Clinic Wellness Team. A key factor to spine or back pain conditions is staying healthy. Overall wellness involves a balanced diet, appropriate exercise, physical activity, restful sleep, and a healthy lifestyle. The term has been applied in many ways. But overall, the definition is as follows.
It is a conscious, self-directed, and evolving process of achieving full potential. It is multidimensional, bringing together lifestyles both mental/spiritual and the environment in which one lives. It is positive and affirms that what we do is, in fact, correct.
It is an active process where people become aware and make choices towards a more successful lifestyle. This includes how a person contributes to their environment/community. They aim to build healthier living spaces and social networks. It helps in creating a person’s belief systems, values, and a positive world perspective.
Along with this comes the benefits of regular exercise, a healthy diet, personal self-care, and knowing when to seek medical attention. Dr. Jimenez’s message is to work towards being fit, being healthy, and staying aware of our collection of articles, blogs, and videos.
Bernadette Banda informs her compelling weight loss story while she clarifies how much her life has changed since she discovered the right fitness regimen with Dr. Alex Jimenez and Daniel “Danny” Alvarado in PUSH Fitness. PUSH became Bernadette Banda’s life philosophy, where she took it on herself never to give up and to always “push” herself towards any fitness goal she wished to attain. With tremendous gratitude, Bernadette Banda praises Danny’s and all the other coach’s efforts and support to help her become healthy.
Chiropractic Weight Loss Treatment
Intentional weight loss is the decrease in total body mass because of attempts to improve fitness and wellness. Weight loss in people who are overweight or obese can decrease health risks, increase health, and may delay the onset of diabetes. It may decrease pain and increase movement in people with osteoarthritis of the knee. Weight reduction may result in a drop in hypertension. Weight loss occurs when the body is expending more energy in metabolism than it’s swallowing from meals or additional nutrients. It is going to then use stored reserves from fat or muscle, slowly resulting in weight loss.
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and/or we have helped you in any way please feel free to subscribe and share us.
Concussions are traumatic brain injuries that affect brain function. Effects from these injuries are often temporary but can include headaches, problems with concentration, memory, balance and coordination. Concussions are usually caused by a blow to the head or violent shaking of the head and upper body. Some concussions cause loss of consciousness, but most do not. And it is possible to have a concussion and not realize it. Concussions are common in contact sports, such as football. However, most people gain a full recovery after a concussion.
Can also happen due to excessive shaking of the head or acceleration/deceleration
Mild injuries (mTBI/concussions) are the most common type of brain injury
Glasgow Coma Scale
Common Causes Of Concussion
Motor vehicle collisions
Falls
Sports injuries
Assault
Accidental or intentional discharge of weapons
Impact with objects
Prevention
Prevention of concussive injuries can be paramount
Encourage Patients To Wear Helmets
Competitive sports, especially boxing, hokey, football and baseball
Horseback riding
Riding bicycles, motorcycles, ATVs, etc.
High elevation activates such as rock climbing, zip lining
Skiing, snowboarding
Encourage Patients To Wear Seatbelts
Discuss the importance of wearing seatbelts at all times in vehicles with all of your patients
Also encourage use of appropriate booster or car seats for children to ensure adequate fit and function of seat belts.
Driving Safely
Patients should never drive while under the influence of drugs, including certain medications or alcohol
Never text and drive
Make Spaces Safer For Children
Install baby gates and window latches in the home
May in areas with shock-absorbing material, such as hardwood mulch or sand
Supervise children carefully, especially when they�re near water
Prevent Falls
Clearing tripping hazards such as loose rugs, uneven flooring or walkway clutter
Using nonslip mats in the bathtub and on shower floors, and installing grab bars next to the toilet, tub and shower
Ensure appropriate footwear
Installing handrails on both sides of stairways
Improving lighting throughout the home
Balance training exercises
Balance Training
Single leg balance
Bosu ball training
Core strengthening
Brain balancing exercises
Concussion Verbiage
Concussion vs. mTBI (mild traumatic brain injury)
mTBI is the term being used more commonly in medical settings, but concussion is a more largely recognized term in the community by sports coaches, etc.
The two terms describe the same basic thing, mTBI is a better term to use in your charting
Evaluating Concussion
Remember that there does not always have to be loss of consciousness for there to be a concussion
Post-Concussion Syndrome can occur without LOC as well
Symptoms of concussion may not be immediate and could take days to develop
Monitor for 48 post head injury watching for red flags
Blurred eyesight or other vision problems, such as dilated or uneven pupils
Confusion
Dizziness
Ringing in the ears
Nausea or vomiting
Slurred speech
Delayed response to questions
Memory loss
Fatigue
Trouble concentrating
Continued or persistent memory loss
Irritability and other personality changes
Sensitivity to light and noise
Sleep problems
Mood swings, stress, anxiety or depression
Disorders of taste and smell
Mental/Behavioral Changes
Verbal outbursts
Physical outbursts
Poor judgment
Impulsive behavior
Negativity
Intolerance
Apathy
Egocentricity
Rigidity and inflexibility
Risky behavior
Lack of empathy
Lack of motivation or initiative
Depression or anxiety
Symptoms In Children
Concussions can present differently in children
Excessive crying
Loss of appetite
Loss of interest in favorite toys or activities
Sleep issues
Vomiting
Irritability
Unsteadiness while standing
Amnesia
Memory loss and failure to form new memories
Retrograde Amnesia
Inability to remember things that happened before the injury
Due to failure in recall
Anterograde Amnesia
Inability to remember things that happened after the injury
Due to failure to formulate new memories
Even short memory losses can be predictive of outcome
Amnesia may be up to 4-10 times more predictive of symptoms and cognitive deficits following concussion than is LOC (less than 1 minute)
Return To Play Progression
Baseline: No Symptoms
As the baseline step of the Return to Play Progression, the athlete needs to have completed physical and cognitive rest and not be experiencing concussion symptoms for a minimum of 48 hours. Keep in mind, the younger the athlete, the more conservative the treatment.
Step 1: Light Aerobic Activity
The Goal: Only to increase an athlete�s heart rate.
The Time: 5 to 10 minutes.
The Activities: Exercise bike, walking, or light jogging.
Absolutely no weight lifting, jumping or hard running.
Step 2: Moderate activity
The Goal: Limited body and head movement.
The Time: Reduced from typical routine.
