The Relationship Between Vitamin D And Breast Cancer

The Relationship Between Vitamin D And Breast Cancer

Vitamin D is a fat-soluble secosteroids.  There are two main forms of vitamin D: vitamin D2, also called ergocalciferol, and vitamin D3, also called cholecalciferol.  Scientific studies suggest that cholecalciferol is the more effective form of the vitamin.  Vitamin D2 is obtained exclusively from the diet and comes mostly from fortified foods and plants like mushrooms grown in UV lights.  Vitamin D3 is found in animal foods like oily fish and fish oil, liver, egg yolks and butter.  Our skin also manufactures vitamin D3 upon exposure to light. 

The Primary Types of Vitamin D and How They Interact With The Body

Specifically, vitamin D3 originates from a compound found in the skin called 7-dihydroxycholesterol when exposed to sunlight, particularly UV-B light.  Vitamin D production is complex and involves metabolic processes that take place in the liver and the kidneys.  In the liver, vitamin D2 and D3 undergo hydroxylation in the presence of mitochondrial and microsomal hydroxylase producing 25-hydroxyvitamin D (25(OH)D), also referred to as calcidiol.  This is further metabolized in the kidneys to produce calcitriol (1,25(OH)2D).  To determine the amount of serum vitamin D, one measures 25(OH)D biomarker with a half-life of around 2 to 3 weeks.

Vitamin D plays an important role in bone health, calcium homeostasis and the immune system as well as the cardiovascular and endocrine systems.  Vitamin D deficiency is also associated with type-2 diabetes, Alzheimer’s disease, osteoporosis, Parkinson’s disease, and cancer.  Recent studies have shown that at least 20 types of cancers are associated with low serum vitamin D.  

Vitamin D and The Mammary Glands

A recent review aimed at studying the connection between vitamin D deficiency and breast cancer revealed a correlation between increased breast cancer risk and vitamin D receptor genetic polymorphism (VDR).  VDR genes regulate hormone differentiation, milk production, and calcium transport during lactation in the mammary glands.  Data from two randomized clinical trials show that women with higher concentrations of vitamin D (>60 ng/ml) had 82% lower incidence rate of breast cancer than women with lower concentrations of vitamin D (<20 ng/ml).  A comparison with the healthy controls indicated a significant risk of breast cancer to women with vitamin D levels less than 20ng/ml developed metastases, and 73% died due to the advanced illness.

Reference

Atoum M, Alzoughool F. Vitamin d and breast cancer: latest evidence and future steps. Breast Cancer (Auckl). 2017 Jan;11:117822341774981.

Folate, Vitamin B12, Vitamin B6, Choline

  1. What is the significance of each of your four vitamins? What roles do they play in the body? What bodily systems are affected? 
  2. What is the RDA level for each of the vitamins? What is the upper limit for each of the vitamins? What are the signs or symptoms of deficiency and toxicity for each of the vitamins? 
  3. Where are these vitamins found in the diet and what may impede availability and absorption? How does the concept of food poverty impact a client’s ability to obtain these vitamins? (For more information on food poverty, click this link Sustain.  
Is Obesity a Disease?

Is Obesity a Disease?

The scientific community is still in disagreement as to whether or not obesity is a disease. While some still consider obesity a self-inflicted disease caused by poor eating habits and lack of exercise, there is growing evidence to support the claim that obesity is a disease. 

According to Pi-Sunyer (2002), not only is obesity a disease but within the United States it is considered to be a condition of epidemic proportions. Statistics show that, in our country, over 20% of adults are diagnosed as clinically obese (Pi-Sunyer, 2002).  The rationale that obesity is a disease is due to the fact that it causes many different comorbidities such as high blood pressure, diabetes, heart disease, etc. 

Has Obseity Reached Epidemic Proportions In Western Countries?

I agree with Conway and Rene (2004) who believe that obesity is not only a condition that has reached epidemic proportions, but it is a disabling, multifaceted disease that causes changes in organ function and can come with a host of comorbidities. The excess body weight puts a strain on the heart, leading to changes in anatomical structure and the function of the organ. Obesity has also repercussions on the immune system (de Heredia et al., 2012), endocrine system (Poddar et al., 2017), and pulmonary system (Dixon & Peters, 2018). These repercussions are caused by both mechanical and functional alteration of tissues and organs. 

Data Suggests That Obseity Is Associated With Several Very Serious Health Concerns

Research studies show that obesity is associated with an increased risk of developing cancer in at least 13 different organs (Avgerinos et al., 2019). Obesity is also linked to type-2 diabetes (Maggio & Pi-Sunyer, 2003), arthritis (Moroni et al., 2020). At the same time, a systematic review of scientific data that was published in 2017 shows that weight-loss interventions in the obese adult population decrease all-cause mortality (Ma et al., 2017). The same review shows that weight loss has a positive impact on cardiovascular mortality and cancer mortality (Ma et al., 2017). 

