically contain vitamins D and K2. These products are also sometimes referred to as “ossein-hydroxyapitate complex” supplements, or OHC in research.

MCHA Calcium

A number of clinical trials have evaluated the benefits of MCHA / OHC calcium by comparing its effects to those of calcium carbonate supplements in patients with osteopenia and osteoporosis, and found benefit. One such study followed a cohort of 54 women for three years and found statistically significant improvements in bone density and serum osteocalcin in the MCH calcium group (12).

A 2015 meta analysis of studies from 1966 to 2013 compared the benefits of OHC calcium supplements to calcium carbonate and concluded that the OHC form was superior to “calcium [carbonate] supplements in maintaining bone mass in postmenopausal women and in different conditions related to bone loss.” They also observed that in patients with osteopenia or osteoporosis who took OHC, pain symptoms were decreased and fractures healed more quickly (13).

In addition to other trace minerals important for bone health, MCH / OHC calcium also contain fat-soluble vitamins like vitamin D and K2, which are important as well. Without these other nutrients in addition to calcium, bone density may not be improved and calcium supplements alone can contribute to kidney stones.

Vitamin D

It’s well known that optimal vitamin D levels are critical for bone health. Dietary vitamin D increases calcium absorption and adequate blood levels are associated with significantly reduced risk of fracture (14). Of course, significantly elevated levels of vitamin D can also be problematic, so we like to keep blood levels between 35-60 ng/dL.

Vitamin K2

This important nutrient fulfills several job duties in the body related to bone density. It is a cofactor in the carboxylation of osteocalcin, which promotes normal bone mineralization and appears to regulate the growth of hydroxyapitate crystals. A number of animal studies demonstrate the vitamin K2 improves bone density in rats that are ovariectomized or treated with glucocorticoids like prednisone. It appears to stimulate bone formation and suppress bone resorption, or breakdown.

In human clinical trials, vitamin K2 has been demonstrated to support lumbar bone mineral density and prevent osteoporotic fractures with age-related osteoporosis and prevent vertebral fractures associated with glucocorticoid use. It also increases bone density of extremities in patients with cerebrovascular disease and maintains lumbar bone mineral density in liver-dysfunction induced osteoporotic patients (15).

One well-designed clinical trial on a cohort of 63 postmenopausal women in Indonesia found that adding 45mg of vitamin K2 to 1500mg of calcium carbonate per day significantly increased lumbar bone mineral density and decreased undercarboxylated osteocalcin levels over a 48 week treatment period (16).

Japanese research has corroborated these findings in a few studies which used 30-45mg of Vitamin K2 per day to increase bone density. One such trial from 2010 found that 45mg of Vitamin K2 daily prevented fractures and sustained lumbar bone mineral density in a cohort of 241 osteoporosis patients (17). A similar European study found similar benefit in a smaller sample size. Researchers suggest that Vitamin K2 therapy should be started early, starting at menopause to effectively prevent spine bone mineral density loss (18). Other research on Caucasian women has found similar benefit as well, confirming that Vitamin K2 is an effective way to prevent bone loss in multiple ethnicities of women (19).

Vitamin A

The last fat soluble nutrient we’ll talk about is Vitamin A, which at high doses is associated with increased risk of fracture. One review study found that high retinol (the active form of Vitamin A from animal sources) induces fractures in animals, and asserts that intake double the recommended amount can cause adverse effects in females. This is only true for retinol and not pro-vitamin A precursors like beta carotene.

One factor that we were not able to find more information on was the ratio of Vitamin A to the other fat-soluble vitamins. It is fairly well established at this point that the fat-soluble vitamin levels must remain in correct proportions to each other, and Vitamins A and D in particular protect against toxic levels of each other. It would be interesting to know what the nutrient status for Vitamin D was in these patients.

Other therapy options

In addition to these nutrients there are some other therapies that have shown benefit for maintaining and restoring bone mineral density, which we’ll cover in the following section.

Genistein and soy

Certain soy foods and other genistein-containing foods have also shown to be very helpful. Found in soy, fave beans, garbanzo beans and coffee, genistein is an phytoestrogenic isoflavone that shows promising benefits for bone mineral density and osteoporosis. In fact, genistein has the strongest estrogenic activity of any flavone, which makes it a great treatment option for menopausal osteoporosis.

Eating fermented soy in moderate quantities is a great way to get more genistein into the diet. Miso, tempeh and natto are all great sources of genistein. It is important, however to keep quality in mind, as more than 90% of soy grown at this point is genetically modified. When selecting soy products, there are two main labels to look for: organic and non-GMO. These labels ensure that the product is non-GMO.

A well-designed trial of 389 osteoporotic postmenopausal women found that 54mg of genistein aglycone combined with calcium and vitamin D3 increased bone mineral density compared to calcium and D3 alone over a 24 month period. One possible area of concern with phytoestrogens is possibly raising the risk of estrogen-based cancers like breast cancer. To address that concern, this study also measured markers for breast cancer including BRCA1 and BRCA2 expression and mammography and found that gene expression did not increase and mammographic density did not change significantly (20). These results suggest that genistein is safe and effective in postmenopausal women.

Other research has found supporting evidence in rats (21) and postmenopausal women (22) (23). It is unclear whether this research would extend to premenopausal women or men. Both of these human studies used a dose of 54mg of genistein per day.

Genistein supplements are also available, and there are a few non-GMO options, including:

  • Source Natural Genistein
  • Bluebonnet non-GMO Soy Isoflavones Plus Genistein

These are both isoflavone complexes that also contains daidzen and glycitein.

Another option that is more of a bone building complex, combining genistein with vitamin D3, vitamin K2, calcium, magnesium and zinc is:

  • Designs for Health Osteoben

In addition to these nutrients, one constituent of cannabis has research also has some research behind it.

Cannabidiol

Cannabidiol (CBD) is a non-psychoactive constituent of marijuana. One study found that the administration of CBD enhanced the healing of femoral fractures in rats. This action was not seen in administration of THC alone, which is the main psychoactive component of marijuana. CBD increased production of an enzyme that catalyzes lysine hydroxylation, which in turn is involved in collagen crosslinking and stabilization. This effect led to CBD improing fracture healing (24).

Magnet therapy

One last treatment option with some research behind it is magnet therapy. One rat study found that long-term extremely low frequency magnetic field (ELFMF) was effective at increasing bone mineral content and bone mineral density. In addition, bone specific alkaline phosphatase levels were increased in the ELFMF group, leading researchers to conclude that ELFMF may offer benefits in the treatment of osteoporosis (25).

Resistance training

We mentioned the important of weight-bearing exercise earlier. Quite a bit of research confirms the importance of this type of exercise in preventing bone mineral density loss as we age. The importance of weight-bearing exercise cannot be overstated, and it’s a “better late than never” type of thing. No matter at what age one begins weight bearing exercise, it is a critical piece to slow and stop bone mineral loss, and can even help increase bone mineral density in some cases. By creating a mild positive stress, or eustress, on the bones, it triggers them to increase their strength and mineral composition.

A 1999 review study found that out of nearly two dozen trials evaluating the effects of resistance training found that the vast majority showed “a direct and positive relationship between the effects of resistance training and bone density,” and the few that did not show a benefit may have been poorly designed (26). A more recent study compared weight bearing exercise to non-weight bearing in a cohort of 40 osteoporosis patients in their 60s. Compared to the non-weight bearing exercise group, the weight-bearing group showed more impressive increases in bone mineral density as well as overall quality of life (27).

