Personal Health Update

I haven’t written about my health in quite a while because there wasn’t anything positive to share. At the end of 2014 I was feeling fairly good and started taking prerequisite science classes so I could pursue a degree in Human Nutrition. Then my health took a turn for the worse with chronic urinary tract infections that lead to a bladder ulcer. The long term antibiotics to heal the ulcer caused systemic yeast infections and SIBO (small intestine bacterial overgrowth), which significantly impacted my health and increased my fatigue. While my gut health still isn’t where it was prior to the antibiotics, I made a few changes this spring that has improved my fatigue and a few other symptoms plus allowed me to reduce doses on some medications and supplements.

I added a low dose (1000mg) of D-ribose twice a day and saw almost immediate improvements in my fatigue. D-ribose is a sugar molecule required for the production of RNA, DNA, NADH, and ATP. ATP is the major energy currency of cells and is required for proper metabolism. High doses of D-ribose (5g 2-3x a day) has been studied in patients with congestive heart failure and ME/CFS as well as in athletes for recovery from physical activity with fair results, but personal anecdotes from patients with fatigue suggested smaller doses were more effective. Due to inflammation reactions and occasionally asthma attacks from sucrose sugar, starting at a lower dose made the most sense for me. I started at 500mg once a day and over a few weeks increased to 1000mg twice a day (morning and afternoon). I tried 1500mg twice a day and 1000mg three times a day, but saw increases in my inflammation and worsening sleep quality that I didn’t get at 1000mg twice a day. Within weeks my fatigue had improved to the point where I could reduce my CoQ10/Ubiquinol dose from 400mg twice a day to 200mg twice a day and reduce my acetyl l-carnitine from 1000mg twice a day to 500mg twice a day. Within a month I also was able to eliminate Cytomel T-3 only thyroid medication completely and my thyroid hormone levels are stable on levothyroxine alone. Apparently a deficiency in ATP depresses the utilization of iodine required for thyroid hormone production so increasing my ATP production with D-ribose also improved my hypothyroidism. This explains why my hypothyroidism got so much worse when my fatigue became severe and why I had such a hard time balancing my thyroid meds since then.

I added rhodiola rosea twice a day to my treatment plan about a month before I started taking D-ribose. It’s an adaptogen that helps with oxidative stress and fatigue from psychological and physiological stressors. It seems to have helped me with heat stress this summer, though I also increased my salt intake by 1/2 a teaspoon per day added to my water, lemonade, or herbal tea. Increased salt intake has improved my tachycardia by more than 10bpm and reduced the incidents of dehydration I used to get from swimming outdoors in the summer heat.

Another big change in my routine is my eating plan. While I still follow a low carb diet, I began experimenting with intermittent fasting. First I tried 4:3 fasting, which is eating for four days a week and restricting food to no more than 500 calories three days a week. I lost 12lbs in the month I did 4:3 fasting, but it wasn’t very sustainable. I then switched to 18 hour overnight fasts with lunch as my main meal. I fast from about 7pm to 1pm the next day. I’ve lost 8lbs since I’ve been doing it and I plan to continue it. My fasting blood glucose has improved more with intermittent fasting than it did on a low carb diet alone and avoiding type 2 diabetes is a bigger long term goal for me than weight loss. Research suggests that intermittent fasting along with a low carbohydrate diet also improves mitochondrial function.

Below is my current medication/supplement treatment regime:

Myalgia/Sleep Disorders

  • Cyclobenzaprine (generic Flexeril) – 10mg/day at 7pm
  • Naltrexone, Low Dose (LDN) – 3mg/day at 11pm
  • Magnesium Oxide – 1000mg/day; 500mg at 3pm and 11pm
  • Melatonin – 250mcg/day at 11pm
  • Potassium Glutamate – 99mg as needed for leg cramps

Mitochondrial Dysautonomia & Nutrient Deficiencies

  • Acetyl L-Carnitine – 500mg 2x/day at 9am and 3pm
  • Alpha Lipoic Acid – 300mg/day; 150mg at 9am and 3pm
  • Calcium Citrate – 400mg/day at 3pm
  • CoQ10/Ubiquinol – 200mg 2x/day at 9am and 3pm
  • Coenzymated B Complex – 2x/day at 9am and 3pm
  • D-ribose – 1000mg 2x/day at 9am and 3pm
  • Probiotics – 2 tab/day at 9am and 3pm
  • Rhodiola Rosea – 100mg 2x/day at 9am and 3pm
  • Thiamine (coenzymated) – 25mg 2x/day at 7am and 11pm
  • Vitamin D3 – 2000UI/day at 3pm
  • Vitamin K2 (MK-7) – 100mg/day at 3pm

Hypothyroidism

  • Synthroid (levothyroxine) – 75mcg/day at 7am

Other Genetic Mutations (COMT)

  • L-theanine – 100mg 2x/day at 9am and 3pm

Mold/Biotoxin Illness & High Clotting Factor VII

  • Losartan – 25mg/day at 7pm
  • Aged Garlic Extract (Kyolic 100) – 600mg before meals
  • Vitamin C – 150mg/day at 7pm
  • Zinc – 15mg/day at 11pm

Allergies

  • Allertec (generic Zyrtec) – 25mg/day at 11pm
  • Guaifenesin (generic Mucinex) – 400mg 2x/day at 9am and 11pm
  • Immunotherapy vaccines (allergy shots) – every 4 weeks

Liver Issues

  • Milk Thistle – 175mg 2x/day at 9am and 11pm

Perimenopause

  • Chaste tree Vitex – 225mg/day at 11pm
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The pH Miracle: Miracle Diet or Pseudoscience?

Note: This is a critical analysis of the best selling fad diet book The pH Miracle written for one of my graduate level nutrition classes. I’ve substantially added to the paper since it was submitted. There was so much poor science literacy and pseudoscience in the book, I didn’t have space to cover it all. Even this expanded version misses a few key topics.

The pH Miracle: Miracle Diet or Pseudoscience?

Abstract

A brief overview of the diet in book The pH Miracle by Robert O Young and Shelley Redford Young along with critical examination of some of the scientific claims supporting the diet as a treatment for a multitude of health problems, including cancer. The paper concludes that Young has little knowledge of human biology or medical science and he based many of his ideas on outdated research done in the 1860’s and 1920’s before technology allowed a greater understanding of microorganisms, cell biology, and human metabolism.

Background

The pH miracle diet is an acid-ash diet popularized by a series of books by Robert O. Young and his wife.1 They also own a residential healing center in California, the pH Miracle Living Center, where they practiced the principles discussed in the book on paying clients.2 The diet is based on personal experiences, Young’s own self-published research, and his clinical practice as a Naturopathic Doctor and nutritionist. Young has an MS in nutrition (1993) and a DSc in chemistry and biology (1995) from American College, and a PhD in nutrition (1997) and a doctorate in naturopathy (1999) from Clayton College of Natural Health.2 American College in Birmingham, Alabama changed its name to Clayton College of Natural Health in 1997; all of Young’s graduate degrees were obtained from one institution.3 It was a non-accredited, distance-learning college that closed in 2010 after being in operation since 1980.3 There is great concern about the quality of the education and the degrees handed out by this institution. Young was arrested in 2014 and convicted in 2016 on two counts of practicing medicine without a license and faces up to 3 years, 8 months in prison in California.4 The jury was deadlocked on charges of grand theft; the prosecutor plans to refile charges against Young.4

Scientific Claims

Young bases the scientific principles of his diet on research done by Antoine Bechamp in the late 1800’s and his own research, which he calls New Biology, and claims it proves that cells in the body can transform into bacteria, yeasts, and molds in an acidic environment.1(18) Young calls these organisms microforms and he believes they cause all diseases.1(18) Young maintains that he has video evidence of bacilli bacteria transforming into cocci bacteria and then into yeast, and fungus, and then mold in an acidic environment and a reversal of the transformation from mold back into a bacilli bacteria in an alkaline environment.1(20) None of this is scientifically plausible and any biology course that discusses cellular structures and microbes can dispute it.5(62)

In general, the diet is built around the acid-ash hypothesis, the idea that foods that contain chlorine, iodine, phosphorus, and sulfur leave acidic ash behind during metabolism while foods that contain calcium, copper, iron, magnesium, potassium, silver, sodium, and zinc leave alkaline ash.1(65) By eliminating or reducing acid causing foods and eating alkaline foods, Young believes the pH of tissues within the body will be alkaline enough that cells can’t transform into microforms. According to Young, if the proper pH balance is achieved then all symptoms of disease will disappear.1(3) Young asserts that the symptoms of an overacidic body include fatigue, aches and pain, infections, hormone imbalances, gastrointestinal issues, mental health issues, asthma, dry skin, etc.1(16) The list encompasses more than half a page and nearly every illness, disease, or minor health problem one can imagine. Young promises that his diet, supplements, and lifestyle will cure all the health problems he lists, up to and including cancer.

Young calls the eating program involved in the pH Miracle diet COWS: Chlorophyll, Oil, Water, Salts.1(66) Chlorophyll is from green vegetables; 70-80% of an alkalizing diet should be made up of them, particularly grasses in the form of green juice, sprouts, capsules, or powdered supplements because grasses are more nutrient dense than other green vegetables as evidenced by the fact that they sustain the lives of cattle, horses, and other ruminant animals.1(69) He claims that humans only need one ounce of protein per day and that can be easily obtained by a plant based diet with soy added once or twice a month; the diet contains only 5-7% protein.1(95,138) 20-30% of the diet should be made up primarily of polyunsaturated fatty acids, a.k.a. oils.1(70,138) Young recommends cold pressed oils like grape seed, hemp seed, flax seed, and borage as well as olive oil, raw nuts, and avocados.1(70) Water seems self explanatory, but Young takes it to another level. He recommends drinking one gallon of alkaline water with a pH of at least 9.5 per day.1(122) He suggests buying his company’s water filtration, electron charging, and pH system for optimal hydration, though he discusses the cheaper options of buying bottled alkaline water from his company or sodium/potassium bicarbonate drops to increase the pH of water.1(125-126) Salt doesn’t mean sodium chloride, but encompasses mineral salts of magnesium, potassium, and calcium as well as sodium bicarbonate.1(74) He recommends adding mineral salt drops or powder to water, sprinkling mineral salts on food at every meal, and drinking alkaline water with one teaspoon to one tablespoon of sodium bicarbonate two to three times per day; again he recommends products sold by his company.1(78-79)