Lastly, obesity’s status and acceptance as a disease are pivotal in determining its treatment, reimbursement for treatment, and the development of widespread interventions. For these reasons, I believe that obesity should be recognized as a disease.

References

Avgerinos, K. I., Spyrou, N., Mantzoros, C. S., & Dalamaga, M. (2019). Obesity and cancer risk: Emerging biological mechanisms and perspectives. Metabolism: clinical and experimental, 92, 121–135. https://doi.org/10.1016/j.metabol.2018.11.001

Conway, B., & Rene, A. (2004). Obesity as a disease: no lightweight matter. Obesity Reviews, 5(3), 145–151. https://doi.org/10.1111/j.1467-789x.2004.00144.x 

de Heredia, F. P., Gómez-Martínez, S., & Marcos, A. (2012). Obesity, inflammation and the immune system. The Proceedings of the Nutrition Society, 71(2), 332–338. https://doi.org/10.1017/S0029665112000092

Dixon, A. E., & Peters, U. (2018). The effect of obesity on lung function. Expert review of respiratory medicine, 12(9), 755–767. https://doi.org/10.1080/17476348.2018.1506331

Ma, C., Avenell, A., Bolland, M., Hudson, J., Stewart, F., Robertson, C., Sharma, P., Fraser, C., & MacLennan, G. (2017). Effects of weight loss interventions for adults who are obese on mortality, cardiovascular disease, and cancer: systematic review and meta-analysis. BMJ (Clinical research ed.), 359, j4849. https://doi.org/10.1136/bmj.j4849

Maggio, C. A., & Pi-Sunyer, F. X. (2003). Obesity and type 2 diabetes. Endocrinology and metabolism clinics of North America, 32(4), 805–viii. https://doi.org/10.1016/s0889-8529(03)00071-9

Moroni, L., Farina, N., & Dagna, L. (2020). Obesity and its role in the management of rheumatoid and psoriatic arthritis. Clinical rheumatology, 39(4), 1039–1047. https://doi.org/10.1007/s10067-020-04963-2

Pi-Sunyer, F. X. (2002). The obesity epidemic: Pathophysiology and consequences of obesity. Obesity Research, 10(S12), 97S-104S. https://doi.org/10.1038/oby.2002.202

Poddar, M., Chetty, Y., & Chetty, V. T. (2017). How does obesity affect the endocrine system? A narrative review. Clinical obesity, 7(3), 136–144. https://doi.org/10.1111/cob.12184

The Four Primary Types Of Gluten Related Disorders

The Four Primary Types Of Gluten Related Disorders

Gluten is a family of storage proteins found in wheat, rye, triticale, and barley. In predisposed individuals, ingestion of gluten causes disease reactions that are grouped under the term gluten-related disorders (GRD). Only a decade ago, GRD were rare in the United States, but the rate of gluten-related disorders has greatly increased since then. It is now estimated that GRD affect close to 10% of the population (Sapone et al., 2012). 

There are five kinds of gluten-related disorders recognized by the medical community. Each disorder presents with unique pathophysiology and etiology. Celiac disease, dermatitis herpetiformis, and gluten ataxia are autoimmune conditions; wheat allergy is an allergic disease (Taraghikhah et al., 2020), and non-celiac gluten sensitivity is a non-autoimmune-allergic disease (Sharma et al, 2020).   

Celiac Disease and Gluten

Celiac disease (CD) is a chronic, auto-immune condition that affects genetically predisposed individuals. It is thought that genetically predisposed individuals develop an immune response to unknown environmental factors which is then triggered by the ingestion of gluten (Lebwohl et al., 2018). CD can cause atrophy of the small intestinal villi, which leads to malabsorption, diarrhea, and failure to thrive. But manifestations of CD can also be minimal, like negligible mucosal lesions, or it can have an asymptomatic presentation, which often causes delayed diagnosis. Celiac disease can also present with extraintestinal manifestations ranging from neurologic disorders, psychiatric disorders, infertility, recurrent miscarriages, osteoporosis and osteopenia, arthritis, aphthous stomatitis (a disease my mother suffers from), dental enamel hypoplasia, and elevations in transaminases (Barker & Liu, 2008). 

Dermatitis Herpetiformis and Gluten

Dermatitis Herpetiformis (DH), also known as Duhring-Brocq disease, is an auto-immune condition that affects the skin and causes chronic blistering and lesions. The lesions and blisters generally cover the areas of the scalp, knees, elbows, ankles, and buttocks, producing intense burning and itching. The skin of people affected by DH presents with the same protein IgA1 with J chain and secretory component found in the small intestinal mucosa in adult celiac disease, suggesting a strong correlation between the two conditions (Cohen et al., 1997). For this reason, DH is also called the “celiac disease of the skin”, and the European Society for Pediatric Gastroenterology, Hepatology and Nutrition now states that a dermatitis herpetiformis diagnosis confirms the celiac disease diagnosis without the need for intestinal biopsy. People affected by DH can suffer from various degrees of gastrointestinal issues that vary from milk lesions of the mucosal lining of the small intestine to villous atrophy (Mendez et al., 2013).