Despite concerns that using heavy weight for resistance training could lead to fracture, one Australian study found that heavy weights may actually confer a greater benefit than moderate weight. Participants completed either a high weight resistance training program or a low intensity program of the same duration and dose. The heavy weight group improved in height, bone mineral density and functional performance compared to the low intensity group (28). And best of all, there were no injuries! A patient’s initial bone mineral density should be considered to make sure the weights used are appropriate.

Although much of the research presented so far has focused primarily or exclusively on women, this trial evaluated the effects of resistance training on men, noting that although women are affected more by osteoporosis, 40% of osteoporotic fractures occur in men and that men have significantly greater risk of complications after a hip fracture. Coupled with the fact that men are treated far less often than women and more than 90% of osteoporosis in men goes undiagnosed and untreated, this represents a significant issue for men, especially older men (29).

This trial concluded that both resistance training and jump training, which revolves around jumping exercises increased bone mineral density in men with a mean of 44 years. Osteocalcin was also increased significantly. Resistance training appeared to be the most effective, resulting in more robust bone mineral density increases.

Based on this research and more that was not included here for brevity, resistance training and especially high intensity interval training (HIIT) is extremely important for anyone concerned about bone mineral density and must be included as part of any well-rounded treatment plan. Despite its placement towards the end of this article, it is a critical piece of the osteoporosis puzzle!

In conclusion

Osteoporosis is a significant health problem today, and the bisphosonate drugs commonly used to treat low bone mineral density have significant risks, including not reducing the risk of fracture, or in some cases even increasing that risk! Fortunately, there are many natural treatment options for osteoporosis that are safe and effective. By working with a functional medicine practitioner to correctly identify and treat your root cause, you can prevent or even reverse osteoporosis from developing and leading to a debilitating fracture.

General recommendations for Osteoperosis concern:

  • Weight lifting / resistance training 2-3 days per week, plus short (10-30 mins) High Intensity Interval Training (HIIT) sessions 4-5 days per week.
  • Achieve Vitamin D levels in the blood of 35-60 ng/ml. If supplementing with Vitamin D, be sure to also supplement with Vitamin K2 (see below for specifics).
  • Ensure that you are getting adequate calcium from food (preferred) or if supplementing, use the MCHA form. It is best to get between 800-1300mg of calcium each day, optimally from foods.
  • Vitamin K2 at 15-45mg per day (note that this is mg dosing and many MK-7 Vitamin K2 supplements are in mcg. Usually the MK-4 form will be required to get the 15-45mg per day dosing in a cost-effective way).
  • For post-menopausal women, consider 40mg per day of black cohosh and/or 54mg daily of genistein aglycone (can also consider organic miso, tempeh, and natto consumption if soy is tolerated).
  • If additional support is needed or desired, CBD and/or magnet therapy may be helpful (though there is not enough research to be conclusive on either of these. However, because they are generally safe and well-tolerated, it can be worth pursuing. Please note that magnet therapy is not to be used for anyone with a pacemaker).
  • We do not recommend supplementing with DHEA (a hormone) outside of working with a functional medicine doctor who understands this hormone and is measuring blood levels.

References

  1. Johnell O and Kanis JA (2006) An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. Osteoporos Int 17:1726.
  2. Kanis JA, Delmas P, Burckhardt P, et al. (1997) Guidelines for diagnosis and management of osteoporosis. The European Foundation for Osteoporosis and Bone Disease. Osteoporos Int 7:390.
  3. Kanis JA, Oden A, Johnell O, et al. (2003) The components of excess mortality after hip fracture. Bone 32:468.
  4. Kwek, Ernest Beng Kee, et al. “An Emerging Pattern of Subtrochanteric Stress Fractures: A Long-Term Complication of Alendronate Therapy?” Injury, vol. 39, no. 2, 2008, pp. 224–231., doi:10.1016/j.injury.2007.08.036.
  5. Neviaser, Andrew S, et al. “Low-Energy Femoral Shaft Fractures Associated With Alendronate Use.” Journal of Orthopaedic Trauma, vol. 22, no. 5, 2008, pp. 346–350., doi:10.1097/bot.0b013e318172841c.
  6. Wuttke, Wolfgang, et al. “Effects of Black Cohosh (Cimicifuga Racemosa) on Bone Turnover, Vaginal Mucosa, and Various Blood Parameters in Postmenopausal Women.” Menopause, vol. 13, no. 2, 2006, pp. 185–196., doi:10.1097/01.gme.0000174470.44822.57.
  7. Seidlová-Wuttke, D., et al. “Effects of Estradiol-17β, Testosterone and a Black Cohosh Preparation on Bone and Prostate in Orchidectomized Rats.” Maturitas, vol. 51, no. 2, 2005, pp. 177–186., doi:10.1016/j.maturitas.2004.07.007.
  8. Villareal, Dennis T., et al. “Effects of DHEA Replacement on Bone Mineral Density and Body Composition in Elderly Women and Men.” Obstetric and Gynecologic Survey, vol. 56, no. 4, 2001, pp. 221–222., doi:10.1097/00006254-200104000-00021.
  9. Mühlen, D. Von, et al. “Effect of Dehydroepiandrosterone Supplementation on Bone Mineral Density, Bone Markers, and Body Composition in Older Adults: the DAWN Trial.” Osteoporosis International, vol. 19, no. 5, 2007, pp. 699–707., doi:10.1007/s00198-007-0520-z.
  10. Dukowicz AC, Lacy BE, Levine GM. Small Intestinal Bacterial Overgrowth: A Comprehensive Review. Gastroenterology & Hepatology. 2007;3(2):112-122.
  11. Grace-Farfaglia P. Bones of Contention: Bone Mineral Density Recovery in Celiac Disease—A Systematic Review. Nutrients. 2015;7(5):3347-3369. doi:10.3390/nu7053347.
  12. Ciria-Recasens, Manel, et al. “Comparison of the Effects of Ossein-Hydroxyapatite Complex and Calcium Carbonate on Bone Metabolism in Women with Senile Osteoporosis.” Clinical Drug Investigation, 2011, p. 1., doi:10.2165/11592930-000000000-00000.
  13. Castelo-Branco, C., and J. Dávila Guardia. “Use of Ossein–Hydroxyapatite Complex in the Prevention of Bone Loss: a Review.” Climacteric, vol. 18, no. 1, 2014, pp. 29–37., doi:10.3109/13697137.2014.929107.
  14. Lips, Paul, and Natasja M. Van Schoor. “The Effect of Vitamin D on Bone and Osteoporosis.” Best Practice & Research Clinical Endocrinology & Metabolism, vol. 25, no. 4, 2011, pp. 585–591., doi:10.1016/j.beem.2011.05.002.
  15. Iwamoto, Jun, et al. “Effects of Vitamin K2 on Osteoporosis.” Current Pharmaceutical Design, vol. 10, no. 21, 2004, pp. 2557–2576., doi:10.2174/1381612043383782.
  16. Purwosunu, Yuditiya, et al. “Vitamin K2 Treatment for Postmenopausal Osteoporosis in Indonesia.” Journal of Obstetrics and Gynaecology Research, vol. 32, no. 2, 2006, pp. 230–234., doi:10.1111/j.1447-0756.2006.00386.x.
  17. Shiraki, Masataka, et al. “Vitamin K2 (Menatetrenone) Effectively Prevents Fractures and Sustains Lumbar Bone Mineral Density in Osteoporosis.” Journal of Bone and Mineral Research, vol. 15, no. 3, 2010, pp. 515–521., doi:10.1359/jbmr.2000.15.3.515.
  18. Iwamoto, Ichiro, et al. “A Longitudinal Study of the Effect of Vitamin K2 on Bone Mineral Density in Postmenopausal Women a Comparative Study with Vitamin D3 and Estrogen–Progestin Therapy.” Maturitas, vol. 31, no. 2, 1999, pp. 161–164., doi:10.1016/s0378-5122(98)00114-5.
  19. Knapen MHJ, Schurgers LJ, Vermeer C. Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women. Osteoporosis International. 2007;18(7):963-972. doi:10.1007/s00198-007-0337-9.
  20. Marini, Herbert, et al. “Breast Safety and Efficacy of Genistein Aglycone for Postmenopausal Bone Loss: A Follow-Up Study.” The Journal of Clinical Endocrinology & Metabolism, vol. 93, no. 12, 2008, pp. 4787–4796., doi:10.1210/jc.2008-1087.
  21. Bitto, A, et al. “Effects of Genistein Aglycone in Osteoporotic, Ovariectomized Rats: a Comparison with Alendronate, Raloxifene and Oestradiol.” British Journal of Pharmacology, vol. 155, no. 6, 2008, pp. 896–905., doi:10.1038/bjp.2008.305.
  22. Marini, Herbert, et al. “Effects of the Phytoestrogen Genistein on Bone Metabolism in Osteopenic Postmenopausal Women.” Annals of Internal Medicine, vol. 146, no. 12, 2007, p. 839., doi:10.7326/0003-4819-146-12-200706190-00005.
  23. Morabito, Nunziata, et al. “Effects of Genistein and Hormone-Replacement Therapy on Bone Loss in Early Postmenopausal Women: A Randomized Double-Blind Placebo-Controlled Study.” Journal of Bone and Mineral Research, vol. 17, no. 10, 2002, pp. 1904–1912., doi:10.1359/jbmr.2002.17.10.1904.
  24. Kogan, Natalya M, et al. “Cannabidiol, a Major Non-Psychotropic Cannabis Constituent Enhances Fracture Healing and Stimulates Lysyl Hydroxylase Activity in Osteoblasts.” Journal of Bone and Mineral Research, vol. 30, no. 10, 2015, pp. 1905–1913., doi:10.1002/jbmr.2513.
  25. Akpolat, Veysi, et al. “Treatment of Osteoporosis by Long-Term Magnetic Field with Extremely Low Frequency in Rats.” Gynecological Endocrinology, vol. 25, no. 8, 2009, pp. 524–529., doi:10.1080/09513590902972075.
  26. Layne, Jennifer E., and Miriam E. Nelson. “The Effects of Progressive Resistance Training on Bone Density: a Review.” Medicine & Science in Sports & Exercise, vol. 31, no. 1, 1999, pp. 25–30., doi:10.1097/00005768-199901000-00006.
  27. Shanb AA, Youssef EF. The impact of adding weight-bearing exercise versus nonweight bearing programs to the medical treatment of elderly patients with osteoporosis. Journal of Family & Community Medicine. 2014;21(3):176-181. doi:10.4103/2230-8229.142972.
  28. Watson, S. L., et al. “Heavy Resistance Training Is Safe and Improves Bone, Function, and Stature in Postmenopausal Women with Low to Very Low Bone Mass: Novel Early Findings from the LIFTMOR Trial.” Osteoporosis International, vol. 26, no. 12, 2015, pp. 2889–2894., doi:10.1007/s00198-015-3263-2.
  29. Hinton PS, Nigh P, Thyfault J. Effectiveness of resistance training or jumping-exercise to increase bone mineral density in men with low bone mass: a 12-month randomized, clinical trial. Bone. 2015;79:203-212. doi:10.1016/j.bone.2015.06.008.
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February 12, 2018