The Activities: Moderate jogging, brief running, moderate-intensity stationary biking, and moderate-intensity weightlifting
Step 3: Heavy, non-contact activity
The Goal: More intense but non-contact
The Time: Close to typical routine
The Activities: Running, high-intensity stationary biking, the player�s regular weightlifting routine, and non- contact sport-specific drills. This stage may add some cognitive component to practice in addition to the aerobic and movement components introduced in Steps 1 and 2.
Step 4: Practice & full contact
The Goal: Reintegrate in full contact practice.
Step 5: Competition
The Goal: Return to competition.
Microglial Priming
After head trauma microglial cells are primed and can become over active
To combat this, you must mediate the inflammation cascade
Prevent repeated head trauma
Due to priming of the foam cells, response to follow-up trauma may be far more severe and damaging
What Is Post-Concussion Syndrome (PCS)?
Symptoms following head trauma or mild traumatic brain injury, that can last weeks, months or years after injury
Symptoms persist longer than expected after initial concussion
More common in women and persons of advanced age who suffer head trauma
Severity of PCS often does not correlate to severity of head injury
PCS Symptoms
Headaches
Dizziness
Fatigue
Irritability
Anxiety
Insomnia
Loss of concentration and memory
Ringing in the ears
Blurry vision
Noise and light sensitivity
Rarely, decreases in taste and smell
Concussion Associated Risk Factors
Early symptoms of headache after injury
Mental changes such as amnesia or fogginess
Fatigue
Prior history of headaches
Evaluation Of PCS
PCS is a diagnosis of exclusion
If patient presents with symptoms after head injury, and other possible causes have been ruled out => PCS
Use appropriate testing and imaging studies to rule out other causes of symptoms
Headaches In PCS
Often �tension� type headache
Treat as you would for tension headache
Reduce stress
Improve stress coping skills
MSK treatment of the cervical and thoracic regions
Constitutional hydrotherapy
Adrenal supportive/adaptogenic herbs
Can be migraine, especially in people who had pre-existing migraine conditions prior to injury
Reduce inflammatory load
Consider management with supplements and or medications
Reduce light and sound exposure if there is sensitivity
Dizziness In PCS
After head trauma, always assess for BPPV, as this is the most common type of vertigo after trauma
Dix-Hallpike maneuver to diagnose
Epley�s maneuver for treatment
Light & Sound Sensitivity
Hypersensitivity to light and sound is common in PCS and typically exacerbates other symptoms such as headache and anxiety
Management of excess mesencephalon stimulation is crucial in such cases
Sunglasses
Other light blocking glasses
Earplugs
Cotton in ears
Treatment Of PCS
Manage each symptom individually as you otherwise would
Manage CNS inflammation
Curcumin
Boswelia
Fish oil/Omega-3s � (***after r/o bleed)
Cognitive behavioral therapy
Mindfulness & relaxation training
Acupuncture
Brain balancing physical therapy exercises
Refer for psychological evaluation/treatment
Refer to mTBI specialist
mTBI Specialists
mTBI is difficult to treat and is an entire specialty both in the allopathic and complementary medicine
Primary objective is to recognize and refer for appropriate care
Pursue training in mTBI or plan to refer to TBI specialists
Sources
�A Head for the Future.� DVBIC, 4 Apr. 2017, dvbic.dcoe.mil/aheadforthefuture.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
�Heads Up to Health Care Providers.� Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 16 Feb. 2015, www.cdc.gov/headsup/providers/.
�Post-Concussion Syndrome.� Mayo Clinic, Mayo Foundation for Medical Education and Research, 28 July 2017, www.mayoclinic.org/diseases-conditions/post- concussion-syndrome/symptoms-causes/syc-20353352.
Pain Anxiety Depression�Everyone has experienced pain, however, there are those with depression, anxiety, or both. Combine this with pain and it can become pretty intense and difficult to treat. People that are suffering from depression, anxiety or both tend to experience severe and long term pain more so than other people.
The way anxiety, depression, and pain overlap each other is seen in chronic and in some disabling pain syndromes, i.e. low back pain, headaches, nerve pain and fibromyalgia. Psychiatric disorders contribute to the pain intensity and also increase the risk of disability.
Depression:�A (major depressive disorder or clinical depression) is a common but serious mood disorder. It causes severe symptoms that affect how an individual feels, thinks, and how the handle daily activities, i.e. sleeping, eating and working. To be diagnosed with depression, the symptoms must be present for at least two weeks.
Persistent sad, anxious, or �empty� mood.
Feelings of hopelessness, pessimistic.
Irritability.
Feelings of guilt, worthlessness, or helplessness.
Loss of interest or pleasure in activities.
Decreased energy or fatigue.
Moving or talking slowly.
Feeling restless & having trouble sitting still.
Difficulty concentrating, remembering, or making decisions.
Thoughts of death or suicide & or suicide attempts.
Aches or pains, headaches, cramps, or digestive problems without a clear physical cause and/or that do not ease with treatment.
Not everyone who is depressed experiences every symptom. Some experience only a few symptoms while others may experience several. Several persistent symptoms in addition to low mood are�required�for a diagnosis of major depression. The severity and frequency of symptoms along with the duration will vary depending on the individual and their particular illness. Symptoms can also vary depending on the stage of the illness.
PAIN ANXIETY DEPRESSION
Objectives:
What is the relationship?
What is the neurophysiology behind it?
What are the central consequences?
Brain Changes In Pain
Figure 1 Brain pathways, regions and networks involved in acute and chronic pain
Davis, K. D. et al. (2017) Brain imaging tests for chronic pain: medical, legal and ethical issues and recommendations Nat. Rev. Neurol. doi:10.1038/nrneurol.2017.122
PAIN, ANXIETY AND DEPRESSION
Conclusion:
Pain, especially chronic is associated with depression and anxiety
The physiological mechanisms leading to anxiety and depression can be multifactorial in nature
Pain causes changes in brain structure and function
This change in structure and function can alter the ability for the brain to modulate pain as well as control mood.
Autoimmunity:�One of the most common things is to leave the doctor�s office with a diagnosis of an autoimmune disease and no nutritional or lifestyle changing insight. Autoimmune diseases are related to inflammation. Keeping� the inflammation down is the goal with autoimmune attacks. The foods you eat make a huge difference in the frequency and severity of flare-ups. Steady dietary changes can help you reach your optimal self.
Is Autoimmune Disease A Result Of The Collective Perturbations Of The Exposome & Its Impact On The Immunometabolic System?
The western diet is associated with inflammation, and inflammation is central to autoimmunity and autoimmune diseases. Keeping the inflammation down can help in lengthening time between attacks. What to eat and what not to eat are the common questions. In order to quiet� inflammation triggers, educate ourselves and live a normal life is the focus.