The diet contains minimal animal products (meat, eggs, and dairy), processed and refined foods, yeasts or vinegar, fermented foods, artificial sweeteners, sweet fruits or berries, natural or refined sugars, alcohol, coffee, chocolate, tea, soda, and most grains and legumes because they are acid causing foods.1(66) Non-starchy vegetables, grasses, sprouted grains and legumes, raw nuts, and a few fruits like lemons, limes, avocados, cucumbers, and tomatoes are considered alkaline and the diet should consist of mostly these food items along with unheated, cold pressed oils.1(66) Raw foods are also considered alkalizing while cooked foods are acidifying, so the majority of the foods eaten should be raw, lightly heated, or quickly steamed.1(82) Young asserts that the human digestive tract is not designed to digest food but to alkalize food so stem cells and red blood cells can be formed in the small intestine.1(134) He doesn’t appear to understand basic human biology on the functions of the digestive tract or the formation of red blood cells in red bone marrow.5(850,636) Young also doesn’t seem to know that enzymes in the digestive tract break down foods into their biochemical components. He believes enzymes are waste products that are released when chewing food and they are harmful, acidifying compounds that will damage healthy cells and tissue.1(55) He even warns that digestive enzymes which break down proteins/meat will break down the human body: “You are meat! It will break you down, too!”1(55) This is another reason why he recommends people avoid meat and dairy. Fermentation of any kind is bad to Young because it creates acid and is performed by bacteria or yeasts. He considers all fermentation molding and even warns that the process of ripening turns sweet fruit into alcohol and mold so it should be avoided.1(22),1(103) Young is anti-probiotics because, even though he states that the bacteria in the human gut can synthesize vitamin B12, which they can’t, he also states that there’s no such things as beneficial bacteria.1(55),1(112) According to Young, bacteria in the gut used to be healthy human cells that were transformed into bacteria and the ideal would be “clean” intestines without bacteria, yeasts, or other microforms.1(55) This is contrary to everything medical research has learned about the commensal relationship between humans and their microbiota.

Combining alkaline and acidic foods in the proper quantities is important in Young’s diet so alkaline minerals aren’t pulled out of bone and tissue in order to counteract the acidity in the food.1(13) This idea appears to be an unfounded expansion of the mineral and bone loss experienced by those with chronic kidney disease (CKD) to encompass everyone.6,7 Proper food combining should include no more than four different types of food in one meal, the majority should be alkalizing vegetables with one serving of a protein or one serving of a complex carbohydrate; acid causing proteins and carbohydrates should not be combined in one meal.1(135)

Even without Young taking the acid-ash hypothesis to extremes, there’s no convincing evidence that a diet based on acid and alkaline foods is best for health or that excessive consumption of acidic foods demineralizes bones and tissue. Meta-analysis of well-designed studies looking at the net acid excretion and calcium excretion in acid-ash diets found that, while in general there is a linear progression of greater calcium excretion with higher acid excretion in urine, there’s no evidence that the extra calcium excreted comes from bone and tissues or that a lower pH contributes to the development of osteoporosis.8 The study authors hypothesize that changes in acidity or alkalinity in the diet alters calcium absorption.8 Another meta-analysis by the same authors as the previous study found that, contrary to the acid-ash hypothesis, there’s no evidence that phosphate contributes to bone demineralization, osteoporosis, or bone calcium excretion in the urine.9 Increased phosphate consumption from supposedly acidic meats, dairy, and grains actually decreased calcium excretion in the urine and increased calcium balance within the body.9 This appears to disprove the main theory behind the acid-ash hypothesis, especially when it comes to bone health and the reason for avoidance of meat, dairy, and grains.

Testing

In order to test the alkalinity of one’s tissues, Young recommends using pH test strips on urine first thing in the morning, before breakfast, after breakfast, between breakfast and lunch, and between lunch and dinner; the ideal pH is 7.2 or higher.1(22-24) He suggests eating alkaline food or drinking water mixed with mineral salts immediately if the results are a pH of 7 or lower.1(22) While eating or drinking alkaline foods or minerals will change the pH of urine, the pH of blood and extracellular fluid is tightly maintained by the kidneys; diet doesn’t change that, though grave illnesses can.5(1006-09) What the diet, especially the mineral salts and sodium bicarbonate added to drinking water, will do is increase the pH of stomach acid, which can have serious health effects including malabsorption of vitamins and minerals and increased susceptibility to food borne illnesses and pathogenic bacteria.5(869-870)

Young also touts the live blood and dried blood analysis services he provides through his pH Miracle Living Center. By looking at blood droplets through a microscope Young claims to be able to see acid crystals, cholesterol, metals, mircoforms, molds, undigested fats, and more.1(25) The patterns in dried blood supposedly match with certain diseases such as arthritis, cancer, diabetes, and heart disease.1(26) The progenitor of live blood microscopy was a German zoologist, Giinther Enderlein, who published a report about it in 1925.10 Enderlein used a technique called darkfield microscopy to illuminate artifacts in the blood that could only be seen with oblique lighting.10 Enderlein used Bechamp’s theories from the 1860’s to label the artifacts he could see in blood and came up with an analysis system that’s still used by some alternative medicine practitioners today.10 Small studies on live blood analysis show that identifying and categorizing Enderlein artifacts in live blood is highly subjective and not very accurate.10 It doesn’t meet the standards used for diagnostic testing in the medical field. The study authors don’t think further studies on live blood analysis should be conducted until questions about biochemical and physical confounders can be answered about the artifacts observed like coagulation, osmotic changes, and blood-glass interaction.10 Currently there’s no evidence that the artifacts seen in live blood analysis aren’t normal coagulation or decomposition processes or that they’re related to identifiable diseases.

Conclusion

The real miracle in the pH Miracle is that Young was able to build a successful business around his ideas since there is little to no actual science in the book. The majority of what he calls New Biology is either unreliable, unproven, or disproved. There’s also a deep lack of understanding about human biology in the book that is indicative of poor scientific literacy and his credentials obtained at an institution that appears to have been a diploma mill.

The people who would benefit most from an acid-ash diet are those with chronic kidney disease (CKD) that disrupts the normal bicarbonate buffering system of the kidneys, but the pH Miracle diet goes far beyond the acid-ash hypothesis. No one would benefit from Young’s COWS eating program with the emphasis on raw foods, grasses, and alkaline water with mineral salts or sodium bicarbonate added. It is deficient in protein, vitamin B12, fat soluble vitamins, and the minerals phosphorous, iodine, and heme iron. It would make someone more susceptible to gastrointestinal problems and nutrient deficiencies by altering the pH of the stomach. The pH Miracle is based on misinformation and pseudoscience masquerading as good nutritional advice from a charismatic man with fraudulent credentials, a prison sentence for practicing medicine without a license, and pending grand theft charges against him for swindling desperate ill people out of hundreds of thousands of dollars.

References

1. Young RO, Young SR. The pH Miracle: Balance Your Diet, Reclaim Your Health. Kindle Edition. New York, NY. Grand Central Publishing; 2010.

2. About Us. PH Miracle Living website. http://www.phmiracleliving.com/t-about.aspx Accessed January 10, 2017.

3. Clayton College of Natural Health. Wikipedia. https://en.wikipedia.org/wiki/Clayton_College_of_Natural_Health Updated December 11, 2016. Accessed January 10, 2017.

4. Figueroa T. Split verdict for ‘pH Miracle’ author. The San Diego Union Tribune. http://www.sandiegouniontribune.com/sdut-criminal-trial-robert-young-ph-miracle-2016feb03-story.html Published February 3, 2016. Accessed January 10, 2017.

5. Marieb EN, Hoehn K. Human Anatomy & Physiology. Ninth Edition. Glenview, IL. Pearson Education; 2013.

6. Bonjour JP. Nutritional disturbance in acid–base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney. Br J Nutr. 2013; 110(7): 1168-1177. doi: 10.1017/S0007114513000962

7. Zheng CM, Zheng JQ, Wu CC, Lu CL, et al. Bone loss in chronic kidney disease: Quantity or quality? Bone. 2016; 87: 57-70. doi: 10.1016/j.bone.2016.03.017

8. Fenton TR, Eliasziw M, Lyon AW, Tough SC, Hanley DA. Meta-analysis of the quantity of calcium excretion associated with the net acid excretion of the modern diet under the acid-ash diet hypothesis. Am J Clin Nutr. 2008; 88(4): 1159-66.

9. Fenton TR, Lyon AW, Eliasziw M, Tough SC, Hanley DA. Phosphate decreases urine calcium and increases calcium balance: A meta-analysis of the osteoporosis acid-ash diet hypothesis. Nutrition Journal. 2009; 8(1): 41. doi: 10.1186/1475-2891-8-41

10. Teut M, Warning A, Lüdtke R. Reliability of Enderlein’s darkfield analysis of live blood. Altern Ther Health Med. 2006; 12(4): 36-41.

Nutritional Management of Crohn’s Disease

Note: This was a research paper for my Vitamins & Minerals graduate class. I made a few additions since turning in the paper, but I believe the conclusions about the best diet for Crohn’s disease apply to everyone with an autoimmune disease, inflammatory disease, or gastrointestinal issues.

Nutritional Management of Crohn’s Disease

Abstract

Crohn’s disease (CD) is a chronic inflammatory bowel disease (IBD) caused by a complex interplay between genetics and environment. This paper looks at a few of the most common underlying factors of CD including several genetic mutations that cause innate and adaptive immune system dysfunction, microbiota changes associated with the disease, and dietary risk factors. It also investigates successful adjunct treatments including diet and nutrition that reduces disease activity and treats or prevents nutritional deficiencies common in CD.

Epidemiology

CD is a relapsing and remitting autoimmune disease that primarily affects the gastrointestinal tract (Baumgart & Sandborn, 2012). Risk of developing CD varies from less than 1 to 16/100,000 people, while prevalence of the disease is estimated at 70-200/100,000 people (Hart & Ng, 2015). Currently North America and Northern and Western Europe have the highest rates, while South America, Africa, and Asia have the lowest (Hart & Ng, 2015). The number of people diagnosed with CD, however, has been increasing, particularly among children under 10 years old and in non-Western cultures (Hart & Ng, 2015).

Risk Factors

Risk factors for CD include family history of IBD, smoking or sustained exposure to second-hand smoke, NSAID use, and gastroenteritis (Baumgart & Sandborn, 2012). Other factors associated with the development of CD include high consumption of monosaccharides like glucose and fructose, trans fatty acids from partially hydrogenated vegetable oils, and omega-6 fatty acids in vegetable oils and diets low in fiber, fruits, vegetables, and omega-3 fatty acids (Owczarek, Rodacki, Domagała-Rodacka, Cibor, & Mach, 2016). Since diet is one of the associated risks of developing CD, there is a high probability that increased global trade in highly processed foods that contain refined sugars and vegetable oils is increasing the prevalence of the disease in cultures that once depended on traditional whole foods diets.