Gluten Ataxia as an Autoimmune

Gluten ataxia (GA) is an autoimmune disease triggered by the ingestion of gluten that affects primarily the cerebellum, the part of the brain responsible for coordination and movement. The cerebellum is also responsible for balance, eye movement, and the kind of motor learning abilities involved in learning movements that require practice and fine-tuning, for example, riding a bike or playing an instrument (Leopold, 2018). In GA, the immune system creates antibodies that attack and destroy the Purkinje cells, causing problems with vision and fine motor skills, gait abnormalities, and balance issues. It can also cause peripheral neuropathy, also known as gluten neuropathy (Hadjivassiliou et al., 2004). The damage to the Purkinje cells is irreversible, and studies involving brain MRIs show that up to 60% of subjects affected by GA suffer from permanent shrinkage of the cerebellum (Sapone et al., 2012).

Wheat Allergies and Gluten

Wheat allergy (WA) is an allergic reaction to gluten in which the immune system produces immunoglobulin E antibodies in response to wheat proteins. It can present with gastrointestinal symptoms similar to celiac disease, but unlike CD, WA has a fast onset. When inhaled (baker’s asthma), WA can cause asthma and rhinitis. When someone affected by WA touches wheat, skin reactions occur. When ingested, wheat causes gastrointestinal pain, diarrhea, malabsorption, and, if untreated, it can lead to failure to thrive. WA can also cause anaphylactic shock, but it does not cause villi atrophy (Elli et al., 2015).

Gluten Sensitivity

Non-celiac gluten sensitivity (NCGS) is a non-autoimmune-allergic disease that presents with gastrointestinal and/or extraintestinal symptoms similar to the ones seen in CD (altered bowel habits, skin rashes, bone pain, headaches, fatigue, and depression). Laboratory testing shows no serum antibodies, and intestinal biopsies do not show villous atrophy. This lack of biomarkers makes NCGS difficult to diagnose, and it also can lead to misdiagnosis. NCGS can be misdiagnosed as IBS, and oftentimes only a strict elimination diet allows for a conclusive diagnosis (Biesiekierski et al., 2011). Molina-Infante et al. (2014) estimate that the prevalence of NCGS is 6 to 10 times higher than CD and WA and that it is more prevalent in family members of CD sufferers. 

References

Barker, J. M., & Liu, E. (2008). Celiac disease: pathophysiology, clinical manifestations, and associated autoimmune conditions. Advances in pediatrics, 55, 349–365. https://doi.org/10.1016/j.yapd.2008.07.001

Biesiekierski, J. R., Newnham, E. D., Irving, P. M., Barrett, J. S., Haines, M., Doecke, J. D., Shepherd, S. J., Muir, J. G., & Gibson, P. R. (2011). Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. The American journal of gastroenterology, 106(3), 508–515. https://doi.org/10.1038/ajg.2010.487

Cohen LM, Skopicki DK, Harrist TJ, Clark WHJ. Elder D, Elenitsas R, Jarsorsky C, Johnson BJ. Lever’s Histopathology of the Skin. 8. Raven: Lippincott; 1997. Noninfectious Vesiculobullous and Vesiculopustular Diseases; pp. 209–252.

Elli, L., Branchi, F., Tomba, C., Villalta, D., Norsa, L., Ferretti, F., Roncoroni, L., & Bardella, M. T. (2015). Diagnosis of gluten related disorders: Celiac disease, wheat allergy and non-celiac gluten sensitivity. World journal of gastroenterology, 21(23), 7110–7119. https://doi.org/10.3748/wjg.v21.i23.7110

Hadjivassiliou, M., Williamson, C. A., & Woodroofe, N. (2004). The immunology of gluten sensitivity: beyond the gut. Trends in Immunology, 25(11), 578–582. https://doi.org/10.1016/j.it.2004.08.011

Lebwohl, B., Sanders, D. S., & Green, P. (2018). Coeliac disease. Lancet (London, England), 391(10115), 70–81. https://doi.org/10.1016/S0140-6736(17)31796-8

Leopold, C. (2018, August 31). Everything you need to know about the cerebellum. Medical News. https://www.medicalnewstoday.com/articles/313265#function 

Mendes, F. B., Hissa-Elian, A., Abreu, M. A., & Gonçalves, V. S. (2013). Review: dermatitis herpetiformis. Anais brasileiros de dermatologia, 88(4), 594–599. https://doi.org/10.1590/abd1806-4841.20131775