My 2006 Seminar Series
�Understanding the Origins of Autoimmune Disease�
Autoimmunity:
The Central Question I Asked In This series,
Are We Allergic to Ourselves?
� Autoantibodies
� Are they really �autoantibodies�?
� Self or Non?self?
I would like to re?explore this question using what we have learned in 2018.
Presence of Anti?Chromatin, DNA and RNA Antibodies
What Biological Processes May Make Self Into Non?Self?
Post?translationalmodificationofProtein � Glycation of protein � Protein Oxidation � Amino Acid Conjugation of Protein (Citrullinated Protein/AntiCCP and RA)
ProteinSynthesisErrors
DNA and RNA Changes � Radiation Induced Crosslinking of DNA � Oxidation of DNA � Copy Errors not corrected by DNA repair process � Epigenetic Changes (the methylome)
Where Do Anti?Cyclic Citrullinated Peptides (AntiCCPs) Come From?
Activation of the immune system resulting in increased iNOS production of nitric oxide
Arginine residues in proteins can be converted in situ into citrulline with the release of nitric oxide by iNOS
The citrulline produced in the protein is now �foreign� and can be recognized by the immune system as such
Antibodies can then be produced against this �foreign protein�
Disease Modifying Anti?Rheumatic Drugs (DMARDs)
The Facts on Methotrexate For Rheumatoid Arthritis Treatment
Methotrexate is the most commonly prescribed drug to treat rheumatoid arthritis, yet it only helps about half of those who try it. Find out how it works and how to lessen its side effects.
Folate Inhibition To Block Immune Cell Proliferation
Food:�Genes that determine illness are triggered by what we put into our bodies, literally what we eat. Our cells are literally created out of the foods we put into our bodies. Like most people do, we are likely eating nutrient-poor foods that create damaged dysfunctional cells. When we learn to eat foods that nourish the body, our cells repair themselves, and the new cells created will be optimal functioning cells.
Unhealthy foods create chronic inflammation, which is destructive to the body. Inflammation is normally the body�s healthy response to injury or infection. However, when inflammation becomes chronic, from constant assault on the gut by consuming the wrong foods, inflammation becomes the cause of destructive diseases, i.e. Lupus, Rheumatoid Arthritis, Colitis and other inflammatory diseases.
Disclosure
Terry Wahls, MD disclosed no relevant financial relationships with any commercial interest.
The two routes by which diet can influence our health:
(A) the metabolism of our cells and
(B) the population of our gut microbiota.
Paolo Riccio, and Rocco Rossano ASN Neuro
2015;7:1759091414568185
Copyright � by SAGE Publications Inc, or the American Society for Neurochemistry, unless otherwise noted.
Manuscript content on this site is licensed under Creative Commons Licenses.
1. Review of MS patient survival on a Swank low saturated fat diet. Nutrition. 2003 Feb;19(2):161-2. Review.
2. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet. 1990 Jul 7;336(8706):37-9.
3. Multiple sclerosis: twenty years on low fat diet. Arch Neurol. 1970 Nov;23(5):460-74
Low-Fat, Plant-Based Diet In Multiple Sclerosis: A Randomized
Controlled Trial
This was a randomized-controlled, assessor- blinded, one-year long study
1. Voitk AJ, Echave V, Feller JH, et, al: Experience with elemental diet in the treatment of inflammatory bowel disease. Is this primary therapy? Arch Surg, 1973;107: 329-333.
2. Tim LO, Odes HS, Duys PJ, et al. The use of an elemental diet in gastrointestinal diseases. S Afr Med J,1976;50: 1752-1756
3. Zoli G, Care? M, Parazza M et al, A randomized controlled study comparing elemental diet and steroid treatment in Crohn’s disease. Aliment
Pharmacol Ther. 1997 Aug;11(4):735-40.
4. Zachos M, Tondeur M, Griffiths AM. Enteral nutritional therapy for induction of remission in Crohn�s disease. Cochrane Database Syst Rev, 2007
January 24;(1)
5. Podas T, Nightingale JM, Oldham R, et al, Is rheumatoid arthritis a disease that starts in the intestine? A pilot study comparing an elemental diet with
oral prednisolone. Postgrad Med J. 2007 Feb;83(976):128-31
6. Podas T, Nightingale JM, Oldham R, et al, Is rheumatoid arthritis a disease that starts in the intestine? A pilot study comparing an elemental diet with
oral prednisolone. Postgrad Med J. 2007 Feb;83(976):128-31
Exclusion Diets
Eliminated specific protein sources � RA Sx ?
Raw vegan, vegan and gluten free vegan
Systematic review of 14 RCTs
Dietary benefits uncertain
Small studies with risk of bias
1. Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, Laerum E, Eek M, Mowinkel P, Hovi K, F�rre O. Controlled trial of fasting and one-year vegetarian diet in rheumatoid arthritis. Lancet. 1991 Oct 12;338(8772):899-902.
2. Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, F�rre Vegetarian diet for patients with rheumatoid arthritis–status: two years after introduction of the diet. Clin Rheumatol. 1994 Sep;13(3):475-82
3. McDougall J, Bruce B, Spiller G, et al, Effects of a very low-fat, vegan diet in subjects with rheumatoid arthritis. J Altern Complement Med. 2002 Feb;8(1):71-5
4. Hafstro?m I, Ringertz B, Spa?ngberg A, et. al, A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford). 2001 Oct;40(10):1175-9.
5. Hagen KB, Byfuglien MG, Falzon L, et, al. Dietary interventions for rheumatoid arthritis. Cochrane Database Syst Rev. 2009 Jan 21;(1):
6. Smedslund G, Byfuglien MG, Olsen SU, et. al, Effectiveness and safety of dietary interventions for rheumatoid arthritis: a systematic review of
randomized controlled trials. J Am Diet Assoc. 2010 May;110(5):727-35
Exclusion Diets
Atopic dermatitis improved n=20
UC � fewer symptoms n=18
Crohn�s food sensitivities identified in half n=42
Antibody cross-reactivity between myelin oligodendrocyte glycoprotein and the milk protein butyrophilin in MS – Inducing antibodies reacting with myelin oligodendrocyte glycoprotein (MOG) and Cerebellar peptides
Liquid cow milk (not cheese) and MS prevalence was highly correlated (rho = 0.836) across 27 countries and 29 populations.