Signs & Symptoms

CD can occur in any part of the gastrointestinal tract, though it is most often found in both the ileum and colon, the ileum alone, or the colon alone (Hart & Ng, 2015). Inflammation and lesions in the mucosal and/or epithelial layers of the intestine tend to be disconnected rather than continuous and can vary in size and depth (Hart & Ng, 2015). If the lesions burrow deep enough, fistulas can form from the affected intestine to other organs including the bladder, skin, or adjoining section of intestine (Hart & Ng, 2015). Symptoms of CD can include blood and/or mucus in the stool, stomach cramps or intestinal pain, urinary incontinence, diarrhea, weight loss, and fatigue (Baumgart & Sandborn, 2012). Twenty-five to forty percent of those with CD develop extraintestinal manifestations (EIM), including musculoskeletal diseases like arthritis, ankylosing spondylitis, and osteoporosis; skin and oral problems like mouth ulcers, lesions or necrotic ulcerations, fissures or fistulas, and psoriasis; eye problems like uveitis, scleromalacia, and corneal ulcers; and hepato-pancreato-biliary diseases like bile duct inflammation and scarring, autoimmune hepatitis, cirrhosis, granulomatous disease, and fatty liver disease (Levine & Burakoff, 2011).

Diagnosis & Treatment

Diagnosis of CD is usually made after laboratory tests of blood and stool, an endoscopy along with multiple biopsies, and imaging tests such as CT or MRI (Baumgart & Sandborn, 2012). Histological signs of CD include pervasive submucosal inflammation, patches of chronic inflammation, and granulomata (Hart & Ng, 2015). A detailed medical history and thorough physical exam should also be done to identify risk factors and check for extraintestinal signs of disease. Diagnosis should not be made based on a single testing method but on the accumulation of medical data.

Conventional medical treatment of CD include medications to suppress the immune system, usually corticosteroids or tumor necrosis factor (TNF) blocking drugs (biologics) are prescribed short term to slow down progression of the disease along with thiopurine drugs, immunomodulators, or methotrexate for long term maintenance (Baumgart & Sandborn, 2012). Too often corticosteroids are prescribed long term, increasing risks of serious side-effects, including bone loss and osteoporosis. Life threatening infections, especially Clostridium difficile, are a concern with drugs that suppress the immune system. Surgeries to repair fistulas or remove segments of diseased intestine should be done judiciously (Hart & Ng, 2015).

There are several alternative or adjunct therapies for CD under investigation. Fecal transplants that colonize the intestines with a healthy community of microbiota have shown some success at remission of CD, but large clinical trials have not been done (Hart & Ng, 2015). Small trials of low dose naltrexone, an opiate antagonist with immune system modulation properties, showed some improvement of CD with the drug, but trials were very small and results were inconsistent (Segal, Macdonald, & Chande, 2014). A trial of medical marijuana in patients who had poor response to standard treatment showed clinically significant improvement in CD disease activity in the treatment group compared to placebo group, but again it was a small trial with little data to extrapolate to a larger population of CD patients (Naftali, et. al., 2013).

Genetics

Susceptibility to CD is genetic and it is thought to be triggered by environmental factors that disturb the natural balance of the microbiota in the gut and disrupt the normal functions of the innate and adaptive immune systems (Baumgart & Sandborn, 2012). Genetic polymorphisms in NOD2, ATG16L1, and IRGM have been strongly associated with the development of CD (Hart & Ng, 2015). All three genes are involved in immune system pathways that respond to microbes and autophagy, the destruction and elimination of cellular material, within intestinal epithelial cells (Billmann-Born, et. al. 2011).

NOD2 is involved in the recognition and protection of the body from certain species of pathogens through its expression in innate immune cells (Billmann-Born, et. al. 2011). Disruption of NOD2 activity due to genetic polymorphisms corrupts the immune system’s natural ability to ignore commensal bacteria and fight pathogens resulting in less tolerance to pathogens and hyperactive immune responses from B cells (Hart & Ng, 2015). NOD2 also interacts with enzymes that synthesize reactive oxygen species (ROS); increased ROS activity can cause cellular damage associated with chronic inflammatory diseases (Billmann-Born, et. al. 2011). Since NOD2 modulates nuclear factor-κB (NFκB), a transcription factor that controls cytokine production, regulation of pro-inflammatory cytokines tumor necrosis factor- α (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6) are disrupted by this gene mutation increasing systemic inflammation as well as intestinal inflammation (Hart & Ng, 2015).

Autophagy in a multi-stage process for isolating, recycling, and eliminating damaged or excess cellular material and intracellular microbes. Autophagy is important for proper innate immune response and also plays a role in adaptive response through antigen presentation in major histocompatibility complex (MHC) class II (Palomino-Morales, et. al., 2009). ATG16L1 is involved in the first step of the autophagy process, the formation of membranes around cellular material (Billmann-Born, et. al. 2011). Altered ATG16L1 results in a disruption in pathogen destruction and antigen processing which causes reduced protection against microbes and protracted immune system activation increasing pro-inflammatory cytokines IL-1β, IL-18, TNF-α, and interferon- γ (IFN-γ) (Palomino-Morales, et. al., 2009). Mutations in the IRGM gene induces inappropriate autophagy against intracellular bacteria resulting in increased destruction of commensal bacteria that protect against pathogenic microbes (Palomino-Morales, et. al., 2009). IRGM haplotypes have been identified that increase risk of developing CD and that are protective against developing the disease (Palomino-Morales, et. al., 2009). Anti-inflammatory T helper 2 (TH2) cytokines IL-4 and IL-13 are regulated by IRGM and dysregulation of them is suspected to be one of the reasons for the autoimmunity found in CD (Hart & Ng, 2015).

Microbiota

There are an estimated hundred trillion microbial organisms residing in the human intestinal tract that affect everything from immune function, metabolism, nutrition, and physiology (Guinane & Cotter, 2013). This microbiota contains thousands of diverse species and disruption of this microbial community (dysbiosis) can have a huge impact on human health; diseases associated with dysbiosis include obesity, malnutrition, diabetes, and IBDs like CD (Guinane & Cotter, 2013). Intestinal inflammation seen in CD is associated with a reduction in microbial diversity and several studies have linked mucosal lesions seen in CD with intestinal microbes, particularly an overabundance of adhesive E. coli (Guinane & Cotter, 2013). Dysbiosis with an increase in adhesive mucosal bacteria has been observed in patients who developed CD after gastroenteritis (Baumgart & Sandborn, 2012). While other causalities have not been established between dysbiosis and CD, a number of phyla and species of microbes have been identified that are reduced or increased in patients with CD compared with healthy controls (Guinane & Cotter, 2013). Manipulation of the microbiota through diet, prebiotics, probiotics, fecal transplants, antimicrobials, or antibiotics have been employed as adjunct treatment for CD. Results have been mixed, with probiotic therapies showing little to no improvement in disease activity (Owczarek, et. al., 2016).

Nutrition

Those with CD are at risk for developing nutritional deficiencies due to intestinal inflammation or lesions, medications used to treat the disease, and other factors like small intestine resections and decreased food intake which impact the digestion and absorption of nutrients. The most common deficiencies are: iron, calcium, vitamin D, vitamin K, vitamin B12 and folate but other deficiencies or sub-optimal levels can occur (Owczarek, et al., 2016). Assessment of nutritional status should include a dietary intake history, physical exam, body composition exam, and anthropometry along with in depth nutritional testing and a medical history. Knowledge of disease activity and active sites of inflammation in the intestinal tract helps with the design of an individualized treatment plan. For example, iron absorption occurs in the duodenum and ileum while vitamin B12 absorption takes place in the ileum. Active disease sites in these areas can greatly affect nutritional status.

Diet

Ideally adequate nutrition for those with CD can be obtained from a diet low in inflammatory foods and high in anti-inflammatory foods. A number of specialized diets have been investigated for the treatment of CD, including the Mediterranean Diet, Specific Carbohydrate Diet (SCD), low FODMAP, vegetarian diets, ancestral or paleolithic diets, and anti-inflammatory diets, all with various levels of success (Owczarek, et. al., 2016). SCD appears to be the most successful and the most studied when it comes to the dietary treatment of children with CD, but clinical trials of specialized diets are small and adherence to many of the diets are difficult (Burgis, Nguyen, Park, & Cox, 2016). Instead of recommending a specific specialized diet for patients with CD, effort should be made to individualize a diet that takes into consideration the patient’s unique needs while increasing anti-inflammatory foods and reducing inflammatory foods. Diets that reduce inflammation in general are whole foods based with low intake of highly processed foods, refined grains, simple sugars, omega-6 fatty acids, and alcohol and high intake of vegetables, fruits, fatty fish and other nutrient dense proteins, natural monounsaturated and omega-3 fatty acids, natural fiber from food sources, and plant polyphenols from tea, cocoa, and berries (Wu & Schauss, 2012). Grains, if eaten, should be intact or cracked rather than milled. Mucosal healing and reduction in inflammation should be the goal of any diet used to as adjunct treatment of CD; whole foods diets rich in vegetables and fruits and that contain minimal processed foods can achieve both (Whalen, et. al., 2016). There’s evidence that a whole foods diet can change and improve intestinal dysbiosis common in CD, as well as change gene expression to reduce pro-inflammatory cytokines (Marlow, et. al., 2013).

Meal Replacement

Depending on symptoms and disease status, adequate nutrition from whole foods is not always possible. While parenteral nutrition (PN) was once thought to help CD patients with active disease obtain remission, the risks of complications with intravenous nutrition are great and it is now seldom used (Hartman, Eliakim, & Shamir, 2009). Enteral nutrition (EN) has shown to be much more successful at improving nutritional status, decreasing inflammatory biomarkers, healing the mucosal lining, and inducing remission (Hartman, Eliakim, & Shamir, 2009). EN can be obtained through elemental or polymeric meal replacement formulas (Hartman, Eliakim, & Shamir, 2009). In rare cases EN formulas can be given though a feeding tube. If EN is given exclusively, effort should be made to transition patients back to eating whole foods as all or part of the diet once the mucosal lining has healed in one to two months (Owczarek, et. al., 2016).