Molina-Infante, J., Santolaria, S., Montoro, M., Esteve, M., & Fernández-Bañares, F. (2014). Sensibilidad al gluten no celiaca: una revisión crítica de la evidencia actual [Non-celiac gluten sensitivity: a critical review of current evidence]. Gastroenterologia y hepatologia, 37(6), 362–371. https://doi.org/10.1016/j.gastrohep.2014.01.005

Sapone, A., Bai, J. C., Ciacci, C., Dolinsek, J., Green, P. H., Hadjivassiliou, M., Kaukinen, K., Rostami, K., Sanders, D. S., Schumann, M., Ullrich, R., Villalta, D., Volta, U., Catassi, C., & Fasano, A. (2012). Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC medicine, 10, 13. https://doi.org/10.1186/1741-7015-10-13

Sharma, N., Bhatia, S., Chunduri, V., Kaur, S., Sharma, S., Kapoor, P., Kumari, A., & Garg, M. (2020). Pathogenesis of Celiac Disease and Other Gluten Related Disorders in Wheat and Strategies for Mitigating Them. Frontiers in Nutrition, 7. https://doi.org/10.3389/fnut.2020.00006

Taraghikhah, N., Ashtari, S., Asri, N., Shahbazkhani, B., Al-Dulaimi, D., Rostami-Nejad, M., Rezaei-Tavirani, M., Razzaghi, M. R., & Zali, M. R. (2020). An updated overview of spectrum of gluten-related disorders: clinical and diagnostic aspects. BMC Gastroenterology, 20(1). https://doi.org/10.1186/s12876-020-01390-0

Food Consumption And Body Metabolism

Food Consumption And Body Metabolism

Our total daily energy expenditure (TDEE) is dictated by three factors: resting metabolic rate (RMR), which is the number of calories our body needs to perform metabolic functions when it is at rest; the number of calories burnt through physical activity, non-exercise activity thermogenesis (NEAT), and exercise; and the number of calories needed to digest and absorb food.  This is called diet-induced thermogenesis (DIT) or thermal effect of feeding (TEF).

Total daily energy expenditure varies from individual to individual and across age, sex, total body weight, physical activity, percentage of fat free mass (FFM), also called lean body mass, versus fat mass (FM), as well as hormones; all play a role in TDEE.  In general, RMR accounts for 60% of TDEE, physical activity account for 25-35% of TDEE, and DIT accounts for 5-15% of total energy expenditure. 

How Is Food Converted Into Usable Energy?

The foods and beverages that we consume are combined with oxygen and converted into energy in the form of ATP.  They also provide the building blocks used to make hormones and enzymes to grow and repair tissue as well as many other processes.  When we eat, digest and assimilate food we burn calories.  Diet-induced thermogenesis begins immediately after we eat and can last several hours, depending on the macronutrient composition of the meal.  The word thermogenesis comes from the Greek θερμός (thermos) and γένεση (genesis), and it means the creation of heat.  Not only does DIT create heat during food digestion and absorption, but it also (by a mechanism still not completely understood) activates the sympathetic nervous system which causes the body to produce heat in brown adipose tissue (BAT).  BAT is only stimulated by cold temperatures (shivering) and food consumption.  

What Exactly Is A Calorie?

A calorie is a unit of energy.  It would be simple to think that a calorie is a calorie and that, therefore, 100 calories of steak are the same as 100 calories of brownies, or butter, or broccoli.  But different macronutrients require different amounts of ATP to be metabolized and stored. This is why different macronutrients have different thermogenic effects, and DIT can vary greatly depending on the macronutrient composition of our diet.  

    Protein and alcohol have the highest thermic effects.  The DIT for protein is calculated to be between 20 to 30%; the DIT of alcohol is between 10 and 30%.  The thermic effect of carbohydrates is between 5 and 10%, and fat has the lowest reported DIT: 0 to 3%.  This means that given the same number of calories, meals rich in protein, fat, carbohydrate, or alcohol have different effect on energy expenditure.  

Studies show that postprandial thermogenesis in healthy subjects is increased 100% on a high-protein/low-fat diet versus a high-carbohydrate/low-fat carbohydrate diet.  In addition, compared to fats and carbohydrates, protein consumption also provides increased satiety.  Satiety scores were higher during high protein/high carbohydrate meals versus high fat meals. For these reasons, high protein diets are favored for weight loss as well as for weight maintenance. 

How Does Food Effect Metabolism?

When researching the effects of food on metabolism, the next logical question to address is the following: would eating many smaller meals burn more calories than eating one to two larger meals in a 24-hour period?  I found contradicting studies when reviewing the literature.  Some studies showed that nibbling throughout the day caused a greater caloric expenditure, while other studies showed that consuming larger meals was linked to greater caloric expenditure.  It seems that when it comes to meal frequency and metabolism the jury is still out.