Iron Man: Lab Markers for Iron Deficiency

Iron Deficiency

by Aaron Mello, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

We wrote in a recent post about functional laboratory testing for anemia. Different forms of anemia result from many different causes, and iron deficiency anemia is the most common form. In this post we’re going to expand on iron dysregulation and some other sequelae of iron deficiency. We’ll also get into markers for iron status that weren’t covered in the anemia post, so keep reading to learn more!

Most of the iron in the body is found in hemoglobin, which is utilized by RBCs to make oxygen transport possible. Much of the remaining iron not utilized by hemoglobin is bound by proteins like transferrin and ferritin because free iron must be tightly regulated to prevent damage. Free iron is extremely reactive and can also be utilized by pathogenic bacteria to proliferate (1).

In this post we’ll go into more detail about iron status markers and iron deficiency, whereas in the previous post on anemia we concentrated more on the RBC section of the CBC. We’ll be focusing on the other side of the coin, iron overload, in an upcoming post. To learn more about how to evaluate iron status and identify iron deficiency, keep reading! We’ll talk about several iron markers, including ferritin, transferrin, serum iron, TIBC, UIBC and iron saturation.

Roles of iron in the body

Let’s begin by talking about how the body utilizes iron in more detail. In our previous post about anemia, we wrote about iron deficiency anemia, which is one of the main consequences of iron deficiency. Other sequelae of iron deficiency we’ll discuss here include heart issues; dry, damaged skin and hair; restless leg syndrome; pica and brittle or spoon-shaped fingernails. Many of these symptoms result from inadequate oxygenation, and as we’ll see from a study we’ll get to shortly, iron deficiency symptoms can be present even without a diagnosis of anemia.

Nitric oxide production is iron-dependent

In addition to negatively impacting the body’s ability to transport oxygen, iron deficiency also reduces the body’s ability to synthesize nitric oxide (NO), which dilates blood vessels. Iron is a necessary cofactor for NO synthesis, so iron deficiency impairs blood vessel dilation is impaired. It’s not just that oxygen can’t be transported, it’s that the flow of blood to peripheral tissues is also impaired due to a lack of NO (2).

Iron necessary for liver detoxification

Iron is not just limited to oxygen transport and utilization. Iron is also a critical nutrient for the function of many cytochrome enzymes, including cytochrome P450 enzymes that are responsible for liver detoxification (2). Consequently, iron deficiency can downregulate phase 1 liver detoxification. Iron also relates to thyroid health, which we wrote about several months ago in a post on Hashimoto’s thyroiditis.

Peroxidase enzymes need iron

Thyroid peroxidase enzyme (TPO) synthesizes thyroid hormone and is dependent on iron. Consequently, thyroid hormone production may fall in iron deficiency. TPO uses hydrogen peroxide (H2O2) to ready iodine for thyroid hormone production. Myeloperoxidase (MPO) is another iron-dependent peroxidase enzyme that controls pathogenic bacteria by producing sodium hypochlorite (NaClO), or bleach, from hydrogen peroxide in order to kill pathogens. MPO malfunction can lead to immune function failure, gut infections and dysbiosis.

Catalase is a third iron-dependent enzyme. It converts hydrogen peroxide (H2O2) to water in order to control levels of H2O2 and prevent cellular and metabolic damage. Free iron that is not bound by a protein can be particularly destructive in the presence of H2O2, with which it can interact to produce dangerous hydroxyl radicals (OH), which causes more damage than just H2O2 or free iron alone (3). It’s easy to see from these examples how far-reaching the roles of iron are.

Like many nutrients, there is a sweet spot for iron levels, and this is doubly true given its role in many metabolic processes, as well as its potential to cause damage. Next we’ll discuss the context of iron deficiency anemia in the larger picture of health before moving on to heme vs non heme iron and some other nutrients required to utilize iron properly.

Anemia is priority

Let’s pause for a second, zoom out and reorient ourselves in the larger picture of health. In challenging patients it can be tempting to sometimes deprioritize anemia and focus on what may appear to be more pressing concerns. Although there may be situations where this is necessary, they are generally few and far between, especially in the chronic disease world. Because nearly every biochemical process in the body is energy dependent – that is – requires ATP, anemia affects every cell with mitochondria and every system in the body.