�By eliminating lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.�
1. Lindeberg, S., Jo?nsson, T., Granfeldt, Y. et al. Diabetologia (2007) 50: 1795. doi:10.1007/s00125-007-0716-y
2. O?sterdahl M, Kocturk T, Koochek A, Wa?ndell PE. Effects of a short-term intervention with a paleolithic diet in healthy volunteers. European Journal of
Clinical Nutrition. 2007;62(5):682�685. doi:10.1038/sj.ejcn.1602790.
3. Jo?nsson T, Granfeldt Y, Ahre?n B, et al. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovascular Diabetology. 2009;8:35. doi:10.1186/1475-2840-8-35.
4. Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter- gatherer type diet. European Journal of Clinical Nutrition. 2009;63(8):947�955. doi:10.1038/ejcn.2009.4.
5. Halberg N, Henriksen M, So?derhamn N, et. al, Effect of intermittent fasting and refeeding on insulin action in healthy men. J Appl Physiol (1985). 2005 Dec;99(6):2128-36.
6. Ryberg M, Sandberg S, Mellberg C, et al. A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women. Journal of Internal Medicine. 2013;274(1):67�76. doi:10.1111/joim.12048.
7. Ruiz-Nu?n?ez B, Dijck-Brouwer DAJ, Muskiet FAJ. The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. The Journal of Nutritional Biochemistry. January 2016. doi:10.1016/j.jnutbio.2015.12.007.
8. Otten J, Stomby A, Waling M, et al. Benefits of a Paleolithic diet with and without supervised exercise on fat mass, insulin sensitivity, and glycemic control: A randomized controlled trial in individuals with type 2 diabetes. Diabetes/Metabolism Research and Reviews. January 2016. doi:10.1002/dmrr.2828.
9. Konijeti GG1, Kim N, Lewis JD, Groven S, Chandrasekaran A. Efficacy of the Autoimmune Protocol Diet for Inflammatory Bowel Disease. Inflamm Bowel Dis. 2017 Aug 29. doi: 10.1097/MIB.0000000000001221.
10. Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012;5:175-89.
11. Eaton SB, Konner MJ, Cordain L. Diet-dependent acid load, Paleolithic nutrition, and evolutionary health promotion. Am J Clin Nutr. 2010;91:295-7. Andersson A, et al. Whole?grain foods do not affect insulin sensitivity or markers of lipid peroxidation and inflammation in healthy, moderately overweight subjects. J Nutr.2007 Jun;137(6):1401?7.
12. Tighe P, et al. Effect of increased consumption of whole ? grain foods on blood pressure and other cardiovascular risk markers in healthy middle?aged persons: a randomized controlled trial. Am J Clin Nutr. 2010 Oct;92(4):733?40.
13. Brownlee IA, et al. Markers of cardiovascular risk are not changed by increased whole?grain intake: the WHOLEheart study, a randomised, controlled dietary intervention. Br J Nutr. 2010 Jul;104(1):125?34.
14. Masters RC, et al. Whole and refined grain intakes are related to inflammatory protein concentrations in human plasma. J Nutr. 2010 Mar;140(3):587?94.
15. Katcher HI, et al. The effects of a whole grain-enriched hypocaloric diet on cardiovascular disease risk factors in men and women with metabolic syndrome. Am J Clin Nutr. 2008 Jan;87(1):79?90.
Nutrient Triage
Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage.
Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose response meta-analysis of prospective cohort studies.
16 studies – 833,234 participants
Risk Of All Cause Mortality Associated With Servings/Day Of Fruit & Vegetables
Dose-Response Relation Between Fruit & Vegetable Consumption & Risk Of All Cause Mortality
BMJ. 2014; 349: g4490.
1. Neuroprotective Effect of Brassica oleracea Sprouts Crude Juice in a Cellular Model of Alzheimer’s Disease. Med Cell Longev.2015;2015:781938
2. Learning and memory promoting effects of crude garlic extract. Indian J Exp Biol.2013 Dec;51(12):1094-100.
3. Enhancement of the neuroprotective activity of Hericium erinaceus mycelium co-cultivated with Allium sativum extract. Arch Physiol Biochem.2015 Feb;121(1):19-25.
4. Mori K, Obara Y, Hirota M, Azumi Y, Kinugasa S, Inatomi S, Nakahata N. Nerve growth factor-inducing activity of Hericium erinaceus in 1321N1 human astrocytoma cells. Biol Pharm Bull. 2008 Sep;31(9):1727-32.
5. Lee DH, Kim HW. Innate immunity induced by fungal ?-glucans via dectin-1 signaling pathway. Int J Med Mushrooms. 2014;16(1):1-16.
6. Akramiene D, Kondrotas A, Didziapetriene J, Kevelaitis E Effects of beta-glucans on the immune system. Medicina (Kaunas).2007;43(8):597-606.
7. Lai PL, Naidu M,Sabaratnam V,Wong K, DaviP, Kuppusamy UR, Abdullah N, Malek SN. Neurotrophic properties of the Lion’s mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia Int J Med Mushrooms.2013;15(6):539-54.
8. Phan CW, David P, Naidu M, Wong KH, Sabaratnam V. Therapeutic potential of culinary-medicinal mushrooms for the management of neurodegenerative diseases: diversity, metabolite, and mechanism. Crit Rev Biotechnol.2015;35(3):355-68.
9. Scientifica (Cairo).2016;2016:3109254.
10. Berry antioxidants: small fruits providing large benefits. J Sci Food Agric.2014 Mar 30;94(5):825-33
11. Dietary and plant polyphenols exert neuroprotective effects and improve cognitive function in cerebral ischemia. Recent Pat Food Nutr Ag. 2013 Aug;5(2):128-43.
12. The impact of fruit flavonoids on memory and cognition. Br J Nutr.2010 Oct;104 Suppl 3:S40-7. d
13. Grape juice, berries, and walnuts affect brain aging and behavior. J Nutr. 2009 Sep;139(9):1813S-7S.
14. Fruit polyphenolics and brain aging: nutritional interventions targeting age-related neuronal and behavioral deficits. Ann N Y Acad Sci.2002 Apr;959:128-32.
15. Reversing the deleterious effects of aging on neuronal communication and behavior: beneficial properties of fruit polyphenolic compounds. Am J Clin Nutr.2005 Jan;81(1 Suppl):313S-316S.
16. Krikorian R, Shidler MD, Nash TA, Kalt W, Vinqvist-Tymchuk MR, Shukitt-Hale B, Joseph JA. Blueberry supplementation improves memory in older adults. J Agric Food Chem.2010 Apr 14;58(7):3996-4000.