There are other nutrients that stimulate metabolism and cause thermogenesis without contributing any calories.  These nutrients are caffeine, capsaicin, and cold water.  Caffeine is an alkaloid found in coffee beans, tea leaves, and cocoa beans.  It is a stimulant and studies show that a cup of coffee can boost metabolism by 3-11%.  A study also showed that caffeine may affect lean people more than overweight people as fat burning in lean women increased by 29% with caffeine consumption but obese women registered an increase of only 10%.  Capsaicin is a compound found in chili peppers that stimulates metabolism and helps reduce energy intake.  Finally, consuming water increases metabolism by 10-30% for about an hour.  Cold water may promote an even greater caloric expenditure, as the body uses extra energy to raise the water temperature to body temperature. 

References:

Raben A, Agerholm-Larsen L, Flint A, Holst JJ, Astrup A. Meals with similar energy densities but rich in protein, fat, carbohydrate, or alcohol have different effects on energy expenditure and substrate metabolism but not on appetite and energy intake. Am J Clin Nutr. 2003 Jan;77(1):91–100.

Westerterp-Plantenga MS, Rolland V, Wilson SA, Westerterp KR. Satiety related to 24 h diet-induced thermogenesis during high protein/carbohydrate vs high fat diets measured in a respiration chamber. Eur J Clin Nutr. 1999 Jun;53(6):495–502.

Acheson KJ: Influence of autonomic nervous system on nutrient-induced thermogenesis in humans. Nutrition. 1993, 9 (4): 373-80.


Hermsdorff HHM, Volp ACP, Bressan J. [Macronutrient profile affects diet-induced thermogenesis and energy intake]. Arch Latinoam Nutr. 2007 Mar;57(1):33–42.

Jequier E. Thermogenic responses induced by nutrients in man: their importance in energy balance regulation. Experientia Suppl. 1983;44:26–44.

Scott CB, Devore R. Diet-induced thermogenesis: variations among three isocaloric meal-replacement shakes. Nutrition. 2005 Jul 1;21(7):874–7.

Nutrition For Female Marathon Runners

Nutrition For Female Marathon Runners

There is no one-size-fits-all in nutrition, and nutrient requirements vary based on age, sex, physical activity, and even illness.  As nutritionists, we need to ensure that our plans meet our client’s unique individuality, as well as their goals. 

Case Example Of a Young Female Marathon Runner

In this case, my 25-year-old marathon runner’s goal is to improve performance and feel her best during each race.  She needs recommendations for what to consumer before, during, and after her races to ensure performance as well as recovery.  A female athlete’s nutritional needs are quite different from those of male athletes: factors that come into play include bone density, as well as differences in caloric consumption and expenditure.  While both male and female athlete require more dietary protein than the average couch potato, the maximal increase is about 100% for male athletes and 50-60% for female athletes.  Proteins are essential for the marathon runner. 

Foods For Faster Recovery

They promote faster recovery after training and race, facilitating muscle growth and repair.  Protein also are needed in the synthesis of new structures, red blood cell development, and antibody production. When glycogen stores are low, the protein stores provide about 15% of the needed energy during muscle activity.  Those who lack protein are at an increased risk of injury, fatigue, and decreased muscle mass, all factors that hinder performance.  My client’s diet plan will include: organic eggs, wild-caught fish, pastured chicken and grass-fed meat, peanut butter and other nuts, if tolerated. 

Carbohydrates and Fats For High Performance Runners

Fats should also be a vital inclusion in marathon runners’ nutritional plan.  Fats are more calorie-dense, providing 9 calories per gram compared to the 4 calories per gram provided by protein and carbohydrates.  Additionally, fats are essential for the transportation of fat-soluble vitamins, for hormone production, brain function, and satiety.  A low-fat diet in athletes can limit athletic performance causing earlier onset fatigue during a race. Sources of fats include coconut oil, extra virgin olive oil and olives, butter and ghee, dairy, avocado, and if tolerated dairy.  

Carbohydrates are important for providing energy during the races.  The runner should be able to consume and maintain optimum carbohydrate intake.  This will help prevent hypoglycemia during the races, maintain the intensity of training, strengthen the immune system, and facilitate post-recovery.  If this client does not consume enough carbohydrates, she will not be able to endure and perform effectively due to increased glucose depletion.  Before a marathon, the total caloric intake should also be increased, including the carbohydrate calories, to achieve an effective carbohydrate-caloric loading effect. 

What Is The General Nutritional Advice Given To Marathon Runners?

The general advice given to marathon runners is to consume fruit juice, honey, molasses, whole-grains, cereals, rice and pasta, starchy carbohydrates and legumes, as well as fruit and high-carbohydrate dairy products such as yogurt.  About 60 to 70% of the calories should be from carbs. Before the race, only quick sources of energy should be consumed because they are absorbed faster.  During the race, she should increase the rate of carbohydrate intake by one gram per minute by consuming carbohydrate-containing drinks.  These drinks should be consumed at regular intervals during the race, and oftentimes an alarm can help keep track.  Additionally, consumption of carbohydrates with high glycemic index such as honey can help during the marathons.  After the races, the goal is to replace the depleted energy stores and fluids.  Attention should also be directed to muscle repair and recovery; hence, micronutrients and proteins will be essential.  Fast recovery is important so that the body can be ready to get back to training.  Carbohydrates will help restore glycogen stores; protein will help with muscle repair and recovery, and electrolytes will help in re-hydrating.  