For this reason it’s often advisable to get the anemia patterns straightened out early on, before moving on to other areas of treatment, unless there is a good reason to start somewhere else first. With that bigger picture in mind, let’s zoom back in and review the importance of heme vs non-heme iron.

Heme vs non-heme iron

One big determining factor for iron intake is the form of iron an individual is consuming. Non-heme iron from vegetarian sources is poorly absorbed and utilized compared to heme iron in meat, especially red meat. This can be an issue for long-term vegans and strict vegetarians, especially those who do not eat any shellfish, which are also a good source of heme iron. Non-heme iron is typically present in an oxidized form, whereas iron needs to be in its reduced form in order to be absorbed (4).

Other factors that affect iron absorption include vitamin C, which increases absorption of non-heme iron by reducing it into more absorbable form (5). Vegetarians who want to increase absorption of plant-based non-heme iron can try consuming with Vitamin C with food. On the other hand, plant foods contain phytates and polyphenols that inhibit iron absorption, so properly soaking seeds and grains before eating is also important to maximize iron absorption.

Calcium also blocks absorption of iron, so calcium-rich foods like spinach and dairy may reduce absorption of iron from iron-rich foods (6). To raise iron levels, concentrate on isolating calcium-rich foods to one meal per day and have another meal that is rich in iron foods like red meat, liver and clams. Now that we’ve covered these factors affecting iron absorption, we’ll next discuss the role copper and vitamin B6 play in iron regulation.

Vitamin B6 and copper

Vitamin B6 and copper affect the body’s ability to absorb and utilize iron. B6 in particular is required to absorb iron. One study on anemic pregnant women treated with iron supplements found that the women who did not initially improve were deficient in B6 and after adding B6 to the iron supplement, anemia improved (7). In addition, both B6 and copper are involved in the utilization of iron to synthesize RBCs.

Copper has a complicated relationship with iron. On the one hand, copper can impede iron absorption by binding to mucosal transferrin at the expense of iron, and excess copper inhibits the ability of spleen reticuloendothelial cells to reuse iron (8). On the other hand, copper is also needed to mobilize sequestered iron from storage tissues. Similar to B6, this can lead to a form of anemia that does not respond to iron supplementation unless copper is also added (9).

It can be worth looking at B6 and copper status and intake in cases of anemia, especially if there are other clues present. Other indicators that copper and B6 may be involved are mood and temperament issues. B6, copper and zinc are required for neurotransmitter synthesis and zinc/copper balance can contribute to aggressive behavior, deficiencies or imbalances in these nutrients may manifest as symptoms of mood, anxiety or temperament (10).

High levels of zinc supplementation for prolonged periods of time without copper supplementation can lead to copper deficiency. This is worth noting for people who supplement with zinc.

Next we’ll talk a bit more about iron deficiency before moving on to related laboratory markers.

Iron deficiency

Iron deficiency is the most common nutritional deficiency worldwide (11). The most prominent consequence of iron deficiency is iron deficiency anemia, which is also the most common form of anemia. Iron deficiency reduces the ability’s body to transport oxygen via iron-containing hemoglobin on RBCs and results in classic anemia symptoms like fatigue, shortness of breath, pale skin and brittle nails.

Although iron deficiency anemia is the main consequence of deficiency, it’s not the only one. We mentioned a study in the introduction about non-anemic iron deficiency. It found that in a population of 198 menstruating women with low ferritin but normal hemoglobin, oral iron supplementation improved fatigue symptoms (12).

Other iron deficiency issues can include:

  • Heart abnormalities like irregular heartbeat, heart palpitations, and in extreme cases enlarged heart, heart murmur or failure
    • When cells are starved of oxygen, the heart must work harder to circulate more RBCs because they can’t carry much oxygen
    • Compounding the issue, the heart itself may lack sufficient oxygen for muscle contractions
  • Dry, damaged skin or hair (13)
    • In a mouse model, reversal of iron deficiency led to a restoration of hair growth
    • Iron deficiency may contribute to hair loss by inhibiting the iron-dependent ribonucleotide reductase enzyme, which is a rate-limiting enzyme for DNA synthesis
    • Hair and skin cell lines both turn over rapidly
  • Restless leg syndrome (RLS)
    • RLS can result from many different causes but iron deficiency is a common cause (14)
    • One study of 251 iron deficiency anemia patients found that RLS was nine times more prevalent in their group than the general population (15)
  • Pica
    • Pica is a condition of craving or eating dirt
    • It can result from many causes, some psychological
    • Iron deficiency pica is characterized by a compulsion to consume iron-containing substances like clay, soil and even small rusty pieces of steel
  • Pagophagia (pica for ice) may also indicate iron deficiency (16)

Because iron plays a central role in transporting and utilizing oxygen to produce ATP, it’s important to resolve iron deficiency and anemia early on in care. Countless critical processes in the body are energy dependent, and if cells are starved for energy they are not going to function properly. In this way, iron deficiency can be central to many diverse health conditions. Next, let’s shift gears and talk in more detail about iron status markers.

Iron status markers

In addition to the anemia markers on the CBC we discussed in our previous post, iron status markers are helpful in cases of suspected iron deficiency anemia or iron overload. In this section we’ll go into more detail about each of the markers and how to use them clinically. As we mentioned earlier, iron is tightly regulated by the body because of its massive reactive potential and the ability of pathogens to use iron to their advantage (17).

In addition, the body has no way to eliminate excess iron other than bleeding and menstruation, so iron status is dependent on two factors – dietary iron intake coupled with how iron is utilized and stored in the body. As mentioned previously, the body strives to keep most iron either in use in hemoglobin or bound to proteins like transferrin and ferritin to prevent free iron ions from creating oxidative stress and encouraging the proliferation of pathogenic bacteria.

With anemia we are looking primarily at cells – RBCs and their components like hemoglobin. These markers are found on a standard CBC.In contrast, the markers on a complete iron panel are not part of a CBC and must be ordered separately to confirm or rule out suspected iron deficiency or overload. We’ll get into each of these iron panel markers in more detail now, as well as a few other markers that can be relevant.

Ferritin: our preferred functional range is 50-150 ng/ml* (Iron Disorders Institute prefers 25-75 ng/ml for those with hereditary hemochromatosis and for anyone levels above 100 ng/ml may indicate an increased disease risk*)

Iron is bound to ferritin to create iron stores in tissues including the liver, spleen and bone marrow. Depressed ferritin may indicate iron depletion, but many factors can affect ferritin and it’s best to view it in the context of a full iron panel. Ferritin sequesters iron in long-term storage to prevent free iron from causing oxidative stress and to make it unavailable to pathogens which will use it for their own growth.

Ferritin on its own without other markers for context can be misleading, as several factors such as oxidative stress and inflammation can elevate ferritin levels. Inflammation can mask iron deficiency and result in a false normal ferritin level. Inflammation can be confirmed by running hsCRP, which we’ll talk about shortly.

Other possible influences on ferritin levels include intake of sulfuraphane (18), milk thistle (19) and green tea extract (20), which can all upregulate ferritin. These products can also lead to anemia by causing the body to store more iron and diverting it away from hemoglobin. Ferritin is also elevated in liver damage, hemochromatosis, neurodegenerative diseases and in response to inflammation.

As we can see, ferritin is impacted by many factors. It also has antioxidant properties, and factors that increase synthesis of glutathione and catalase also increase ferritin because it’s part of the antioxidant defense system (21). Because many biochemical causes can impact ferritin and potentially cancel each other out, it is important to view ferritin in the context of other markers on a complete iron panel, which we will discuss now.