17. Funding for the studies was provided by the US Highbush Blueberry Council, the National Institute on Aging, and Wild Blueberries of North America. Dr. Krikorian has disclosed no relevant financial relationships.
18. Lobo GP Amengual J, Baus D, Shivdasani RA Genetics and diet regulate vitamin A production via the homeobox transcription factor ISX. J Biol Chem.2013 Mar 29;288(13):9017-27
?-carotene Is Not Retinol (Vitamin A)
?-Carotene is converted to vitamin A in the intestine by the enzyme ?-carotene-15,15′- monoxygenase (BCMO1) to support vision, reproduction, immune function, and cell differentiation.
Considerable variability in BCMO1 exists and can effect individual vitamin A status
Nutritional Adequacy (%RDA) US Diet Vs. Study Diet
Multimodal Intervention Improves Quality Of Life
Mood & Cognition
In the setting of progressive MS Improved thinking ability and reduced anxiety and reduced depression
Average daily servings of the study diet recommended (vegetables/fruits) and excluded (gluten/dairy/eggs) foods p < 0.01 difference from baseline to 12 months
Average Scores On The Mood Measures At Each Study Visit
Average Scores On The DKEFS & WAIS Sub-Scales At Each Study Visit.
Relapsing Remitting MS
Reduce Fatigue
?Mental & Physical QoL 16% (> 5 points)
Improved Motor Function
A Simplified Model Of FMD?Mediated Effects On Glucocorticoid, Immune Suppression & Oligodendrocyte Regeneration & Differentiation In MS
N=60 6 Month Human Clinical Trial
FMD 100 ml broth, 1 T flax oil tid, 200 � 350 Kcal, Plus enema as needed 7 days Mediterranean diet
Ketogenic(KD) 160gmfatm<100gPro,<50g CHO
Usual diet
Change at 3 month of (k) overall quality of life, (l) change in health, (m) physical health composite, and (n) mental health composite. The dotted line represents a threshold that is thought to be clinically important
The Two Routes By Which Diet Can Influence Our Health:
(A) the metabolism of our cells and
(B) the population of our gut microbiota.
Paolo Riccio, and Rocco Rossano ASN Neuro
2015;7:1759091414568185
Copyright � by SAGE Publications Inc, or the American Society for Neurochemistry, unless otherwise
noted. Manuscript content on this site is licensed under Creative Commons Licenses.
Gut Brain Immune Axis
Gut microbiota influence the brain and immune system balance
Diet influences the microbiome strongly
Exercise, sleep, stress level also important
Changes in the colon mucosa every early in the disease process
The composition of gut microbiota is influenced by multiple factors, such as diet and host genotype. Within the gut, ecological processes such as selection and evolution take place. The use of antibiotics reduces the numbers and diversity of gut microbiota.
Higher quality diet (food), stress reduction, movement � are relatively safe with large favorable benefits for all cause mortality
3 month trial of a grain free, dairy free, sugar free vegetable rich (or gluten free vegetarian) diet is relatively safe with potential for many favorable benefits
Autoimmunity is the reaction of cells (lymphocytes) or antibodies�of the immune system along with the body�s own tissues leading to certain pathology. Autoimmunity can produce various conditions, which depend upon the target of the attack.�While intrinsic factors, which include age, sex, and genetics contribute to autoimmunity, it is believed that extrinsic factors such as drugs, chemicals, microbes, and/or the environment can trigger the initiation of autoimmune responses.
Autoimmune Disease & Environmental Toxicants
Educational Objectives
Review air pollution, cigarette smoking, and citrullination as models for the genesis of autoimmune disease
Explore the role of general cell stressors in autoimmune disease
Discuss the impact of lung and gut barrier disruption by environmental toxins and food additives in autoimmune disease
Utilize the Functional Medicine ATM model to illustrate the various mechanisms by which toxicants could contribute to the pathophysiology of autoimmune disease.
�Mild forms of the autoimmune response probably occur naturally in most people. But, for people with a predisposition to autoimmunity, environmental factors, such as toxic chemicals, drugs, bacteria or viruses, may trigger a full?fledged response.�
�NOVEL CRYSTAL BALL: One day Y?shaped molecules called autoantibodies in a patient�s blood may tell doctors whether a patient is �brewing� certain diseases and may even indicate roughly how soon the individual will begin to feel symptoms.�
Autoimmune Disease: �Delayed Gratification�
Scientific American, March, 2007
Many autoimmune diseases do not develop spontaneously, but instead evolve through an extended germination period before they become clinically evident…
Well over 10 million people test positive for ANA, years before they have any symptoms.
This implies the presence of additional environmental factors that dampen or amplify the process over time.
Arbuckle MR, et al, N Engl J Med. 2003 Oct 16;349(16):1526?33.
Elevated Levels Of Antibodies Against Xenobiotics In A Subgroup Of Healthy Subjects
Vojdani, A, Kharrazian, D, Mukherjee, PS
Some environmental chemicals, acting as haptens, can bind to a high? molecular?weight carrier protein such as human serum albumin (HSA), causing the immune system to misidentify self?tissue as an invader and launch an immune response against it, leading to autoimmunity
The levels of specific antibodies against 12 different chemicals bound to HSA were measured by ELISA in serum from 400 blood donors.
10% (IgG) and 17% (IgM) of tested individuals showed significant antibody elevation against aflatoxin?HSA adduct.
The percentage of elevation against the other 11 chemicals ranged from 8% to 22% (IgG) and 13% to 18% (IgM).
Detection of antibodies against various protein adducts may indicate chronic exposure to these chemical haptens in about 20% of the tested individuals
J Appl Toxicol. 2015 Apr; 35(4): 383�397.
Could Environmental Toxins Be A Key Missing Link That Pushes The Immune System Over The Brink To Permanently Lose Control Of Its Tolerance To Self?Antigens?
(A Corollary Question: Does The Persistent Presence Of Autoantibodies Or Autoreactive T Cells Imply An Inevitable Progression To Full?Blown Autoimmune Disease?)