Some studies recommend 35-50% of total calories per day (approximately 600 calories) be obtained through EN formulas to maintain remission in patients with CD (Owczarek, et al., 2016). Considering many CD patients eliminate foods they believe worsens their symptoms or can not eat adequate amounts of food to maintain energy or nutrition, supplementing with EN formulas should be seriously considered on a case by case basis.

Supplements

Patients who can not get adequate nutrition from foods may also need supplementation of key nutrients. Iron deficiency occurs in more than 60% of CD patients due to inflammation and low dietary intake (Owczarek, et al., 2016). Symptoms of iron deficiency include fatigue, dizziness, tingling in hands and feet, and shortness of breath. Due to the side-effects and the risk of increasing disease activity in the intestines, intravenous iron infusions should be given to CD patients with active disease or poor tolerance to oral iron supplements (Stein & Dignass, 2013). Iron isomaltoside at 1000mg and Ferric carboxymaltose at 1000mg or less are fast infusing and appear to correct anemia better than some of the other IV iron formulas, though both require maintenance doses at different intervals (Stein & Dignass, 2013). For oral supplementation, ferrous sulfate at 325mg (65mg elemental iron) three times a day is suggested until deficiency is resolved; lower doses may decrease side-effects but also prolong deficiency (Alleyne, Horne, & Miller, 2008). Adding low dose vitamin C supplement (125-250 mg) along with the iron supplement will increase absorption, as will taking it on an empty stomach; coffee, tea, high fiber meals, and taking iron with other minerals will decrease absorption (Alleyne, Horne, & Miller, 2008).

Patients with CD are at increased risk of developing osteoporosis, especially those on long term corticosteroid therapy. Supplementation with calcium, vitamin D, and vitamin K may be required to correct and prevent deficiencies and maintain bone health. Adequate intake of calcium should be between 1000-1500 mg/day (Owczarek, et al., 2016). If this can not be achieved in diet, then supplementation is recommended. 400-500 mg/day of calcium citrate taken once or twice a day along with vitamin D is suggested. Hypercalcemia can occur if calcium is not absorbed and eliminated properly or intake is too high. Symptoms of hypercalcemia include fatigue, confusion, excessive thirst, frequent urination, muscle pain and weakness. Inflammation biomarkers C-reactive protein (CRP), IL-6, and TNF-α decrease in patients with CD when vitamin D levels are optimal (Owczarek, et al., 2016). Supplementation of 2000-5000 IU/day of vitamin Dis recommended, depending on levels and sun exposure. Vitamin D toxicity also causes hypercalcemia. Vitamin K is often low in patients with CD and it is required for proper bone remolding and blood clotting. Vitamin K is synthesized by bacteria in the colon, so active disease states, inflammation, or dysbiosis can affect vitamin K levels. Supplementation of vitamin K1 does not produce measurable changes in bone health in patients with CD (O’Connor, et. al. 2014). However, supplementation of vitamin K2 at 45-100 mg/day improves bone turnover in patients with autoimmune disease on corticosteroids (Shikano, et. al., 2016).

Vitamin B12 is often deficient in patients with CD, particularly if there is active inflammation in the ileum. 5-40 mcg of an 1000-2000 mcg/day oral supplement can be absorbed by passive diffusion; normalization of vitamin B12 and MMA levels occurs after 3-4 months of treatment (Battat, et. al., 2014). Monthly intramuscular injections (IM) should be considered if neurological symptoms of deficiency do not improve with oral treatment. Folate is also a common B vitamin deficiency in those with CD, particularly in those taking the drug sulphasalazin (Owczarek, et al., 2016). Supplementation of 400 mcg/day of methylfolate is suggested to prevent deficiency with higher doses recommended only under medical supervision to correct anemia. Folic acid toxicity can mask B12 deficiency so methylfolate is recommended.

Increased intake of foods containing magnesium, zinc, and vitamin A or vitamin A precursors like β-carotene should be encouraged. Supplementation of these nutrients are only necessary if deficiencies occur (Owczarek, et al., 2016). Because of the gasterointestinal side-effects of magnesium, immune system side-effects of zinc supplementation, and risk of toxicity with vitamin A supplements, food is the best source of these nutrients. Best food sources of magnesium include: leafy greens, nuts and seeds, cold water fatty fish, legumes, and avocados. Shellfish, red meat, poultry, nuts and seeds, cheese, and cooked leafy greens are good sources of zinc. Vitamin A and its precursors are found in organ meats, cold water fatty fish, and orange colored vegetables or fruits like yams, cooked carrots, butternut squash, and dried apricots as well as in cooked leafy greens. Because vitamin A is a fat soluble vitamin, plant sources of vitamin A precursors should be eaten with good fats like the omega-3 fatty acids contained in unheated cold-pressed flaxseed oil, cold-pressed hemp seed oil and cold-pressed extra virgin olive oil or that are in organic, grass fed butter or whole milk yogurt.

Conclusion

CD is a complex gastrointestinal disease that involves genetic mutations as well as environmental factors that cause systemic and localized inflammation. Management of CD should involve nutrition as well as conventional medical treatments in order to modulate the immune system, reduce inflammation, decrease disease activity, improve symptoms, and prevent nutritional deficiencies. Lifestyle changes that include smoking cessation and stress reduction should also be discussed. A whole foods diet that reduces highly processed foods and includes greater quantities of vegetables, fruits, and omega-3 fatty acids is highly recommended. Supplemental nutrition, especially during periods of disease activity, is encouraged. That can include vitamin or mineral supplementation as well as meal replacement formulas depending on the patient’s specific needs. While diet, nutrition, and lifestyle changes alone likely will not cause remission of CD, when combined with other treatments, remission and reduction of recurrences of active disease states should be possible.

References

Baumgart, D.C., & Sandborn W.J. (2012). Crohn’s disease. Lancet, 308(9853), 1590-1605. doi: 10.1016/S0140-6736(12)60026-9

Hart, A.L., Ng, S.C. (2015). Crohn’s disease. Medicine, 43(5), 282-290. doi: 10.1016/j.mpmed.2015.02.006

Owczarek, D., Rodacki, T., Domagała-Rodacka, R., Cibor, D., & Mach, T. (2016). Diet and nutritional factors in inflammatory bowel diseases. World J Gastroenterol, 22(3), 895-905. doi: 10.3748/wjg.v22.i3.895

Levine, J.S., Burakoff, R. (2011). Extraintestinal Manifestations of Inflammatory Bowel Disease. Gastroenterol Hepatol (N.Y.), 7(4): 235–241.

Segal, D., Macdonald J.K., Chande, N. (2014). Low dose naltrexone for induction of remission in Crohn’s disease. Cochrane Database Syst Rev, 2014(2): CD010410. doi: 10.1002/14651858

Naftali, T., Schleider, L.B.L., Dotan, I., Lansky, E.P., Benjaminov, F.S., Konikoff, F.M. (2013). Cannabis induces a clinical response in patients with Crohn’s disease: a prospective placebo-controlled study. Clin Gastroenterol Hepatol, 11(10), 1276–1280. doi: 10.1016/j.cgh.2013.04.034

Billmann-Born, S., Lipinski, S., Böck, J., Till, A., Rosenstiel, P., Schreiber, S. (2011). The complex interplay of NOD-like receptors and the autophagy machinery in the pathophysiology of Crohn disease. Eur J Cell Biol, 90(6), 593-602. doi: 10.1016/j.ejcb.2010.10.015.

Palomino-Morales R.J., Oliver, J., Gómez-García, M., López-Nevot, M.A., Rodrigo, L., Nieto, A., Alizadeh, B.Z., Martín, J. (2009). Association of ATG16L1 and IRGM genes polymorphisms with inflammatory bowel disease: a meta-analysis approach. Genes Immun, 10, 356–364. doi:10.1038/gene.2009.25

Guinane, C.M., Cotter, P.D. (2013). Role of the gut microbiota in health and chronic gastrointestinal disease: understanding a hidden metabolic organ. Therap Adv Gastroenterol, 6(4), 295–308. doi: 10.1177/1756283X13482996

Burgis, J.C., Nguyen, K., Park, K.T., Cox, K. (2016). Response to strict and liberalized specific carbohydrate diet in pediatric Crohn’s disease. World J Gastroenterol, 22(6), 2111–2117. doi: 10.3748/wjg.v22.i6.2111

Wu, X., Schauss, A. (2012). Mitigation of Inflammation with Foods. J. Agric. Food Chem, 60(27): 6703–6717.

Whalen, K. A., McCullough, M. L., Dana Flanders, W., Hartman, T.J., Judd, S., Bostick, R.M. (2016). Paleolithic and Mediterranean Diet Pattern Scores Are Inversely Associated with Biomarkers of Inflammation and Oxidative Balance in Adults. J. Nutr, 146(6), 1217-26. doi: 10.3945/jn.115.224048.

Marlow, G., Ellett, S., Ferguson, I.R., Zhu, S., Karumasignhe, N., Jesuthasan A.C., Han, D.Y., Fraser, A.G., Ferguson, L.R. (2013). Transcriptomics to study the effect of a Mediterranean-inspired diet on inflammation in Crohn’s disease patients. Hum Genomics, 7(1): 24. doi: 10.1186/1479-7364-7-24.

Hartman, C., Eliakim, R., Shamir, R. (2009). Nutritional status and nutritional therapy in inflammatory bowel diseases. World J Gastroenterol, 15(21), 2570–2578. doi: 10.3748/wjg.15.2570.

Stein, J., Dignass, A.U. (2013). Management of iron deficiency anemia in inflammatory bowel disease – a practical approach. Ann Gastroenterol, 26(2), 104–113.

Alleyne, M., Horne, M.K., Miller, J.L. (2008). Individualized treatment for iron deficiency anemia in adults. Am J Med, 121(11): 943–948. doi: 10.1016/j.amjmed.2008.07.012.

O’Connor, E.M., Grealy, G., Mccarthy, J., Desmond, A., Craig, O., Shanahan, F., Cashman, K.D. (2014). Effect of phylloquinone (vitamin K 1 ) supplementation for 12 months on the indices of vitamin K status and bone health in adult patients with Crohn’s disease. Br J Nutr, 112(7), 1163-1174.

Shikano, K., Kaneko, K., Kawazoe, M., Kaburaki, M., Hasunuma, T., Kawai, S. (2016). Efficacy of Vitamin K2 for Glucocorticoid-induced Osteoporosis in Patients with Systemic Autoimmune Diseases. Internal Medicine, 55(15), 1997-2003.