* Cardiovascular and blood sugar disease risk increases with ferritin levels above 100 ng/ml. However, these risks can be mitigated with properly functioning antioxidant defense mechanisms. With properly functioning antioxidant defense, levels of 150 ng/ml or above may be safe.

Transferrin: 

The protein transferrin is largely synthesized in the liver and binds iron for transportation through the blood. In addition to binding iron for transport, transferrin is a major component of iron regulation primarily found in the blood and tissue fluids (22).

Serum transferrin is a somewhat expensive test. We sometimes order TIBC instead, which we’ll talk about shortly, as TIBC can be an indicator of transferrin status. Other factors influencing transferrin include liver disease, which can reduce synthesis, and dietary iron. Transferrin can vary considerably based on the iron content of a person’s last meal, so it needs to be performed with the patient fasting.

Serum iron: 

This is simply the amount of iron in the bloodstream bound to transferrin. It is not the most reliable marker of iron deficiency but it’s a better marker for iron overload like hemochromatosis, especially when combined with iron saturation. We’ll talk more about hemochromatosis in an upcoming post.

TIBC: our preferred functional range is 275-430 ug/dL

Total iron binding capacity (TIBC) measures ability of RBCs to bind to transferrin. TIBC is elevated in iron deficiency, pregnancy and blood loss, and it’s normal in anemia of chronic disease and inflammation. TIBC is depressed in elevated iron loads, liver disease, hypoproteinemia, infection and chronic disease.

UIBC, or unbound iron binding capacity, has an optimal range of 175-350 ug/dL. Lower levels mean higher iron.

Transferrin saturation: our preferred functional range is 17-45% with optimal being 25-35%

Elevated transferrin saturation (TS) stimulates hepcidin, which we’ll talk about next. In turn, hepcidin downregulates iron absorption and increases storage of iron in ferritin. TS is more sensitive than ferritin because TS is what causes ferritin to increase in response to high iron. It’s also more specific to iron status than ferritin, which is influenced by many other factors like inflammation, which we discussed earlier.

Hemoglobin (Hg): 

Hemoglobin is the iron-containing portion of a red blood cell that transports ozxygen from lungs to tissues. Depleted or excessive amounts of hemoglobin can point to imbalanced iron levels.

Mean Corpuscular Volume (MCV):

MCV is a measure of the average volume of red blood cells. Anemias are often referred to in reference to the size of the red blood cell. There is microcytic anemia (low MCV and often is caused by low iron), normocytic anemia (normal MCV), and macrocytic anemia (high MCV – also called pernicious anemia – often caused by low B12 and/or folate levels).

Gamma Glutamyl Tranferase (GGT):

GGT is a liver enzyme that has traditionally been used to primarily look for liver issues. Recently, it has become clear that GGT elevation (even high-normal values) can be associated with increased risk for metabolic syndrome. Levels greater than the lowest 25% of the population are associated with metabolic abnormalities, cardiovascular disease risk, and more.

Hepcidin:

Sometimes referred to as “The Iron Regulatory Hormone,” hepcidin is the master coordinator of iron. High iron hepcidin downregulates iron absorption and directs free iron to be sequestered in ferritin. Hepcidin responds to threats like an infection via inflammation which could use free iron for its own proliferation. Hepcidin also has antimicrobial properties; in fact its name comes from the its location of synthesis, the liver (hep-), and its antimicrobial effects (-cidin) (23).

hsCRP: our functional range is 0-1 mg/L

We talked about hsCRP and inflammation earlier. Inflammation, as measured by high sensitivity C-Reactive Protein (hsCRP) can lead to false normal or even elevated ferritin in the presence of anemia. Anemia of chronic disease results in low absorption and high storage as ferritin, so high ferritin and iron deficiency can exist simultaneously because the small amount of iron that is absorbed is directed into storage instead of hemoglobin synthesis in an effort to sequester it away from pathogenic invaders. hsCRP isn’t an iron marker per se, but it can be useful to confirm or rule out inflammation that may be elevating ferritin.

Now that we have a better understanding of these markers and how to use them to evaluate iron deficiency, let’s review some iron-rich foods before closing. Also be sure to keep an eye out for our upcoming post on iron overload and hemochromatosis.

Iron foods

  • Clams
  • Liver / organ meat
  • Red meat – lamb, beef
  • Prunes
  • Beets
  • Venison
  • Kidney
  • Octopus
  • Oysters
  • Sardines
  • Blackstrap molasses

In Conclusion

Iron is a critical nutrient and iron is the most common deficiency worldwide. Furthermore, iron deficiency anemia is the most common form of anemia, and it impacts every cell of the body because of its role in ATP production. It’s easy to see why resolving iron deficiency is a critical piece for anyone whom is affected by it. Stay tuned for an upcoming post on the other side of the coin from iron deficiency – iron overload and hemochromatosis!

For those low in iron, here are strategies that can help increase iron stores:

  • Make sure low iron is based on lab testing, as iron can be toxic when in excessive quantities
  • Increase iron containing foods (especially those with heme iron like animal products)
  • Add vitamin C with meals (500-1000mg)
  • Contain calcium-containing foods and/or supplements to 1 meal per day (calcium blocks iron absorption)
  • Iron supplementation under the guidance of a functional medicine doctor / practitioner
  • Stop donating blood temporarily until iron stores are back up
  • Avoid chelating substances or protocols intended to chelate metals
  • Be sure you re-test labs so that you know when levels are normal and you can simply maintain
  • If you do not have success with basic practices, see a functional medicine doctor / practitioner to identify root cause issues that might be preventing iron absorption