Rheumatoid Arthritis: Swan neck deformity from chronic synovitis
Anti?Cyclic Citrullinated Peptide Antibody
Current method is 96% specific for RA
Elevated titers detected >10 years before onset of clinical disease
Sensitivity (likelihood of positive test) increases from 50% at Dx to >75% over course of disease
Likely involved in pathogenesis
Citrullinated Ags are highly expressed in inflamed joints
Citrulline is formed by posttranslational modification of arginine residues by peptidyl arginine deiminases (PADs)
PADs are upregulated by inflammation, injury, and toxicants
Inflammation and injury thus increases citrullination of multiple synovial proteins
Multiple HLA?DR variants (shared epitope) associated with RA preferentially display citrullinated Ags on MHCII � activating citrulline?specific autoreactive T cells
Smoking increases risk of +anti?CCP when coupled with HLR?DR shared epitope
Floris van Gaalen et al. J Immunol 2005;175:5575-5580
Autoimmunity To Specific Citrullinated Proteins Gives The First Clues To The Etiology Of Rheumatoid Arthritis
Four citrullinated whole protein antigens, fibrinogen, vimentin, collagen type II, and alpha?enolase, are now well established, with others awaiting further characterization All four proteins are expressed in the joint, and there is evidence that antibodies to citrullinated fibrinogen and collagen type II mediate inflammation by the formation of immune complexes Antibodies to citrullinated proteins are associated with HLA ‘shared epitope’ alleles
Porphyromonas gingivalis, pathogenic bacteria that is a major cause of periodontal disease, expresses endogenous citrullinated proteins
Thus, both smoking and Porphyromonas gingivalis are attractive etiological agents for further investigation into the gene/environment/autoimmunity triad of RA.
Wegner N, Lundberg K, Kinloch A, et al, Immunol Rev. 2010 Jan;233(1):34?54
�More than 20,000 physicians, after Luckies had been furnished them for tests, basing their opinions on their smoking experience, stated that Luckies are less irritating than other cigarettes.�
Mad Men?
Holy Smokes!!
Cigarette Smoking Has Been Strongly Linked To Numerous Autoimmune Diseases
Cigarette Smoking & Autoimmune Disease: What Can We Learn From Epidemiology?
Rheumatoid arthritis and cigarette smoking:
Risk is highest in men: OR up to 4.4 X
Smoking increases risk of seropositive RA 2.4X in women
Smoking intensity and duration both greatly increase risk
Smoking increases severity of symptoms
Increased risk remains for 20 yrs after cessation
�Cigarette smoking is the most conclusively established environmental risk factor for RA�
Smoking & Air Pollution As Pro?Inflammatory Triggers For The Development Of Rheumatoid Arthritis.
Smoking initiates chronic inflammatory events in the lungs.
These, in turn, promote the release of the enzymes, peptidylarginine deiminases 2 and 4 from smoke?activated, resident and infiltrating pulmonary phagocytes.
Peptidylarginine deiminases mediate conversion of various endogenous proteins to putative citrullinated autoantigens.
In genetically susceptible individuals, these autoantigens trigger the production of autoantibodies to anti?citrullinated peptide, an event which precedes the development of RA.
Anderson R, Meyer PW, Ally MM, Tikly M, Nicotine Tob Res. 2016 Jul;18(7):1556?65
Floris van Gaalen et al. J Immunol 2005;175:5575-5580
Cigarette Smoking & Autoimmune Disease: What Can We Learn From Epidemiology?
Systemic lupus erythematosis
Highest risk in current smokers
Current smokers have higher levels of anti?dsDNA Ab
Multiple sclerosis
Increased risk of MS in both current & past smokers
Risk increases with intensity of smoking (more cigarettes per day)
Increased severity of MS in current smokers
Cirtrullination of myelin?basic protein ?? antigenic
Graves� hyperthyroidism
Smoking is esp. strong risk factor for opthalmopathy
Industrial Air Emissions & Proximity To Major Industrial Emitters, Are Associated With Anti?Citrullinated Protein Antibodies.
Randomly sampled 1586 subjects out of 20,000 population from Quebec, Canada
After adjusting for age, sex, smoking, and ethnicity, found
Positive association between anti?CCPA and annual industrial PM 2.5 and sulfur dioxide emissions (i.e. living closer to emitters increases anti?CCPA)
Negative association between anti?CCPA and to a major industrial emitter of both PM 2.5 and SO2 (living further away from emitters decreases anti?CCPA)
�These analyses suggest that exposure to industrial emissions of air pollutants is related to ACCPA positivity.�
Bernatsky S, Smargiassi A, Joseph L, et al, Environ Res. 2017 Aug;157:60?63
Air Pollution As A Determinant of Rheumatoid Arthritis
The induction by air pollution of an inflammatory environment with high citrullination levels in the lung may induce iBALT formation, thereby causing a transition toward a more specific immune response via the production of anti?citrullinated peptide antibodies.
Air pollution not only triggers innate immune responses at the molecular level, increasing the levels of proinflammatory cytokines and reactive oxygen species, but is also involved in adaptive immune responses.
Thus, via the aryl hydrocarbon receptor (AHR), diesel exhaust particles can trigger a T?cell switch to the Th17 profile.
Sigaux J, et al Joint Bone Spine. 2018 Mar 7. pii: S1297?319X(18)30043?5
The Aryl Hydrocarbon Receptor Links TH17?Cell? Mediated Autoimmunity To Environmental Toxins
The aryl hydrocarbon receptor (AhR) is a ligand?dependent transcription factor that mediates a range of critical cellular events in response to halogenated aromatic hydrocarbons and non?halogenated polycyclic aromatic hydrocarbons such as dioxin (TCDD)
In a murine model of multiple sclerosis, which is mediated by Th17 cells, activation of cells using the AhR exacerbated disease, whereas mice deficient in the AhR had attenuated autoimmune disease.
This paper thus links activation of Th17 cells with environmental toxins, suggesting a plausible hypothesis for the increase in such diseases with industrialization.
Veldhoen, M., Hirota, K., Westendorf, A.M, et al Nature. 2008 May 1;453(7191):106?9
J Inflamm (Lond). 2015; 12: 48.
Does Rheumatoid Arthritis (& Other Autoimmune Diseases) Start In The Gut, Or In The Lungs?
Gomez?Mejiba SE, Zhai Z, Akram H, et al. Inhalation of Environmental Stressors & Chronic Inflammation: Autoimmunity and Neurodegeneration.
Mutation research. 2009;674(1?2):62?72.
Citrullination & Autoimmunity
Environmental exposure to cigarette smoke and nanomaterials of air pollution may be able to induce citrullination in lung cells prior to any detectable onset of inflammatory responses, suggesting that protein citrullination could be considered as a sign of early cellular damage
Citrullination has been reported to be a process present in a wide range of inflammatory tissues. Indeed, citrullinated proteins have been detected also in other inflammatory arthritides and in inflammatory conditions other than arthritides (multiple sclerosis, polymyositis, inflammatory bowel disease and chronic tonsillitis)
Histone hypercitrullination can activate neutrophil extracellular traps (NETS)� high inflammatory
These data support the hypothesis that rather than being a disease?dependent process, citrullination is an inflammatory?dependent condition that plays a central role in autoimmune diseases.