Every Athlete Has Unique Nutritional Requirements

While the general advice has been used in sports nutrition for decades, I like to use a more individual approach with my athletes.  In my work, I have found that using a continuous glucose monitor is paramount to study each individual athlete’s response to carbohydrates and glucose.  Too much or too little glucose can be detrimental to athletic performance leading up to and during an event. Glucose levels are complex and many factors can influence them.  Plus, every athlete has unique fueling requirements. A continuous glucose monitor is my preferred tool when working with athletes.  For this reason, I will recommend that this client use this tool to learn how her body responds to different carbohydrates.  This will help us find the perfect nutrition for performance.  Athletes usually begin glucose loading 3 days before a race.  Knowing how her body responds to different foods will allow this client to eat meals that provide a stable and sustainable glucose rise and that will keep her in optimal fuel range. 

Hydration is extremely important. Before and during a marathon, my client will make sure to keep well hydrated.  I recommend electrolyte supplements, mineral-rich water, and coconut water.  

Other factors to consider are vitamins and minerals.  Calcium, for example, is an essential mineral needed for bone growth, density, and prevention of bone loss and fractures.  Consumption of calcium-rich foods help maintain strong bones that can endure the intensity of the races.  Therefore, this client should consume foods rich in calcium like dairy products, green leafy vegetables, spinach, and broccoli. 

B Vitamins And The Health Of Female Athletes

Vitamins are essential nutritional components for the marathon runner.  The most important vitamins are vitamin D and B complex vitamins.  The body needs vitamin D to metabolize calcium.  Vitamin D is necessary for a healthy immune system and hormone production. Therefore, I will advise my client to include fatty fish in her diet and supplement with vitamin D3 if needed.  Vitamin B6, B12, and Folate are also important.  For example, vitamin B12 and folate are essential for red blood cell development, protein synthesis, and tissue repair.  These are important in improving the oxygen-carrying capacity and building endurance during long races. 

My client will begin adopting her new dietary plan during training so that she can get used to the changes and, if needed, we can modify the plan according to her needs well before the race.  

References


Tarnopolsky MA. Gender differences in metabolism; nutrition and supplements. J Sci Med Sport. 2000 Sep;3(3):287–98.

Burke, L. M., Jeukendrup, A. E., Jones, A. M., & Mooses, M. (2019). Contemporary Nutrition Strategies to Optimize Performance in Distance Runners and Race Walkers. International journal of sport nutrition and exercise metabolism, 29(2), 117–129. 

Costa, R., Knechtle, B., Tarnopolsky, M., & Hoffman, M. D. (2019). Nutrition for Ultramarathon Running: Trail, Track, and Road. International journal of sport nutrition and exercise metabolism, 29(2), 130–140. 

Smith-Ryan, A. E., Hirsch, K. R., Saylor, H. E., Gould, L. M., & Blue, M. (2020). Nutritional Considerations and Strategies to Facilitate Injury Recovery and Rehabilitation. Journal of athletic training, 55(9), 918–930. 

Thomas, D. T., Erdman, K. A., & Burke, L. M. (2016). American College of Sports Medicine Joint Position Statement. Nutrition and Athletic Performance. Medicine and science in sports and exercise, 48(3), 543–568. 

Fibromyalgia: Conventional Treatments & Functional Medicine

Fibromyalgia: Conventional Treatments & Functional Medicine

Differences Between Conventional Medicine and Functional Medicine 

  Fibromyalgia is a syndrome that affects between 2% and 8% of the population (Clauw D. J., 2014). It is more prevalent in women than in men, and it presents with chronic pain that affects the musculoskeletal system, fatigue, sleep problems, mood disorders, memory issues and other symptoms (Bair & Krebs, 2020). Fibromyalgia is not an illness with objective markers, and its diagnosis is usually made by studying a patient’s history and symptoms and then excluding other diseases that cause chronic widespread pain (Häuser, 2016). According to Galvez-Sánchez & Reyes Del Paso (2020) this has historically created problems in the diagnosis, management, treatment, and even social recognition of the disease. Old diagnosing guidelines called for the examination of so-called tender points: these are specific points on the body that are tested for pain and/or tenderness. In order to be diagnosed with fibromyalgia, a patient had to respond positively for tenderness to 11 out of 18 points. This was an inaccurate method, as fibromyalgia symptoms change from day to day. Current diagnostic guidelines now include widespread pain on both sides of the body for a minimum of three months (Fibromyalgia: Understand How It’s Diagnosed, 2020). After diagnosis, the patient is generally referred to a specialist in rheumatology for further treatment. 