References

  1. Cassat JE, Skaar EP. Iron in Infection and Immunity. Cell host & microbe. 2013;13(5):509-519. doi:10.1016/j.chom.2013.04.010.
  2. Galleano, M. “Nitric Oxide and Iron: Effect of Iron Overload on Nitric Oxide Production in Endotoxemia.” Molecular Aspects of Medicine, vol. 25, no. 1-2, 2004, pp. 141–154., doi:10.1016/j.mam.2004.02.015.
  3. Kadiiska, Maria B., et al. “A Comparison of Cobalt(II) and Iron(II) Hydroxyl and Superoxide Free Radical Formation.” Archives of Biochemistry and Biophysics, vol. 275, no. 1, 1989, pp. 98–111., doi:10.1016/0003-9861(89)90354-8.
  4. West AR, Oates PS. Mechanisms of heme iron absorption: Current questions and controversies. World Journal of Gastroenterology : WJG. 2008;14(26):4101-4110. doi:10.3748/wjg.14.4101.
  5. Teucher, et al. “Enhancers of Iron Absorption: Ascorbic Acid and Other Organic Acids.”International Journal for Vitamin and Nutrition Research, vol. 74, no. 6, 2004, pp. 403–419., doi:10.1024/0300-9831.74.6.403.
  6. Lynch, Sean R. “The Effect of Calcium on Iron Absorption.” Nutrition Research Reviews, vol. 13, no. 02, 2000, p. 141., doi:10.1079/095442200108729043.
  7. Hisano, M, et al. “Vitamin B6 Deficiency and Anemia in Pregnancy.” European Journal of Clinical Nutrition, vol. 64, no. 2, 2009, pp. 221–223., doi:10.1038/ejcn.2009.125.
  8. Chan, W Y, and O M Rennert. “The Role of Copper in Iron Metabolism.” Annals of Clinical and Laboratory Science, vol. 10, no. 4, 1980, pp. 338–44.
  9. Sharp, Paul. “The Molecular Basis of Copper and Iron Interactions.” Proceedings of the Nutrition Society, vol. 63, no. 04, 2004, pp. 563–569., doi:10.1079/pns2004386.
  10. Walsh, W, et al. “Elevated Blood Copper/Zinc Ratios in Assaultive Young Males1.” Physiology & Behavior, vol. 62, no. 2, 1997, pp. 327–329., doi:10.1016/s0031-9384(97)88988-3.
  11. “Micronutrient Deficiencies.” WHO, World Health Organization, www.who.int/nutrition/topics/ida/en/.
  12. Clenin, G E. “The Treatment of Iron Deficiency without Anaemia (in Otherwise Healthy Persons).” Swiss Medical Weekly, vol. 147, no. 2324, 2017, doi:10.4414/smw.2017.14434.
  13. Guo EL, Katta R. Diet and hair loss: effects of nutrient deficiency and supplement use. Dermatology Practical & Conceptual. 2017;7(1):1-10. doi:10.5826/dpc.0701a01.
  14. Allen, Richard P., and Christopher J. Earley. “The Role of Iron in Restless Legs Syndrome.”Movement Disorders, vol. 22, no. S18, 2007, doi:10.1002/mds.21607.
  15. Allen, Richard P., et al. “The Prevalence and Impact of Restless Legs Syndrome on Patients with Iron Deficiency Anemia.” American Journal of Hematology, vol. 88, no. 4, Dec. 2013, pp. 261–264., doi:10.1002/ajh.23397.
  16. Uchida, T, and Y Kawati. “Pagophagia in Iron Deficiency Anemia.” The Japanese Journal of Clinical Hematology, vol. 55, no. 4, 2014, pp. 436–9.
  17. Nanami, M. “Tumor Necrosis Factor- -Induced Iron Sequestration and Oxidative Stress in Human Endothelial Cells.” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 25, no. 12, Jan. 2005, pp. 2495–2501., doi:10.1161/01.atv.0000190610.63878.20.
  18. Evans PC. The influence of sulforaphane on vascular health and its relevance to nutritional approaches to prevent cardiovascular disease. The EPMA Journal. 2011;2(1):9-14. doi:10.1007/s13167-011-0064-3.
  19. Hutchinson C, Bomford A, Geissler CA. The iron-chelating potential of silybin in patients with hereditary haemochromatosis. European journal of clinical nutrition. 2010;64(10):1239-1241. doi:10.1038/ejcn.2010.136.
  20. Toolsee NA, Aruoma OI, Gunness TK, et al. Effectiveness of Green Tea in a Randomized Human Cohort: Relevance to Diabetes and Its Complications. BioMed Research International. 2013;2013:412379. doi:10.1155/2013/412379.
  21. Theil EC. Ferritin iron minerals are chelator targets, antioxidants, and coated, dietary iron. Annals of the New York Academy of Sciences. 2010;1202:197-204. doi:10.1111/j.1749-6632.2010.05575.x.
  22. Rouault, Tracey A. “How Mammals Acquire and Distribute Iron Needed for Oxygen-Based Metabolism.” PLoS Biology, vol. 1, no. 3, 2003, doi:10.1371/journal.pbio.0000079.
  23. Rossi E. Hepcidin – the Iron Regulatory Hormone. Clinical Biochemist Reviews. 2005;26(3):47-49.
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December 29, 2017

Diagnosing Anemia with Functional Medicine

anemia

by Aaron Mello, CNTP, MNT and Dr. Miles Nichols, DAOM, MS, LAc

Anemia is a complex and varied condition characterized by low levels of erythrocytes (red blood cells) and hemoglobin. There are many types of anemia. In a recent post on B12 injections, we talked about B12 deficiency anemia. In this post we’ll expand on the anemia piece and talk more about different types of anemia including iron deficiency anemia, hemolytic anemia and sickle cell anemia. We’ll also delve into some of the lab markers that are used to distinguish different types of anemia.

Anemia is a large topic so we’ll get to as much as we can in this post, and expand in future posts. We’ll also touch on ways that anemia can interact with other conditions like Small Intestine Bacterial Overgrowth (SIBO) and chronic inflammation. In addition, we’ll talk about iron and iron deficiency anemia, especially as it relates to vegan and strict vegetarian diets, which are often deficient in heme iron as well as vitamin B12. There is a lot to cover and you’re bound to learn something new, like how B12 analogues from spirulina can actually block B12 absorption! Keep reading to learn more.

Definition of anemia

For a quick recap, anemia is a deficiency of erythrocytes, or red blood cells (RBCs), which transport oxygen to all the cells of the body where it is used to fuel the mitochondria. Erythropoesis, or manufacture of RBCs, takes place in the bone marrow. The RBCs are then transported to the bloodstream where they live for about 120 days in a healthy individual. Depressed hemoglobin levels can also cause anemia.

Generally speaking, most anemia has one of two broad causes:

  1. Decreased production of RBCs and/or hemoglobin
  2. Increased loss or destruction of RBCs, such as a bleeding disorder (1)

RBCs are the most abundant blood cell by far and make up 40-45% of the blood by volume. Even though RBCs live about four months, the body must manufacture an astonishing two million erythrocytes every second to keep up with the equally high rate of RBC destruction. The anatomy of RBCs is highly specialized to provide optimal oxygen transportation abilities.

Symptoms of anemia

Because depressed RBCs negatively affect the body’s ability to fuel its cells with oxygen, many of the symptoms of anemia revolve around difficulty supplying cells with enough oxygen such as low energy levels and shortness of breath.

Symptoms of anemia include: 

  • Fatigue
  • Weakness
  • Pale or yellowish skin
  • Irregular heartbeats
  • Shortness of breath
  • Dizziness or lightheadedness
  • Chest pain
  • Cold hands and feet
  • Headache (1)

Now that we know what anemia is and what the symptoms are, let’s look more in depth at how RBCs carry oxygen and get into more detail about the etiology of anemia, as well as different forms. One of the most important components of RBCs is hemoglobin, which is the iron-containing component of erythrocytes.

Hemoglobin & Iron

Each RBC contains about 280 million hemoglobin molecules and each hemoglobin molecule contains four heme, nonprotein pigments that contain iron ion (Fe2+) which are able to reversibly combine with oxygen molecules, making oxygen transport possible. Hemoglobin also transports about 23% of carbon dioxide, a metabolic waste product, for excretion (2).

Because the iron in hemoglobin binds oxygen for transport by RBCs, a deficiency of iron can lead to iron deficiency anemia, the most common form. We’ll talk about iron-deficiency more shortly. Now that we’ve reviewed relevant erythrocyte anatomy and physiology, let’s move on to the different forms of anemia.

Forms of anemia

Primary or secondary anemia can result from many different causes. In this section we’ll review some of the most common kinds.

Iron deficiency anemia

We touched on this form of anemia earlier. Iron is critical for the manufacture and proper function of RBCs. Iron deficiency primarily results from inadequate intake or absorption, excessive loss through bleeding, or increased iron demand, and it is the most common form of anemia. Individuals eating a strict vegetarian or vegan diet are among the most likely to have inadequate iron intake (3). Iron malabsorption is common with gastric ulcer, parasites, H. pylori infection (4), hypochlorhydria, and in digestive disorders like Crohn’s and celiac disease (5).

Increased iron loss is common in women with heavy menses and in cases of internal bleeding (6). The presence of blood in the stool, especially dried blood that resembles coffee grounds is a strong indication of intestinal bleeding. An occult blood test can also identify blood in the stool that is not visible. When diagnosing iron deficiency anemia, we include more serum markers than with some other forms of anemia, like megaloblastic anemia. An anemia panel for iron deficiency that we use in our clinic includes ferritin, serum iron, UIBC, transferrin saturation, and an CBC w/ differential (at a minimum for comprehensive diagnosis…we sometimes include other markers as well).