Battat, R., Kopulov, U., Szilagyi, A., Saxena, A., Rosenblatt, D.S., Warner, M., Bessissow, T., Seidman, E., Bitton, A. (2014). Vitamin B12 Deficiency in Inflammatory Bowel Disease: Prevalence, Risk Factors, Evaluation, and Management. Inflamm Bowel Dis, 20(6), 1120–1128. doi: 10.1097/MIB.0000000000000024

Nutritional Management of Biochemical Abnormalities in Idiopathic Intracranial Hypertension

Note: This is the research paper I wrote earlier this year for my Biochemistry of Nutrition graduate school class. I haven’t looked at it since I turned it in. I originally wanted to add more to it on specific IH research topics (coagulation factors, thyroiditis) that I didn’t have the time or space to write about originally, but my health took a turn this spring and I’m just now recovering from it.

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Nutritional Management of Biochemical Abnormalities
in Idiopathic Intracranial Hypertension

Abstract

Idiopathic Intracranial Hypertension [IIH], historically known as Pseudotumor Cerebri and Benign Intracranial Hypertension, is a rare disorder where there is greatly increased cerebrospinal fluid pressure in the skull without an obvious cause like a head injury or chiari malformation. It can occur in any age group and any sex, but the largest population is obese women of child bearing age. IIH mimics the symptoms of a brain tumor and common symptoms include: chronic headaches, visual disturbances or vision loss from papilledema, tinnitus or pulsating heartbeat in head, nerve pain and paresthesia, dizziness and lightheadedness, nausea and vomiting, fatigue, memory and cognitive difficulties, and exercise intolerance. There are a number of hypotheses about the biochemical mechanisms involved with IIH but recent research implicates increased levels of pro-inflammatory cytokines associated with the reduction in cerebrospinal fluid drainage. High levels of cortisol and several other pro-inflammatory cytokines are also associated with impaired secretion and absorption of cerebrospinal fluid. Nutrient deficiencies and genetic polymorphisms that affect absorption of one or more of the vitamins required for one carbon metabolism are not uncommon with IIH; those vitamins include riboflavin, folic acid, vitamin B12, and vitamin B6. Typical medical treatments for IIH include: lifestyle changes like weight loss and reductions in salt and caffeine in the diet; medications like acetazolamide or loop diuretics to help reduce the build-up of fluids in the skull; and medical procedures or surgeries such as multiple lumbar punctures to remove cerebrospinal fluid, optic nerve sheath fenestration to improve visual field, and shunt or stent implantation to control cerebrospinal fluid drainage. Nutritional management of IIH includes normalizing homocysteine levels with the appropriate bioavailable forms of B vitamins and healthful, low calorie or low carbohydrate diets to promote weight loss, reduce cortisol levels, and control inflammation.

Signs, Symptoms, and Diagnosis

Idiopathic Intracranial Hypertension [IIH] involves a dysfunction in the mechanisms that secrete or absorb cerebrospinal fluid in the brain. It is a rare disease that is becoming increasingly more common. There’s some debate whether this increase is due to rising obesity rates or improved diagnostics; it is likely a combination of both. 92% of those diagnosed with IIH are obese women between the ages of 22-44, but it can be found in any population. Occurrence rates in the general population are approximately 1/100,000; however, in obese women of childbearing age the rate is 20/100,000. A small but significant population of those prone to IIH are astronauts. 29% of astronauts experience either intracranial hypertension or other visual changes related to changes in cerebrospinal fluid dynamics. NASA has partnered with The Intracranial Hypertension Research Foundation to study causes and improve diagnostics and treatment of Intracranial Hypertension.

Associated risk factors for the development of IIH include disorders like hypothyroidism, hyperthyroidism, Cushing’s disease, Lyme’s disease, and aldosteronism. Secondary intracranial hypertension has been associated with sleep apnea, pregnancy, anemia, meningitis, medications or drugs (antibiotics, lithium, vitamin A, steroids, hormone birth control), chiari malformation, and living in a microgravity environment.

Severity of symptoms vary but disabling chronic headaches is the most common symptom and permanent vision loss is experienced by nearly a quarter of IIH patients. Due to the diverse and often nonspecific nature of the symptoms, it takes an average of 5 years before the diagnosis of IIH is made. IIH is commonly misdiagnosed as chronic migraines or dismissed as symptoms of other health problems. The previous name of IIH, Psuedotumor Cerebri (meaning: false brain tumor), clearly shows the symptoms apply to other diseases. Because symptoms and treatments can be disabling, the medical profession has moved away from the name Benign Intracranial Hypertension because it undermines the seriousness of the condition.

A diagnosis of IIH is usually made after brain imaging, an ophthalmological exam, and a lumbar puncture. Brian imaging is used to rule out brain tumors, hydrocephalus, lesions, venous sinus thrombosis, or other structural problems. Signs of IIH that appear in imaging include flattening of posterior globe near the optic nerve and an empty cella. These occur 80% and 70% of the time in IIH, respectively.

An ophthalmological exam looks for papilledema, swelling of the optic disc from increased intracranial pressure. It is another common, though not universal, symptom of IIH. Permanent vision loss, either partial or full, is a serious complication of IIH. Permanent vision loss is more likely in patients who don’t receive a prompt diagnosis and appropriate treatment.

Measuring the opening pressure of cerebrospinal fluid during a lumbar puncture is the gold standard for diagnosing IIH. Opening pressure must be 250mm (25cm) or greater for a diagnosis of IIH. Occasionally a second lumbar puncture is required because the opening pressure was low on the first one and other causes for the symptoms were ruled out. A lumbar drain for 6 to 24 hours to monitor cerebrospinal fluid pressure is seldom required to make a diagnosis.

Physiological and Biochemical Mechanisms

While IIH is characterized by increased intracranial pressure, the exact physiological processes is yet unknown though four possible mechanisms of impaired cerebrospinal fluid dynamics have been suggested: increased cerebrospinal fluid secretion in the choroid plexus, increased cerebral volume, increased cerebrospinal fluid outflow resistance at the arachnoid granulations, and increased cerebrospinal venous pressure. There is no consensus though small studies show some IIH patients exhibit signs of at least one of these fluid dynamics disorders.

arachnoid-granulations

There are a number of hypotheses about the biochemical mechanisms involved with IIH, including endocrine dysfunction since IIH occurs most often in women. However, if hormones were the only factor involved, IIH would be more common. Another major factor in the development of IIH is obesity, with 94% of patients diagnosed with IIH falling into the clinically obese category. But again, if obesity was the only factor, there would be more cases of IIH. It is possible that both endocrine dysregulation and obesity, along with a combination of other factors, play a role in the development of IIH. Recent research implicates systemic inflammation along with glucocorticoid dysregulation, and one carbon metabolism errors due to nutrient deficiencies or genetic polymorphisms, though no group of patients exhibits abnormalities in every biomarker. However, it gives doctors and researchers alternative diagnostics using laboratory testing and can help establish new treatments.

Obesity is an established cause of low grade systemic inflammation. Numerous studies show pro-inflammatory cytokines in adipose tissue in those with obesity. Those cytokines include: CC-chemokine ligand 2 [CCL2], interleukin-1β [IL-1β], interleukin-6 [IL-6], interleukin-8 [IL-8], tumor necrosis factor-α [TNF-α], hepatocyte growth factor [HGF], nerve growth factor [NGF], and plasminogen-activtor inhibitor type 1 [PAI-1]. Resistance to the adipose hormone that controls appetite, leptin, and elevated serum leptin levels are also associated with obesity.

Pro-inflammatory cytokines associated with obesity, TNF-α, IL-1β, Il-6, and leptin also regulate the glucocorticoid enzyme 11β-hydroxysteroid dehydrogenase type 1 [11β-HSD1]. 11β-HSD1 regulates corticosteroid hormone activity by activating cortisol from cortisone. Elevated 11β-HSD1 is associated with altered lipid metabolism and insulin resistance because it controls cortisol availability which drives gluconeogenessis. Dysregulation of 11β-HSD1 can disrupt sex hormone metabolism and cortisol production. Cortisol dysregulation through altered 11β-HSD1 activity may have an effect on cerebrospinal fluid homeostasis through the regulation of the arachnoid granulation. There is also evidence of 11β-HSD1 immunoreactivity in the cerebrospinal fluid secreting cells in the choroid plexus.

Hematological and cerebrospinal fluid laboratory analysis in patients with IIH show high levels of pro-inflammatory cytokines, both ones associated with obesity and ones not associated with it. Systemic inflammation is linked to changes in cerebrospinal fluid dynamics and could be one of the underlying causes of IIH. Recent research implicated pro-inflammatory cytokines CCL2 and IL-17 in the reduction of cerebrospinal fluid outflow resistance and the association of high levels of homocysteine, cortisol, TNF-α, and IL-6 with altered compensatory mechanisms in the secretion and absorption of cerebrospinal fluid. Transforming growth factor-β [TGF- β], C reactive protein [CRP], leptin, and cortisol are also often elevated in patients with IIH. The leptin levels in patients with IIH is much greater than the levels found in obese patients without IIH.

One carbon metabolities, namely homocysteine, are also often elevated in patients with IIH, indicating B vitamin deficiencies or genetic polymorphisms that affect one carbon metabolism. Two genetic polymorphisms have been identified as increasing the risk for elevated homocystine as well as increasing the risk of developing IIH: gene MTRR with one or two G alleles and gene SHMT1 1420 with C alleles. The two identified genetic polymorphisms affect absorption of one or more of the vitamins required for one carbon metabolism; those vitamins include riboflavin, folic acid, vitamin B12, and vitamin B6. Improving the nutritional status of patients with elevated homocysteine could improve IIH symptoms and reduce the likelihood of recurrence.

Conventional Medical Treatments

Since IIH is linked to obesity, conventional treatment for IIH includes a recommendation for weight reduction. Besides extreme dieting that includes very low caloric intake, weight loss surgery is often suggested. More reasonable dietary advice for patients with IIH is to reduce sodium and caffeine intake in order to improve fluid dynamics. Excess sodium can increase intracranial pressure while caffeine increases the production of cerebrospinal fluid.

Besides lifestyle changes, medications are the first line of treatment. Carbonic anhydrase inhibitors act as a mild diuretic as well as reduce the reabsorption of bicarbonate and sodium chloride thereby slowing down fluid transport and reducing intraocular and intracranial pressure. Two popular carbonic anhydrase inhibitors used to treat IIH are acetazolamide and topiramate. Topiramate has the added benefits of reducing chronic headaches and acting as an appetite suppressant, which can aid in weight loss. If carbonic anhydrase inhibitors are not tolerated, loop diuretics that reduce the production of cerebrospinal fluid are used. Furosemide is the most popular loop diuretic prescribed for IIH. Glucocorticoids like Prednisone are sometimes used on a short term basis to reduce inflammation. They are thought to improve the outflow of cerebrospinal fluid at the arachnoid granulations in the brain. Other drugs used to treat migraines may be prescribed since chronic headaches is one of the most debilitating symptoms of IIH.