Valesini G, Shoenfeld Y, et al Autoimmun Rev. 2015 Jun;14(6):490?7 Wang S,
Wang Y.Biochim Biophys Acta. 2013 Oct;1829(10):1126?35
Air Pollution In Autoimmune Rheumatic Diseases: A Review
Environmental factors contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica dust in rheumatoid arthritis and systemic lupus erythematosus
Scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica dust.
Primary vasculitis associated with anti?neutrophil cytoplasmic antibody (ANCA) may be triggered by silica exposure
Air pollution is one of the environmental factors involved in systemic inflammation and autoimmunity
Farhat SC, et al, Autoimmun Rev. 2011 Nov;11(1):14?21
Silica, Silicosis & Autoimmunity
Exposure to respirable crystalline silica (<10 ?m in size) occurs most often in occupational settings � the �dusty� trades
Epidemiological studies link occupational exposure to crystalline silica dust with systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis
Findings from human and animal model studies are consistent with an autoimmune pathogenesis that begins with activation of the innate immune system leading to proinflammatory cytokine production (NLRP3 inflammasome), pulmonary inflammation leading to activation of adaptive immunity, breaking of tolerance, and autoantibodies and tissue damage
Pollard KM, Front Immunol. 2016; 7: 97.
Asbestos = Magnesium Silicate
Assessment Of Autoimmune Responses Associated With Asbestos Exposure In Libby, Montana, USA
The population in Libby, Montana, provides a unique opportunity for study because of both occupational and environmental exposures that have occurred as a result of the mining of asbestos?contaminated vermiculite near the community
Libby serum samples showed significantly higher frequency of positive ANA and ENA tests, increased mean fluorescence intensity and titers of the ANAs, and higher serum IgA, compared with Missoula serum samples
The results support the hypothesis that asbestos exposure is associated with autoimmune responses and suggests that a relationship exists between those responses and asbestos?related disease processes.
Pfau JC, et al Environ Health Perspect, 2005, Vol 113: 25-30
Air Pollution, Oxidative Stress & Exacerbation Of Autoimmune Diseases
Particulate matter present in air pollution can induce oxidative stress and cell death, both by apoptosis and necrosis of human cells leading to aggravation of chronic inflammation, i.e. the tissue damaging reaction observed in autoimmune diseases.
Therefore, identification of strong inducers of oxidative stress among components of PM seems to be crucial for their neutralization and elimination from the ambient environment.
It seems likely that PM 2.5 may exacerbate the onset of the SLE because they were attributed to a significant increase of the level of anti?dsDNA antibodies, and the presence of the renal casts in SLE patients
Exposure to ozone, sulphates, and other pollutants present in the air has been associated with type 1 diabetes in children
MS occurrence and hospitalization was associated with exposure to air pollutants such as PM10, SO2, NO2, and NOx
In addition to tobacco smoke and silica, pollution emissions from road traffic may be an environmental factor responsible for exacerbation of RA
Gawda, A, et al, Central European Journal of Immunology 2017; 42(3)
What Do Environmental Pollutants, Toxins, Infections & Unhealthy Diets Have In Common?
Increase inflammation and additional free radical production,
Which damages tissues (bystander effect), disrupts barriers, and/or modifies DNA…
Creating �foreign?like� tissues that break immune tolerance (eg anti?nuclear antibodies)
Cell Stressors
Macario, A. J.L. et al. N Engl J Med 2005;353:1489-1501
Damage Associated Molecular Patterns
Molecular structures that activate immunologic receptors
Released with cellular injury and/or necrosis after exposure to cellular stressors
DNA fragments
Mitochondria
Misfolded proteins
Advanced glycation end products have similar biological effects
Initiate and perpetuate inflammatory response (esp NLRP3 inflammasome)
Ojcius D, Sai?d?Sadier N. Alarmins, inflammasomes and immunity. Biomedical Journal. 2012;35(6):437.
Vakrakou AG, Boiu S, Ziakas PD, et al, Systemic activation of NLRP3 inflammasome in patients with severe primary Sjo?gren’s syndrome fueled by inflammagenic DNA accumulations.
J Autoimmun. 2018 Mar 15. pii: S0896?8411(17)30789?8.
Environmental Xenobiotic Exposure & Autoimmunity
We argue that localized tissue damage and chronic inflammation elicited by xenobiotic exposure leads to the release of self?antigens and damage?associated molecular patterns …
As well as the appearance of ectopic lymphoid structures and secondary lymphoid hypertrophy,
Which provide a milieu for the production of auto-reactive B and T cells that contribute to the development and persistence of autoimmunity in predisposed individuals.
Pollard KM, Christy JM, Cauvi DM, Kono DH, Current Opinion in Toxicology, Volume 10, August 2018, Pages 15?22
The Functional Medicine Paradigm (Slightly Modified)
Immune disruption = increased susceptibility to triggers
Overload in hepatic detoxification pathways
Effect on triggers:
Synergistic action (immunotoxicant)
Adjuvant: chemical modification of self?antigen to make it appear foreign or immunogenic (neoantigens)
Enhanced apoptosis: danger/damage signals (DAMPs)
Effect on mediators:
Amplified inflammatory pathways
Increased oxidative stress
Disruption of pro?resolution counter?regulatory mechanisms
Functional Toxicology
Changes In Intestinal Tight Junction Permeability Associated With Industrial Food Additives Explain The Rising Incidence Of Autoimmune Disease
The incidence of autoimmune diseases and food additive consumption are both increasing in parallel
Dysfunction of intestinal tight junctions is common in multiple autoimmune diseases
Commonly used industrial food additives including glucose, salt, solvents, emulsifiers, gluten, microbial transglutaminase, and nanoparticles increase intestinal tight junction leakage.