Megaloblastic anemia

Megaloblastic anemia is also known as “B12 deficiency anemia” because it is caused by a lack of vitamin B12 and/or folate. Both of these B vitamins are required for erythropoesis, or RBC synthesis. Pernicious anemia (PA) is a common cause of B12 deficiency and megaloblastic anemia, and results from an inability to produce intrinsic factor, which binds to B12 in the stomach and makes absorption in the small intestine possible. PA can also be autoimmune and is confirmed with a positive intrinsic factor antibody blood test. To learn more about megaloblastic anemia, refer back to our recent post on B12 injections.

As we discussed in that post, another common underlying cause of B12 deficiency is a strict vegetarian or vegan diet that does not include any fish or shellfish. Microalgae like spirulina are often believed to contain B12, but instead mostly contain B12 analogues that not only are inactive in the body, they actually block the absorption of usable B12! We don’t recommend spirulina for B12, as it can actually contribute to deficiency by blocking absorption of active B12 (7).

Another interesting aspect of megaloblastic anemia we have observed clinically is a relationship between Small Intestine Bacterial Overgrowth (SIBO) and megaloblastic anemia. It’s fairly well known that SIBO can push B12 low by preventing absorption, and it can also increase folate (8). Some of the SIBO bacteria produce folate, and what we have observed clinically is that sometimes after treating SIBO,  B12 comes back up and folate levels drop, so it can be worth retesting both of these B vitamins after treating SIBO in cases of anemia, as both can change significantly with successful SIBO treatment.

Anemia of chronic inflammation

This type of anemia is secondary to chronic inflammation and is initiated by the activation of inflammatory cytokines like interleuken-6 (IL-6). Anemia that presents with elevated inflammatory cytokines may indicate anemia secondary to inflammation. The spike in cytokines leads to inflammation by several mechanisms:

  • Increases hepatic production and secretion of hepcidin, a peptide which inhibits iron transport and absorption
  • Hepicidin also prevents the stores from being released and utilized
  • Suppresses erythroid precursor proliferation in the bone marrow
  • Inhibits erythropoietin from the kidney
  • Shortens lifespan of RBCs (9)

Chronic disease can also produce a similar type of anemia. Chronically increased WBC production to support an elevated immune response can come at the expense of RBC production and lead to decreased erythropoesis.

Hemolytic anemia

In hemolytic anemia, RBC plasma membranes rupture prematurely and release hemoglobin into the bloodstream. This can overload and damage the glomeruli units in the kidneys that filter blood. Hemolytic anemia can result from many different causes, including inherited defects like altered RBC enzymes, or from exogenous influences like parasites and toxins (10).

Thalassemia is a related group of hereditary hemolytic anemias, which are characterized by deficient synthesis of hemoglobin. In thalassemia, RBCs are small (microcytic), pale (hypochromic) and short-lived. We’ll get into terms for the size and color of RBCs shortly.

Sickle cell disease

Sickle cell anemia is characterized by misshapen RBCs that contain an abnormal kind of hemoglobin and as a result become long, sickle-shaped and unable to carry oxygen. As a result of their abnormal shape, sickle cells rupture easily and die prematurely, resulting in low RBCs. Sickle cells also clump together and can cause blockages in blood vessels (11).

Describing anemic RBCs

Different types of anemia are described in terms of the size and color of the RBCs.

  • Size: 
    • Large – macrocytic
    • Medium – normocytic
    • Small – microcytic
  • Color:
    • High – hyperchromic (or megaloblastic)
    • Medium – normochromic
    • Low – hypochromic

We can see how the types of anemia already discussed can fall into these categories:

  • Mirocytic hypochromic:
    • Iron deficiency
    • Anemia of blood loss
    • Anemia of chronic inflammation / disease
    • Thalassemia
  • Normocytic normochromic:
    • Anemia of chronic inflammation / disease
    • Anemia of acute blood loss
    • Hemolytic anemia
    • Sickle cell
  • Megaloblastic:
    • B12/folate deficiency
    • Pernicious anemia

These distinctions will come into play into the next section on lab testing. One primary way different types of anemia are distinguished from each other is by looking at color and size of the RBCs.

Lab testing for anemia

There are many anemia patterns, as anemia can have many different etiologies. These manifest differently on labwork. Anemia is primarily diagnosed through the RBC section of the Complete Blood Chemistry (CBC). We’ll go over those in this section, discuss some patterns and also a few other markers that can be useful to run.

Anemia in general is identified by depressed RBCs, hemoglobin (HGB) and hematocrit (HCT). From there we look first at Mean Corpuscular Volume (MCV), Mean Corpuscular Hemoglobin (MCH) and Mean Corpuscular Hemoglobin Concentration (MCHC) to begin to distinguish different types. Red Blood Cell Distribution Width (RDW) is also useful, especially when mixed anemia is present.

  • Anemia is defined as:                                                            ideal ranges
    • Low RBCs (below the following ideal range)           (M) 4.4-4.9         (F) 3.9-4.5
    • Low HGB (below the following ideal range)            (M) 14-15 g/dL   (F) 13.5-14.5 g/dL
    • Low HCT (below the following ideal range)            (M) 39-55%        (F) 37-44%
  • MCV looks at cell size:                   defined as
    • Depressed – microcytic          <80 fL
    • Normal – normocytic             80-100 fL
    • Elevated – macrocytic            >100 fL
  • MCH & MCHC look at cell color:            defined as
    • Depressed – hypochromic     MCH <85 pg          MCHC <32 g/dL
    • Normal – normochromic       MCH 85-92 pg      MCHC 32-36 g/dL
    • Elevated – hyperchromic       MCH >92 pg          MCHC >36 g/dL

Let’s look at these markers in a little more detail before moving on to other important anemia markers.

  • RBCs: the absolute number of cells per liter of blood, which if low may indicate deficient synthesis, increased destruction, or excessive blood loss. High RBCs are associated with high altitude, dehydration, bone marrow disorders or renal disorders.
  • Hemoglobin (HGB): The main iron-containing oxygen-transport metalloprotein in RBCs which carries oxygen to the cells and carbon dioxide to the lungs for expiration.
  • Hematocrit (HCT): A measurement of the RBC-containing fraction of whole blood.
  • Mean Corpuscular Volume (MCV): The average volume of an RBC, which is used to distinguish microcytic, normocytic and macrocytic anemia from each other.
  • Mean Corpuscular Hemoglobin (MCH): The average mass of hemoglobin per RBC.
  • Mean Corpuscular Hemoglobin Concentration (MCHC): The average concentration of hemoglobin in the cells. This is used to distinguish between hypochromic, normochromic and megaloblastic (hyperchromic) anemia.
  • Red Blood Cell Distribution Width (RDW): This is a measure of the variation in RBC size. High RDW may indicate a mixed anemia like concurrent microcytic and macrocytic or early stage anemia when there is more variation in the size of RBCs being produced.

Next, we’ll talk about how iron status can impact the presentation of anemia before talking about how to correctly identify and treat the root cause.

Iron markers and disorders

Because of the crucial role iron plays in oxygen transport and anemia, iron disorders overlap with anemia quite a bit. Iron analysis markers are useful in classifying some types of anemia and distinguishing anemia from non-anemia iron disorders. Iron is also essential for erythropoiesis (RBC creation) and DNA synthesis (12). Iron disorders are a large subject all on their own, which we may cover in a future post. We’ll just discuss iron here briefly as it relates to anemia.