What Does The Data Reveal?

 A study published in 2005 in The Journal of Rheumatology concluded that fibromyalgia can manifest hand in hand with neurotransmitter and neuroendocrine dysfunction, namely, higher than normal levels of excitatory neurotransmitters (catecholamines, serotonin, acetylcholine and histamine), low levels of biogenic amines as well as imbalances of the hypothalamus-pituitary-adrenal axis (HPA) (Mease P., 2005). Despite these findings, conventional medicine does not test for those biomarkers; instead, it manages fibromyalgia with the use of antidepressants (tricyclic and selective serotonin reuptake inhibitors (SSRI)), anti-seizure medications, muscle relaxants, and nonsteroidal anti-inflammatory drugs (NSAIDS).  Other drugs prescribed include sedatives, norepinephrine/serotonin reuptake inhibitors, and experimental drugs. Exercise, acupuncture and massage are complementary alternative therapies that are often recommended in conjunction with medication (Chinn et al., 2016).    

Conventional Medicine’s Approach To Treatment

Conventional medicine has a reductionist approach to illnesses such as fibromyalgia, while functional medicine uses a holistic approach in the treatment of such conditions. It is frustrating to see such disparities. It is even more frustrating when there are numerous peer-reviewed studies that share important findings demonstrating that addressing the several underlying causes of fibromyalgia can bring this syndrome into remission. These findings have been reviewed, published and shared with the medical community, but conventional medicine is not yet using this knowledge to treat the root causes of the syndrome. The conventional medicine approach uses pharmaceutical drugs to manage symptoms;

this Band-Aid approach is not only unsustainable, it is also faulty. 

Functional Medicine’s Approach To Treatment

 Functional medicine recognizes fibromyalgia as a painful neuropathic pain syndrome that can have root causes in several systems. HPA imbalances, neurotransmitters dysfunction, endocrine issues, nutrient deficiencies, autoimmunity and stress can all play a role in fibromyalgia (Martínez-Lavín M., 2020). The functional medicine approach to treating fibromyalgia aims at finding the root causes of the disease and correcting them, while continuing to support the patient holistically through the use of targeted therapies as well as with complementary alternative therapies (CAM) like massage therapy, nutrient therapy, acupuncture, etc. (Pfalzgraf et al., 2020). 

Among the factors and conditions that are taken into consideration by functional medicine doctors when working with fibromyalgia patients are celiac disease, non-celiac gluten sensitivity, candida overgrowth, hypothyroidism, nutrient deficiencies, leaky gut and small intestine bacterial overgrowth, adrenal fatigue, mercury toxicity, and glutathione deficiency. While the research is still in its early stages, preliminary findings show that people affected by celiac disease and non-celiac gluten intolerance suffer from fatigue, musculoskeletal pain, and brain fog (Isasi et al., 2016). Several studies show that many patients affected by fibromyalgia, myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) also suffer from abdominal discomfort syndrome (ADS) and irritable bowel syndrome (IBS). A study from Maes et al. (2014) shows that the ME/CFS patients also presenting with ADS have higher than normal levels of “IgA and IgM responses to LPS or commensal bacteria” (Maes et al., 2014). Small intestine bacterial overgrowth and leaky gut are also associated with fibromyalgia. Treating the bacterial imbalance has been shown to ameliorate gastrointestinal and fibromyalgia symptoms (Logan & Beaulne, 2002).

 Hypothyroidism can cause secondary fibromyalgia (Corsalini et al., 2017); therefore, failure to test and to address thyroid function will perpetuate fibromyalgia symptoms. 

A Holistic Overview Of The Treatment OF Fibromyalgia

 The functional medicine approach also looks at nutrient status and possible deficiencies: a meta-analysis of 40 observational studies show that fibromyalgia sufferers have lower levels of vitamin D, vitamin B12, magnesium and vitamin E compared to a control group (Joustra et al., 2017) (Pagliai et al., 2020). Studies also show that they have significantly lower levels of glutathione compared to control (Shukla et al., 2020).

 The adrenal glands are our stress response system. Fibromyalgia patients are shown to have either hyper-cortisol or hypo-cortisol output, as well as HPA axis imbalances (Eller-Smith et al., 2018).

 There are other factors that are assessed by functional medicine doctors who work with fibromyalgia patients. While there I was not able to find peer reviewed studies on them, I was able to find quite a bit of anecdotal evidence online. According to Dr. Amy Myers, MD, factors to consider are exposure to mold, mercury toxicity, and MTHFR gene mutations. 