Medical procedures aren’t uncommon in severe cases of IIH that are resistant to treatment with medications. Repeated lumbar punctures to remove excess cerebrospinal fluid are often used on a temporary basis before surgical interventions are attempted or scheduled. Repeated lumbar punctures aren’t without risk. There’s always a possibility of permanent nerve damage and increased risk for serious infection.

Optic nerve sheath fenestration is used after rapid or progressive vision loss occurs due to increased pressure on the optic nerves. Incisions are made in the meninges in order to relieve the intracranial pressure on the optic nerve and improve the visual field. It’s not a cure for IIH but it can reduce further vision loss from chronic papilledema due to high intracranial pressure. Optic nerve sheath fenestration can lead to permanent blindness or other complications.

Venous sinus stents are a relatively new procedure in the treatment of IIH, but they’re gaining in popularity. A tubular support is placed in the venous sinus in order to widen an area narrowed by either intracranial pressure or blockage in order to improve cerebrospinal fluid flow. They seem to be nearly as effective as shunts but with fewer complications. The biggest complication is the risk for blot clots but that is usually controlled with medication. In IIH patients with confirmed venous sinus stenosis that impedes cerebrospinal fluid absorption, venous sinus stenting across the arachnoid granulation normalizes cerebrospinal fluid pressure and reduces IIH symptoms. Long term studies are still required but currently stenting is a surgical alternative to shunts.

Two different type of shunts are used to improve cerebrospinal fluid drainage with IIH. Shunts involve the placement of a catheter either in the brain or the spine connected to a drain tube in the peritoneal cavity in the abdomen in order to drain cerebrospinal fluid more effectively. Neuronavigation-assisted ventriculoperitoneal (VP) shunts with programmable valves are have a slightly higher risk of initial failure (14% vs 11%), but revision rates of lumboperitoneal (LP) shunts is much higher (60% vs 30%). Both often require multiple surgeries and the risk of infection is high. Shunts should be considered as a last resort.

Nutritional Management

There are three nutritional targets for the management of IIH: weight loss, reduction of inflammation, and normalization of homocysteine levels. Low sodium and limited caffeine intake may also be helpful in the management of IIH.

Studies show that weight loss using a short term (3 months) very low carbohydrate diet improves abnormal 11β-HSD1 activity and normalizes cortisol levels. Very low calorie diets have also shown to improve IIH symptoms, though biochemical markers weren’t checked. While doctors often recommend surgical weight loss procedures in the treatment of IIH, diet based weight loss has fewer complications as long as micronutrient needs are met.

Research into diets that mitigate pro-inflammatory cytokines and other pro-inflammatory biochemicals have identified a few factors that should be included in a diet in order to reduce systemic inflammation. Those factors include: monounsaturated and omega-3 fatty acids like those found in avocados, olive oil, nuts, flaxseed, chia seed, and oily fish; a greater quanity of fruits, vegetables, and nuts; minimally processed whole grains; and polyphenols including tea, cocoa, red wine, and berries. Studies suggest that diets with higher fruit and vegetable intake are associated with reduced levels of pro-inflammatory cytokines including IL-1, IL-6, and TNF-α and CRP.

Dietary factors that increase inflammation include: trans fats and omega-6 fatty acids like those found in vegetable oils; highly processed foods with a high glycemic index; and diets without adequate fruits, vegetables, and nuts.

New research shows that diets which contain mostly fresh foods with limited sugar and processed foods reduce inflammation. A Mediterranean style diet and a Paleolithic style diet were used in the trial and both decreased CRP. Pro-inflammatory cytokine levels weren’t tested.

Normalization of homocysteine levels can be managed through diet alone if genetic polymorphisms aren’t present. The micronutrients required for one carbon metabolism can easily be gained from food as long as genetic polymorphisms don’t hinder the conversion of them into usable forms. Bioavailable or coenzymated vitamins may be added to the patient’s treatment regime if vitamin conversion is a problem. Folate can be obtained from leafy greens, citrus, beans, nuts, and whole grains. Vitamin B12 is in mollusks, liver, red meat, fish, poultry, eggs, and dairy products. Vitamin B6 can be found in organ meats, fish, beans, potatoes, and bananas. Riboflavin (vitamin B2) is most plentiful in dairy products, nuts, red meat, fish, eggs, and pork.

Designing a diet that the patient can turn into a lifestyle change for the long term is key to any nutritional management of disease. Neither very low carbohydrate nor very low calorie diets are easy or safe for long term, though both can be used for short term weight loss in order to improve biomarkers and symptoms of IIH. For the treatment of IIH, a whole food diet rich in omega-3 fatty acids, vegetables, fruits, nuts, and nutrient rich meats and low in highly processed foods with high glycemic index and high omega-6 fatty acids seems to be the best place to start.

Conclusion

Idiopathic Intracranial Hypertension is a disabling disease that can cause permanent vision loss and chronic headaches that mostly affects obese women between the ages of 22-44. While the cause of the symptoms are well documented, increased cerebrospinal fluid pressure, the underlying causes of the abnormal cerebrospinal fluid dynamics are still heatedly debated and researched. Newer research implicates a number of biochemical changes including systemic inflammation, glucocorticoid dysregulation, and one carbon metabolism errors. Conventional medical treatment for IIH currently does little to identify or treat these underlying biochemical abnormality. Nutritional management of the biochemical irregularities though a carefully designed diet and supplemental vitamins, if required, is a good adjunct treatment to conventional medicine that should reduce symptoms and recurrence of IIH.

Bibliography

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Intracranial Hypertension and Thyroid

I started graduate school last month with the intention of earning an MS in Human Nutrition. For my Biochemistry of Nutrition class I have to do a research project on a metabolic disease. Originally I planned to do one on mitochondrial disease but from my Pathophysiology class I’ve learned that mitochondrial dysfunction underlies nearly every chronic illness from autoimmune diseases to cardiovascular disease to Parkinson’s disease to Alzheimer’s disease. Now I plan to do it on Secondary Intracranial Hypertension, if my professor agrees. The causes of Idiopathic Intracranial Hypertension are unknown but there have been multiple risk factors found for SIH, including endocrine disruption due to pituitary gland dysfunction, hormone birth control, steroids, hyperthyroidism, and hypothyroidism. Endocrine disruption makes some, not all, SIH a metabolic disease.

I believe quite strongly that facultative hyperthyroidism due to improper/negligent medical care was the cause of my SIH. This post lists all the reasons I believe this. Unfortunately there is no way to prove it since I didn’t have many labs done in the five months I was taking the wrong dosage of thyroid medication (or if I did, I don’t have copies of the results).

In July of 2009 I started seeing a naturopathic “doctor” because none of the multiple treatments I tried with my Internal Medicine PA, even experimental ones like Viagra, helped relieve the “Fibromyalgia” (I usually call it mold induced myalgia now) and I was getting sicker and sicker. It culminated with my PA taking me off all medications and admitting she couldn’t help me. The ND could prescribe a promising medication I had researched, Low Dose Naltrexone, that my PA was unable to prescribe since it came from a compounding pharmacy. Unfortunately I allowed the ND to talk me into trying many more things, most of which made my symptoms worse or caused new problems. Even though my hypothyroidism was very mild and I’d taken a low dose of Synthroid for years without any problems, she thought I needed to take both slow acting T4, like Synthroid, and a fast acting T3 thyroid medication because my body wasn’t converting the T4 to T3 properly. It’s possible this is true since mold illness increases systemic inflammation and interferes with the function of the pituitary gland which signals the thyroid gland to produce more T4 and T3 with Thyroid Stimulating Hormone (TSH). Inflammation can also inhibit the body’s ability to convert T4 into T3. Not everyone with hypothyroidism requires a T4/T3 medication, but there are some health issues that make it a better choice. A full thyroid serum panel that includes TSH, Free T3, Free T4, and Reverse T3 can help a doctor find the best treatments for a patient. Thyroid antibodies can also be tested if an autoimmune disease is suspected.

Instead of switching me to a natural dessicated thyroid medication that comes in standardized doses from a pharmaceutical company like Armour, Naturethroid, or Westhroid, my ND prescribed an 80/20 T4/T3 drug from a compounding pharmacy. Here’s where the negligence comes in. I was taking 37.5mcg of Synthroid and I switched to 40mcg of 80/20 T4/T3 combination in mid-September. This breaks down to 32mcg of T4 and 8mcg of T3. The problem with this dosage is that T3 medications are almost 4x as potent as T4 medications. Most thyroid medication conversion charts equates 12.5mcg of T3 to 50mcg of T4. Using that conversion, I was prescribed the equivalent of 32mcg (8×4) T3 along with another 32mcg of T4 for a total of 64mcg, almost twice the dose I was taking before. If the conversion had been done properly, I should have been prescribed 25mcg of T4 and 5mcg of T3 (5×4=20+20=40). I know math is hard, but it is a doctor’s job to know how to prescribe medications at the right doses. This is doubly so if the drug is compounded and not standardized. This dosage mistake had huge repercussions for my health.

I don’t like to play “what if” games because it would drive me insane. There are too many decisions that were made either by me or my health care providers that contributed to the worsening of my  health, from where I lived to what medications I took, but a dosage mistake is not the same thing as hidden mold or unforeseen medication side-effects. It is negligence and possibly malpractice.

At the end of December 2009, my IH headaches began and continued to worsen. Based on the location of the headaches at the top of my head, I thought they were thyroid related. My mom gets similar headaches when her thyroid meds are out of balance. I asked my ND to test my thyroid levels in early February 2010. She said everything was within normal range but I still wasn’t converting T4 to T3 properly. She convinced me to take the herb chaste tree to help regulate my period, which had been irregular and sometimes occurring twice a month since January. My health continued to decline and the headaches got worse. The problems with my period are also hallmarks of hormone/thyroid imbalance for me. Often that’s my first major sign that something is wrong since fatigue and muscle pain are normal for me.