Iron-deficiency anemia is a form of microcytic hypochromic anemia characterized by depressed ferritin, serum iron and iron saturation and elevated TIBC and transferrin. There can be many causes of iron-deficiency anemia, many of which involve either reduced iron intake or absorption, or increased blood loss, or both.

Common causes of iron-deficiency anemia:

  • Reduced iron intake:
    • Evaluate diet for iron intake, vegetarian/veganism
    • Heme iron vs non-heme iron
  • Reduced iron absorption:
    • H. pylori
    • Hypochlorhydria
    • Celiac disease
    • Parasites (hookworms, roundworms, pinworms)
  • Increased blood loss:
    • Gastric ulcer
    • Internal bleeding
    • Heavy menses
    • Occult blood in stool

One thing we often see in our office is vegetarians and vegans who are deficient in iron, despite making a concerted effort to eat iron-rich vegetable sources like spinach. Vegetable sources of iron contain non-heme iron, which must be converted into heme iron to be utilized in the body. In contrast, animal sources of iron are much higher in heme iron. One of the best sources is red meat. As we discussed in our previous post on B12 injections, plant foods do not contain B12. Consequently, strict vegans and vegetarians who do not eat any fish or shellfish are at increased risk of B12 deficiency, as well as iron deficiency.

Because iron status is such a large subject on its own, we will continue the iron discussion in a future post with information on iron overload, non-anemia iron deficiency and hereditary hemochromatosis. Now that we’ve covered some of the common markers, let’s emphasize focusing on root-cause diagnosis before putting it all together with some anemia patterns.

What’s the root cause?

As we have seen in many other cases, it’s critical to correctly identify the underlying root cause of anemia. For example, just within the category of iron deficiency anemia, it is important to identify if a person is anemic because of a yet undaignosed H. pylori infection, or the anemia could be secondary to heavy menses that are depleting iron. These are just two of many possible root causes of iron deficiency.

Lab testing to order

The markers we talked about earlier like RBCs, HCT, MCV, MCH, MCHC and RDW are all part of a standard CBC. That is a great starting point. Other important markers to consider are iron status markers like ferritin, serum iron, UIBC, and transferrin saturation if iron deficiency anemia is suspected. We will go into these more in our upcoming post on iron. If, on the other hand megaloblastic anemia is suspected, markers of B12 and folate status are important (such as serum B12, serum folate, RBC folate, homocysteine, Methylmalonic Acid (MMA), and possibly holotranscobalamin if available in your area. Pernicious anemia can be confirmed with a positive intrinsic factor antibody in cases of suspected pernicious anemia.

Getting started

Start with the RBC breakdown on the CBC to determine whether the anemia is micro-, normo- or macrocytic and hypo-, normo- or hyperchromic. Once you’ve identified the type, look at possible underlying causes and order further testing as appropriate, whether it’s a SIBO breath test, an iron panel, inflammatory cytokines or MMA and folate. Getting a serum B12, homocysteine, and ferritin value are also standard orders for nearly every patient in our clinic (on top of a CBC with differential).

If you are vegan or strictly vegetarian, you may need to supplement with vitamin B12, iron, zinc, and possibly other trace minerals (best to check and confirm deficiencies as excessive amounts of some nutrients like iron or zinc can be toxic. B12 is generally considered to be safe with low chances for toxicity even with excessive doses). Some people decide to become vegetarian or vegan for health reasons. While there are conditions that can improve from various diets, vegetarian and vegan diets included, there are times when the health benefits can be exaggerated or the negative health impacts can be ignored. An example is the “What the Health” documentary. This movie has been the subject of several of our patients who have inquired about whether they should be eliminating animal products from their diet.

Unfortunately, this movie does a great job of touching into peoples emotions, but is very poor in citing any well-done, peer-reviewed research (although some people watching it think that it must be valid evidence). It is our professional opinion that the research cited in this movie is of poor quality and that the perspective was biased without considering both sides of the issue. We do not generally recommend vegetarian or vegan diets for health reasons in most cases. However, we completely understand ethical / religious reasons for choosing these kinds of diets and support clients who consciously choose these kinds of diets with recommendations for how to avoid nutrient deficiencies (especially by supplementing with some of the nutrients listed above and choosing certain foods that are rich in nutrients that are commonly deficient). For pescatarians (or vegetarians that are comfortable eating things that do not have faces), clams are a fantastic source of vitamin B12 and iron (plus other minerals). Oysters are the highest source of zinc. Just one or two servings of clams per week can correct some of the nutrient deficiencies that are common in vegetarians / vegans who are willing to eat shellfish.

If you struggle with some or all of:

  • Fatigue
  • Weakness
  • Dizziness
  • Pale skin

Plus you have some of the risk factors like:

  • Vegan diet
  • Excessive bleeding
  • Gastrointestinal (gut) infections
  • Extreme exercise

It is worth getting lab testing from a functional medicine doctor who can assess for functional ranges and help identify the root cause(s) behind anemia or other conditions that can also cause some of the same kinds of symptoms.

Check back soon for our future posts which will expand this information. We’ll get more detailed about iron markers and other anemia patterns.

References

  1. National Institute on Health. “Anemia: Symptoms – National Library of Medicine – PubMed Health.” National Center for Biotechnology Information, U.S. National Library of Medicine, www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022311/.
  2. Tortora GJ. and Grabowski SR. (1993) Principles of Anatomy and Physiology. Harper Collins College Publishers.
  3. Pawlak R, Lester SE, Babatunde T. The prevalence of cobalamin deficiency among vegetarians assessed by serum vitamin B12: a review of literature. Eur J Clin Nutr. 2014;68(5):541-8.
  4. Ciacci C, Sabbatini F, Cavallaro R, et al. Helicobacter pylori impairs iron absorption in infected individuals. Dig Liver Dis. 2004;36(7):455-60.
  5. Saboor M, Zehra A, Qamar K, Moinuddin. Disorders associated with malabsorption of iron: A critical review. Pakistan Journal of Medical Sciences. 2015;31(6):1549-1553. doi:10.12669/pjms.316.8125.
  6. Moschonis G, Papandreou D, Mavrogianni C, et al. Association of Iron Depletion with Menstruation and Dietary Intake Indices in Pubertal Girls: The Healthy Growth Study. BioMed Research International. 2013;2013:423263. doi:10.1155/2013/423263.
  7. Watanabe F, Katsura H, Takenaka S, et al. Pseudovitamin B(12) is the predominant cobamide of an algal health food, spirulina tablets. J Agric Food Chem. 1999;47(11):4736-41.
  8. Dukowicz AC, Lacy BE, Levine GM. Small Intestinal Bacterial Overgrowth: A Comprehensive Review. Gastroenterology & Hepatology. 2007;3(2):112-122.
  9. Nemeth E, Rivera S, Gabayan V, et al. IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. Journal of Clinical Investigation. 2004;113(9):1271-1276. doi:10.1172/JCI200420945.
  10. Dhaliwal G, Cornett PA, Tierney LM. Hemolytic anemia. Am Fam Physician. 2004;69(11):2599-606.
  11. Dubert M, Elion J, Tolo A, et al. Degree of anemia, indirect markers of hemolysis, and vascular complications of sickle cell disease in Africa. Blood. 2017;130(20):2215-2223.
  12. Wu CJ, Krishnamurti L, Kutok JL, et al. Evidence for ineffective erythropoiesis in severe sickle cell disease. Blood. 2005;106(10):3639-3645. doi:10.1182/blood-2005-04-1376.
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