 Lastly, functional medicine also focuses on the mind-body connection when treating fibromyalgia: a systematic review of the Cochrane Central Register of Controlled Trials shows that mind-body therapy is effective in improving quality of life, pain management, and mood issues in fibromyalgia sufferers. Mind-body therapy uses techniques such as biofeedback, mindfulness, relaxation and movement therapy (Theadom et al., 2015). 

References:

Bair, M. J., & Krebs, E. E. (2020). Fibromyalgia. Annals of internal medicine, 172(5), ITC33–ITC48. https://doi.org/10.7326/AITC202003030

Chinn, S., Caldwell, W., & Gritsenko, K. (2016). Fibromyalgia Pathogenesis and Treatment Options Update. Current pain and headache reports, 20(4), 25. https://doi.org/10.1007/s11916-016-0556-x

Clauw D. J. (2014). Fibromyalgia: a clinical review. JAMA, 311(15), 1547–1555. https://doi.org/10.1001/jama.2014.3266

Corsalini, M., Daniela, D. V., Biagio, R., Gianluca, S., Alessandra, L., & Francesco, P. (2017). Evidence of Signs and Symptoms of Craniomandibular Disorders in Fibromyalgia Patients. The open dentistry journal, 11, 91–98. https://doi.org/10.2174/1874210601711010091

Eller-Smith, O. C., Nicol, A. L., & Christianson, J. A. (2018). Potential Mechanisms Underlying Centralized Pain and Emerging Therapeutic Interventions. Frontiers in cellular neuroscience, 12, 35. https://doi.org/10.3389/fncel.2018.00035

Fibromyalgia: Understand how it’s diagnosed. (2020, September 18). Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/fibromyalgia/in-depth/fibromyalgia-symptoms/art-20045401

Galvez-Sánchez, C. M., & Reyes Del Paso, G. A. (2020). Diagnostic Criteria for Fibromyalgia: Critical Review and Future Perspectives. Journal of clinical medicine, 9(4), 1219. https://doi.org/10.3390/jcm9041219

Häuser W. (2016). Fibromyalgiesyndrom Basiswissen, Diagnostik und Therapie [Fibromyalgia syndrome: Basic knowledge, diagnosis and treatment]. Medizinische Monatsschrift fur Pharmazeuten, 39(12), 504–511.

Isasi, C., Tejerina, E., & Morán, L. M. (2016). Non-celiac gluten sensitivity and rheumatic diseases. Reumatologia clinica, 12(1), 4–10. https://doi.org/10.1016/j.reuma.2015.03.001

Joustra, M. L., Minovic, I., Janssens, K., Bakker, S., & Rosmalen, J. (2017). Vitamin and mineral status in chronic fatigue syndrome and fibromyalgia syndrome: A systematic review and meta-analysis. PloS one, 12(4), e0176631. https://doi.org/10.1371/journal.pone.0176631

Logan, A. C., & Beaulne, T. M. (2002). The treatment of small intestinal bacterial overgrowth with enteric-coated peppermint oil: a case report. Alternative medicine review : a journal of clinical therapeutic, 7(5), 410–417. 

Lord, R.S., & Bralley J. A. (2012) Laboratory evaluations for integrative and functional medicine. 2nd edition. Metametrix.

Maes, M., Leunis, J. C., Geffard, M., & Berk, M. (2014). Evidence for the existence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with and without abdominal discomfort (irritable bowel) syndrome. Neuro endocrinology letters, 35(6), 445–453. 

Martínez-Lavín M. (2020). Holistic Treatment of Fibromyalgia Based on Physiopathology: An Expert Opinion. Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases, 26(5), 204–207. https://doi.org/10.1097/RHU.0000000000001455

Mease P. (2005). Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. The Journal of rheumatology. Supplement, 75, 6–21. 

Pfalzgraf, A. R., Lobo, C. P., Giannetti, V., & Jones, K. D. (2020). Use of Complementary and Alternative Medicine in Fibromyalgia: Results of an Online Survey. Pain management nursing : official journal of the American Society of Pain Management Nurses, 21(6), 516–522. https://doi.org/10.1016/j.pmn.2020.07.003

Pagliai, G., Giangrandi, I., Dinu, M., Sofi, F., & Colombini, B. (2020). Nutritional Interventions in the Management of Fibromyalgia Syndrome. Nutrients, 12(9), 2525. https://doi.org/10.3390/nu12092525

Shukla, V., Kumar, D. S., Ali, M. A., Agarwal, S., & Khandpur, S. (2020). Nitric oxide, lipid peroxidation products, and antioxidants in primary fibromyalgia and correlation with disease severity. Journal of medical biochemistry, 39(2), 165–170. https://doi.org/10.2478/jomb-2019-0033

Theadom, A., Cropley, M., Smith, H. E., Feigin, V. L., & McPherson, K. (2015). Mind and body therapy for fibromyalgia. The Cochrane database of systematic reviews, 2015(4), CD001980. https://doi.org/10.1002/14651858.CD001980.pub3

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