Intestinal entry of foreign antigen activates the autoimmune cascade
Lerner A, Matthias T. Autoimmunity Reviews 14 (2015) 479�489
Autoimmunity Reviews 14 (2015) 479�489
Autoimmune Disease: �Two?Hit� Signal Theory
Barrier disruption allows immune system to be repeatedly exposed to a combination of an autoantigen & an �adjuvant� [Adjuvants can be toxicants, microbes, foods]
This triggers a genetically predisposed immune system to react to the autoantigen as a non?self �stranger�
�Danger� signals released at the site of clearance of dead cells amplify the process; shaping the features & severity of the resulting autoimmune disease
Persistent �Stranger + Danger� = loss of tolerance
Based on this model, strategies aimed at preventing the accumulation of dying cells lowering the adjuvant (toxic) load may be beneficial for the prevention & treatment of autoimmune disease
Anaya JM, Ramirez?Santana C, Alzate MA, Molano?Gonzalez N, Rojas?Villarraga A, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
Oxidatively Modified Autoantigens In Autoimmune Diseases
Oxidative modification of proteins has been shown to elicit antibodies in a variety of diseases, including SLE, diabetes mellitus & RA.
Oxidatively modified DNA & LDL occur in SLE, a disease in which premature atherosclerosis is a serious problem. AGE pentosidine & AGE?modified IgG have been shown to correlate with RA disease activity.
In the face of overwhelming evidence for the involvement of oxidative damage in autoimmunity, the administration of antioxidants is a viable untried alternative for preventing or ameliorating autoimmune disease…�
Kurien BT, Hensley K, Bachmann M, Scofield RH., Free Rad Biol & Med, 2006, Vol 41: 549-556
Oxidative Stress In The Pathology & Treatment Of Systemic Lupus Erythematosus.
Oxidative stress is increased in SLE, and it contributes to immune system dysregulation, abnormal activation and processing of cell? death signals, autoantibody production and fatal comorbidities.
Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE.
Reactive oxygen intermediates (ROI) mostly originate from mitochondria, and T cells from patients with SLE exhibit mitochondrial dysfunction
In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine?protein kinase mTOR undergoes redox?dependent activation.
In turn, reversal of glutathione depletion by application of its amino acid precursor, N?acetylcysteine, improves disease activity in lupus? prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research.
Antioxidant therapy might also be useful in ameliorating damage caused by other treatments.
Oxidative stress (OS) plays an important role in the pathogenesis of a variety of autoimmune diseases (ADs) and many environmental agents participate in this process.
Environmental agents, including trichloroethylene (TCE), silica, pristane (TMPD in mineral oil), mercury, and smoke, are known to induce an autoimmune response, potentially through OS?mediated mechanisms.
Antioxidants can attenuate SLE disease activity by down regulating NLRP3 inflammasome activation and activating Nrf2 signaling.
Khan MF, Wang G. Curr Opin Toxicol. 2018 Feb;7:22?27.
Metals & Minerals Associated With Autoimmune Diseases
Heavy metals
Mercury
Cadmium
Lead
Gold
Minerals & Metalloids
Silica (crystalline silicon dioxide)
Asbestos (chrysotile = magnesium silicate)
Arsenic
Lithium
Iodine
Bigazzi PE., Metals and kidney autoimmunity. Environ Health Perspect. 1999 Oct;107 Suppl 5:753?65
Biologic Markers in Immunotoxicology National Research Council (US) Subcommittee on Immunotoxicology. Washington (DC): National Academies Press (US); 1992.
Anaya JM, et al, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
Messages To Take Home
Autoimmune and autoinflammatory diseases are steadily increasing in our society
The rise in exposure to environmental pollutants and other toxins is increasing the total body burden of xenobiotics
A central theme in the development of autoimmune diseases is the loss of immune tolerance
Immune tolerance can be broken by disruption of barriers (skin, lung, gut, brain) and/or immune dysregulation
Numerous xenobiotics have been shown to disrupt healthy barriers and dysregulate immune responses
Xenobiotics may play a central role in the initiation and perpetuation of autoimmune disease
Explosion Of Autoimmune Diseases: The Mosaic Of Old & Novel Factors
Modern life and exposures to novel chemical and xenobiotic compounds may lead to the development of new complexes of symptoms that do not necessarily belong to one of the well?known autoimmune diseases
As physicians and scientists, we must continue to study novel pathogenic mechanisms and susceptible alleles to help us identify new therapeutic venues.
Agmon?Levin N, Lian Z, Shoenfeld Y. Cell Mol Immunol. 2011 May; 8(3): 189�192.
IFM Annual International Conference Hollywood, Florida May, 2018
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The Ecology Of The Exposome
Exposome & The Alteration Of �Self�
The Exposome Connections To Autoimmune Diseases Converting Self Into Non?Self
Multi?Organ Network Biology
In Autoimmunity, Warburg Metabolism Is Increased Through Increased Activity Of GAPDH
Origin Of IL?17 Producing Th17 Cells
What Is The Relationship Of The Gut Microbiome To Autoimmune Disease?
80% Of Patients With Autoimmune Disease Are Female
4?Hydroxyestrogens & DNA reactivity
Relationship Of Hepatic Drug Detoxification To Anti?Nuclear Antibody Development
Endocrine Thyroid
Endocrine?Thyroid
Musculoskeletal
Musculoskeletal & Kidney
Neurological
Autoimmunity
Presence of Anti?Chromatin, DNA and RNA Antibodies
What Biological Processes May Make Self Into Non?Self?
The Facts on Methotrexate For Rheumatoid Arthritis Treatment
Autoantibodies Are Increasing At Least Five Years Before Diagnosis Of SLE
The Argument For Preventing Self From Becoming Non?Self
Nat Rev Rheumatol. 2017 Jun;13(6):348-358.
Paolo Riccio, and Rocco Rossano ASN Neuro
BMJ. 2014; 349: g4490.
Reduce Fatigue
The composition of gut microbiota is influenced by multiple factors, such as diet and host genotype. Within the gut, ecological processes such as selection and evolution take place. The use of antibiotics reduces the numbers and diversity of gut microbiota.
Arbuckle MR, et al, N Engl J Med. 2003 Oct 16;349(16):1526?33.
Floris van Gaalen et al. J Immunol 2005;175:5575-5580
J Inflamm (Lond). 2015; 12: 48.
Gomez?Mejiba SE, Zhai Z, Akram H, et al. Inhalation of Environmental Stressors & Chronic Inflammation: Autoimmunity and Neurodegeneration.
Macario, A. J.L. et al. N Engl J Med 2005;353:1489-1501
Autoimmunity Reviews 14 (2015) 479�489
Anaya JM, Ramirez?Santana C, Alzate MA, Molano?Gonzalez N, Rojas?Villarraga A, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
Bannerjee, B.D., Toxicology Letters, 1999, Vol 107: 21-31
Garza, A, Drug?Induced Autoimmune Diseases. Pharmacy Times 1?20?16
Anaya JM, et al, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
IFM Annual International Conference Hollywood, Florida May, 2018