By early March I knew the compounded thyroid meds were making me more ill, even if I couldn’t prove it; my fatigue and muscle pain were almost unbearable, I had severe sleep issues, I bled constantly, I lost weight very fast (over 10lbs in one month), and the headaches were uncontrollable. I finally saw my PA on March 12th and switched back to Synthroid at my previous dose of 37.5mcg. Of course it was too late by then; I already had IH. March 19th I tried a migraine medication in an attempt to stop the pain cycle. The next day the left side of my face and my left forearm went numb and the headache expanded to encompass my entire head. On March 23rd I started losing vision in my left eye. On March 24th I saw my PA and had an emergency MRI of my head. She talked me into trying an opiate in an attempt to stop the headache cycle. The MRI didn’t show any abnormalities so on March 26th I had an emergency appointment with an eye doctor. My eye pressure was elevated and there was bulging on my optic nerves indicating elevated cerebrospinal fluid in my skull. He diagnosed me with Pseudotumor Cerebri aka Intracranial Hypertension. Later that day it was confirmed with a lumbar puncture with an opening pressure of 35 (normal is under 25). 30cc’s of CSF was removed in an attempt to reduce the pressure in my skull and ease the four weeks of continuous headache.

I won’t go into depth about my experience with IH in this post since I’m building a chain of evidence that the IH and my thyroid problems are linked. It took several years for the IH symptoms to ease up and mostly disappear, but my thyroid problems weren’t over. In late 2011, I once again had issues with irregular periods despite doing okay on 37.5mcg of Synthroid since switching back to it in 2010. My TSH was too high, which meant my body wasn’t getting enough thyroid hormones. My Synthroid dose was increased to 100mcg. My energy levels were greatly improved for about a month and I weighed less than I did at age 16, but then my TSH dropped too low, which meant I was taking too much medication. My dosage was adjusted downward and I gained most of that weight back in the space of two months. In late 2012, I tried Armour thyroid, a natural dessicated thyroid medication that contains both T3 and T4 hormones. I didn’t do well on it and the IH headaches, which were mild at that point, got much worse. They eased up once I was back on Synthroid.

After a year of struggling to get my thyroid levels balanced with Synthroid I asked to try a T3 medication, Cytomel, alone in late 2013. By that time my IH symptoms were basically gone. I’d get an IH headache a few days a month around my period, but that was it. I was no longer on Nortriptyline for neuropathy nor diuretics to remove extra CSF, both of which were used to treat my IH. Within a few days of slowly increasing the dosage of Cytomel, I knew it was a problem. After two weeks the IH headaches were too severe for me to continue on Cytomel. I switched back to Synthroid and soon the IH headaches were gone again. My MD still wanted me to try both T4 and T3 medications since blood tests showed I wasn’t converting T4 to T3 properly. I have copies of that lab work showing it to be true. At that point I was taking between 93.75mcg and 87.5mcg of Synthroid. We dropped Synthroid down to 50mcg and added 5mcg of Cytomel twice a day.  Even though the conversion of this dose was close to what I was taking of Synthroid (10×4=40+50=90mcg), once again the IH headaches returned. I dropped the Cytomel dose down to 5mcg in the morning and 2.5mcg in the evening and the headaches became bearable, though they were a constant presence. I’ve stayed fairly close to that dose since then though I still have to adjust the doses of Sythroid and Cytomel several times a year to find the best dose that keeps the headaches away, yet keeps my energy levels up enough I can function. If one or both of the doses gets too low or too high, not only does the IH headaches worsen, my fatigue gets worse, so do my PMS symptoms, and eventually my periods become irregular. Currently I’m taking 56.25mcg of Synthroid and 5mcg of Cytomel in the morning and 2.5mcg in the evening and I have a constant, yet mild, IH headache. I took 62.5mcg of Synthroid and 5mcg of Cytomel in the morning and 1.25mcg in the evening for several months but my fatigue worsened. Somewhere between 6.25mcg and 7.5mcg of Cytomel is my perfect dose, but I can’t cut the 5mcg tablets that small. I may ask my MD about trying a sustained release compounded form of T3 in 6.75mcg.

In the process of writing this, I realized that I’m having so much trouble adjusting my thyroid medications and keeping it balanced due to pituitary gland problems. I’ll have to ask my MD about this as well. I’m not sure there’s anything we can do to treat it directly, but it is something that mold illness affects and it’s the gland responsible for MSH production, and we know my MSH levels are much too low.

Anyway, all my experiences with Cytomel and how tiny dosage changes make my IH symptoms return made me go back and take a hard look at the compounded thyroid medication I was taking when the symptoms began. I’ve read a lot about hypothyroidism and how the body converts T4 into T3 since 2012, and I have a much better understanding of how my body reacts when my thyroid levels are out of balance. Too bad I didn’t have this knowledge before my health was ruined by IH and the treatments for it. Dealing with mold illness was bad enough without adding thyroid problems and IH on top of it. Without the lab reports or copies of the prescription, I don’t think I can prove any of my suspicions to the state naturopath licensing board, but I wonder how many other prescribing mistakes she’s made. We trust health care practitioners, especially if they call themselves doctors, to know what they’re doing. We literally put our lives in their hands. They should be at least be reasonably competent. If I can figure out dosing conversions after looking at a couple of charts online, a medical professional should have even better resources they can reference.

Eating Plans to Improve Health

Changing ones diet is the simplest thing one can do to make a huge impact on their health but many people resist making changes to the way they eat. I’ve tried many different diets in order to improve my health. Some helped, some made things worse, some I didn’t see any results either way. I’ve listed them below with a brief description and how I did on them. What most of them have in common is a focus on unprocessed or minimally processed foods.

Yeast Elimination Diet: There are several different yeast elimination diets online or in books. This diet is used to kill overgrowth of candida yeast. Candida overgrowth can manifest as a skin rash, chronic vaginal yeast inflections, gastrointestinal issues, and/or increased fatigue. The diet involves eliminating all foods that feed the candida microbes in the gut. This includes: sugar, yeasts, carbohydrates, fermented foods, & vinegars. Once yeast overgrowth symptoms are gone for several weeks, foods can slowly be reintroduced. Supplements to help kill the yeast and mitigate the effects of yeast die-off can be taken but I’ve done the diet many times without supplements.

I first tried it in 1997 when a brown rash developed on my neck under my hair and kept spreading. My medical doctors told me since it didn’t itch it was just cosmetic and there was nothing they could do about it. My chiropractor suspected it was yeast so I read up on candida and ways to get rid of it. I came across a 4 step yeast elimination diet and tried it. It worked and since then I’ve had to go back to it multiple times, including for a few months this year. For me, a decrease in beneficial gut microbes from years on antibiotics and Prednisone allowed the candida microbes to grow unchecked in my gut.

Anti Inflammatory Diet: There are multiple types of anti inflammatory diets but most recommend eliminating inflammatory foods like sugar, nightshade vegetables (tomatoes, potatoes, peppers, eggplant), trans fat and omega 6 fatty acids, alcohol, dairy, MSG, and gluten. They recommend adding whole grains, leafy greens, nuts, ginger & turmeric, olive oil, garlic & onions, bright colored fruits & veggies, and omega 3 fatty acids from foods like salmon, tuna, mackerel, sardines, chia seeds, & flax seeds, all of which have anti inflammatory properties.

After I got sick in 2008 many of these items increased my inflammation so I eliminated them out of necessity. Some I still have reactions to but others I don’t. After a year of eliminating all inflammatory foods, I added those I don’t have a sensitivity to back into my diet. I’ve had to be vigilant, though, since I got inflammation reactions from foods that are supposed to be anti inflammatory like leafy greens, and ginger & turmeric have a tendency to cause a rash if I over saturate my system with them.

Neurotoxin Diet: This diet was recommended to a friend by an Integrative Medicine doctor and she suggested I try it. It’s currently not well known. I believe the doctor is working on a book about it. The diet eliminates foods with high levels of heavy metals like arsenic in factory farmed chicken & rice, cyanide in tapioca, nuts, seeds, legumes, spinach, and mercury in certain varieties of fish. It also eliminates latex fruit (avocados, bananas, & mangoes) that have been artificially ripened with calcium carbide, artificial sweeteners, and MSG.

I tried this diet for about six months in 2011 but didn’t notice any changes in my health so I eventually reintroduced most of the foods back into my diet. I still don’t notice any harmful effects from these items other than soy, rice, and artificial sweeteners but those are for other reasons (soy changes my menstrual cycle due to hormone increases and rice & artificial sweeteners cause inflammation from the release of cytokines due to my MSH deficiency).

Medical Weight Loss Plan: The clinic I went to emphasized low calories, low fat, low carbohydrates, and high protein along with handfuls of supplements to make up for the nutrients not being obtained by food. It pushed a lot of things I don’t consider acceptable food items (highly processed whey or soy protein bars, protein powders, and snacks with artificial sweeteners). I focused on vegetables and meat.

I did this for about 3 months in 2011 after my weight loss plateaued. With Intracrainal Hypertension, weight loss was strongly recommended as a way to keep the cerebrospinal fluid drains in the neck open and avoid brain surgery. Nothing motives a person to lose weight like the threat of brain surgery. I lost about 15 pounds on the program and it kicked my metabolism back into weight loss mode even though I was miserable on the diet and my health continued to decline. I’m glad I did it but I know so much more about healthful eating and weight loss now than I did then. Between 2010-2011 I lost 60lbs. I regained 30lbs between 2012-2014 due to improving my malabsorption issues and increasing thyroid meds but the weight loss did help. Not only did the extra fluid in my skull start draining properly, reducing the pressure on my optic nerves, it also completely resolved my obstructive sleep apnea.

Specific Carbohydrate Diet(TM): This diet is supposed to improve gut health and has been around in one form or another since the 1950’s. It eliminates grains, starches, and sugars as well as processed foods. The theory behind it is that some people can’t digest complex carbohydrates so only monosaccharide carbohydrates are allowed.

Of all the diets I’ve tried, I had the hardest time with this one. While I understood the rules from a scientific standpoint, it was hard to remember exactly which carbohydrates were allowed. I only lasted two months on it. In that time I didn’t notice any improvements.

Modified Paleo/The Wahls Protocol(TM): This diet was created by an MD who healed her MS through a modified Paleo diet and Functional Medicine. The diet stresses eating 9 cups of non-starchy fruits and veggies per day: 3 cups of colored fruits & veggies (berries, beets, carrots, etc.), 3 cups of leafy greens, and 3 cups of sulfur veggies (cabbage, broccoli, cauliflower, garlic, onions). It focuses on organic, whole foods without additives like artificial sweeteners, pesticides, herbicides, and antibiotics. It eliminates all cereal grains, legumes, potatoes, refined sugar, refined vegetable oils, and limits dairy.

Dr. Wahls’ website was recommended on my first visit with my Integrative Medicine MD in 2012. I tried the diet for just over a month and ended it because I became sensitive to leafy greens & peppers and gained 20lbs. I think it’s a great diet for those with an autoimmune disease and a functioning gut but not so great for people like me who has MTHFR gene mutations affecting the processing of nutrients and other nutrient deficiencies that create food sensitivities. Her book “Minding My Mitochondria” was very informative and interesting, though. It lists the nutrients needed for optimal mitochondrial and cell function in the foods she recommends.

CORE Diet: This diet was recommended by a nutritionist in 2012. It’s both marketed as a weight loss diet as well as a way to eat well-balanced meals. It consists of food lists with average calorie counts per serving size for those who want to count calories as well as a Daily Plate chart that recommends each meal consist of 20% lean protein, 30% healthful fats like olive oil, coconut oil, avocados, and nuts/seeds, and 50% carbohydrates with an emphasis on vegetables and whole grains. It emphasizes quality (low sugar, low gluten, high fiber, organic), quantity (small frequent meals, portion control, minimum 2 fruits/3 non starchy veggies per day), timing (eat every 3-4 hours, last meal 2-3 hours before bed), and balance (protein and fat with every meal or snack). It can also be easily modified for carbohydrate restriction and vegetarians.

I still have the pages given to me by my nutritionist on the fridge. It’s a very sensible eating plan that can be modified for almost everyone. I never used it as much as I should have.

Rotation Diet: This diet is for people with multiple food sensitivities. It rotates food groups in a 4 day rotation in order to reduce new food sensitivities. Four days works better than 3, which I tried, because it gives the immune system enough time to eliminate antibodies from foods rather than keep building them up. There are no foods eliminated on this diet, only restrictions on what can be eaten on which days.

It took visits to two different nutritionists and food allergy blood testing for me to get a decent rotation diet that worked but it was one of the best things I did. I was on a rotation diet of one form or another for most of 2012-2014. I only recently stopped it as I feel that my nutrition levels are finally up to levels where my body is functioning properly enough that it can eliminate antibodies like it’s supposed to.

Low/No Amylose Diet: Amylose is a natural polymer made up of glucose that is broken down by the enzyme amylase that’s in saliva. Eliminating foods high in amylose and glucose helps burn fat without increasing blood sugar. It’s recommended by Dr. Shoemaker to help his mold patients both lose weight and balance hormones. It helps with leptin resistance, glucose resistance, and pre-diabetes. It’s similar to the Paleo diet and the Atkins diet only it’s less restrictive and much easier to understand than the Specific Carbohydrate Diet. It eliminates cereal grains except waxy corn, simple sugars including dextrins, starchy root vegetables including peanuts, bananas & plantains, and commercially prepared juices. It emphasizes no fasting or skipping meals and 6-8 ounces of protein per day.

I’ve been on the edge of pre-diabetes for years and there’s a family history of it. I did this diet for almost a year and the first six months I was very strict about it. I felt okay on it but didn’t lose weight and my fasting blood glucose levels didn’t decrease. It did, however, increase my Transforming Growth Factor Beta-1 levels.

Low Protein Diet: The absolute minimum protein a woman needs is 46 grams per day. A man needs 56 grams. Most people feel better with more, however, there are exceptions. Notably, people with kidney disease are often put on low protein diets. The only restrictions on this diet is the amount of protein.

My reading up on Transforming Growth Factor Beta-1 lead me to this diet. There’s studies that show low protein diets have positive effects on TGF-B1 levels and, since the medication I’ve taken since April hasn’t helped, I thought it was worth trying. An added benefit to this diet was I didn’t have to eliminate anything other than foods I get a reaction from (though I need to keep an eye on my blood glucose levels). The diet makes sense for me since TGF-B1 has been implicated in kidney disease as well as diabetic neuropathy. The reason diabetics are often put on medications to protect their kidneys is to keep TGF-B1 levels from rising. Those same medications are used to reduce TGF-B1 in kidney disease patients and mold/biotoxin patients.

 Shangri-La Diet: This weight loss diet was the idea of the late psychologist Seth Roberts, PhD. Besides experimenting on himself, he did in depth studies on it as well. The concept is based on the idea that the body stores more calories from familiar tasting foods than from neutral or unfamiliar foods and eating/drinking high caloric flavorless foods can reset the appetite controls in the brain, making it so a person eats less. There are no food restrictions on this diet but it does add 1-2 Tablespoons of flavorless oil or sugar/honey water twice a day. The oil/sugar gives the body the calories it needs to function without storing it as fat. The book recommends a person gets enough nutrients by taking multivitamins or other supplements.

I read the book in October. I started this diet around the same time I started the low protein diet and drastically changed my thyroid meds. So far I’ve lost 11lbs and I haven’t been following it as strictly as I could be (some days I only do 2 tbs of extra light olive oil once a day). I don’t feel deprived of food and I don’t have to count calories. I mostly eat nutrient dense foods for my two meals a day because quality of nutrients matters to me. Breakfast usually consists of a fruit smoothie and lunch/dinner is a roasted veggie blend with a small amount of meat or fish. My weight has fluctuated up and down depending on the dose of my thyroid meds since 2012. This is the longest I’ve maintained any weight loss since 2011 and I’m hopeful I can lose the rest of the extra weight I gained and maintain it thanks to this diet.

My Food Sensitivity History

I’ve had a complicated relationship with food since I was an infant that only increased as I got older. I now know that much of my food sensitivities were caused by my compounded heterozygous MTHFR gene mutations. Decreased ability to process folate and B12 from foods affects methylation and detoxification. This results in increased sensitivity to foods, drugs, and environmental stimuli. MTHFR gene mutations are often the root cause of Multiple Chemical Sensitivity.

My first major food sensitivity noticed by my mom was to cow’s milk. It would cause sinus drainage and excess phlegm. Cheese didn’t cause such a dramatic reaction but milk did. Unlike most children I didn’t grow up on cold cereal and glasses of milk. It improved as I got older, most likely because I had allergy shots from age 10 to age 22, but worsened in 2008. My 5 year anniversary gift from my job was an ice cream/sorbet maker. I spent months making and eating ice cream, most of it milk based. I started getting pain in my right side that worsened. Gallbladder issues were suspected but none of the tests showed gallbladder problems. In 2009 I finally connected the pain to dairy consumption and eliminated it from my diet. This July I reached the one year mark on the current round of allergy shots and my allergist assured me that the sinus issues from dairy should be resolved.  I started adding dairy back into my diet, mostly in the form of cheese, and it’s going okay. My sinuses do better with cooked dairy and I have to limit the amount I eat or the pain in my side returns but it’s not something I have to watch strictly. I still use coconut or almond milk as a milk substitute in most recipes and I doubt I’ll ever return to using milk or cream. Cheese, though, is much harder to substitute.

The second food I reacted to as a child was chocolate. At age 7 or 8, I ate too much and broke out in hives. I had to be very careful about the amount of chocolate I had until after the eight month course of Prednisone I was on in 2010-2011. Since then I haven’t had a problem with chocolate. At least one good thing came out of that drug experience.

My last childhood food sensitivity was to sugar. When I was around 10 we made doughnuts and I was dipping them in a confectioner’s sugar glaze, often licking my fingers. Before too long I had an asthma attack. Sensitivity to sugar is pretty common in my family. My dad gets stomach aches if he eats too much and my sister gets a horrible barking cough that kept her out of elementary school for a month. My tolerance level to sugar was fairly high and lemon juice was a good counteracting agent if I ate too much. Then in 2010 my hands would swell if I had sugar and I’d experience increased pain and  inflammation in joints I’ve damaged. I eliminated it from my diet. I tried to add it back in last year but the pain in my SI joints/hips increased and I felt like I was in a mini myalgia flare. Eliminating sugar again decreased the pain.

I didn’t have any major issues with other foods until after college. My first job after college was working at the salad bar of a grocery store. We were encouraged to sample the fruits we cut up to test for ripeness. By the end of the nine months I worked there I couldn’t eat any fruits or berries except lemons and bananas without my eyes swelling and itching, and breaking out in a rash. For awhile I couldn’t even touch acidic foods like pineapples or hot peppers. This lasted from 1996 to 2009. It took a couple more years before I was able to eat tomatoes again.

It’s still kind of a mystery why I reacted to the next foods. Starting in 2000 every time I ate pork I had terrible gastrointestinal issues. Bacon was the exception. Then in 2003 I had the same reaction to beef, elk, deer, wild boar, and buffalo. Originally we thought it was due to hormones but I reacted to wild game and organic meats, too. This reaction continued until 2010. With mitochondrial dysfunction there are sometimes issues with protein metabolism. Another possibility is my liver dysfunction decreased protein metabolism. Currently I’m okay with most forms of protein except canned legumes. Fresh, frozen, and dried are fine just not canned. The only thing I can think is that canning changes the protein structure of them in some way that my body can’t handle.

In 2010 after the worst of my myalgia flare was under control, I noticed inflammation reactions to more foods. I suspect the mold illness and dysregulation of inflammatory cytokines have a lot to do with it. Wheat/gluten and potatoes besides sugar made my hands swell so I eliminated them. Soy changed my menstrual cycles so I eliminated it. In 2012 before I started the supplement regime that helped my methylation errors, I tried Dr. Terry Wahls’ modified Paleo diet for autoimmune diseases. I saturated my system with too many leafy greens and peppers and got the same pain in my right side from them that I got from dairy. I eliminated them. This year I was slowly adding grains back into my diet after being on a grain free diet and noticed that I got an inflammation reaction from rice. It is now out of my diet. One the plus side, I was able to add potatoes, leafy greens, and peppers in moderation back in last year and my tolerance to sugar is a little higher than it was.

Looking back at all the foods I had to eliminate due to adverse reactions it’s not surprising I had nutrient deficiencies. Vitamins are obtained from food sources since the body can’t create them itself. I eliminated major sources of vitamin C and antioxidants (fruits & berries), B1 (pork & whole grains), B12 (red meat & dairy), and folate/folic acid (leafy greens & enriched wheat products). Even if I didn’t have MTHFR gene mutations, decreased microbes in my gut due to Prednisone and antibiotic use, and MSH deficiency from mold illness, I probably would have had nutrient deficiency issues, just not quite so severe as to cause Mitochondrial Dysautonomia.

Overall my food sensitivities have improved a great deal and there’s hope that once I’m completely healed from mold/biotoxin illness the rest of them will improve as well. In a later post I’ll discuss in more detail the various diets I’ve tried to improve my health, including rotation diets meant to avoid any further food sensitivities.