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Marshall Protocol in chronic illnesses

Dr. Renata Trister DO

The Marshall Protocol is a medical treatment used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including Chronic Fatigue Syndrome, Fibromyalgia, Crohn’s Disease, Sarcoidosis and Rheumatoid Arthritis.  Dr. Marshall started his research after to being diagnosed with sarcoidosis. After reading studies that demonstrated Rickettsia DNA in sarcoid patients, and by noting that his disease was worsened by sunlight. He developed a hypothesis, and a treatment protocol to treat chronic inflammatory illnesses.

Sarcoidosis is a disease whose etiology is unknown, but is characterized by non-caseating granulomas.  Granulomas are an immunologic response to infections, often fungal or mycobacterial. Sarcoidosis frequently causes dysregulation of vitamin D with increased levels in the blood, the vitamin D being made in the granulomas.

The Marshall Protocol is based on the hypothesis that “chronic diseases (termed T-helper [Th1] illnesses) are the result of infection by an intraphagocytic, metagenomic microbiota of chronic bacterial forms that are often referred to as the Th1 pathogens”. The term intraphagocytic refers to the fact that these bacteria have developed the ability to remain alive and proliferate undetected inside the cytoplasm of the cells they infect. These cells include macrophages (cells of the innate immunity), the very cells that the body uses to kill invading pathogens. Once inside these cells, they cause our own cells to release inflammatory cytokines (proteins that often generate pain and inflammation).

The term metagenomic indicates that there is a tremendous number of different species of these chronic bacterial forms. Finally, the term microbiota refers to the fact that these bacteria are also thought to sustain themselves by grouping into communities called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics.

Many of the Th1 pathogens are also postulated to be in a chronic state referred to as the L-form. Under certain conditions, L-form bacteria mutate from classical bacteria and lose their cell walls. Since L-form bacteria lack a cell wall, many antibiotics (that target bacterial cell walls) are not effective, furthermore these pathogens cannot be detected by standard laboratory tests.

The ability of the Th1 pathogens to proliferate in the body is directly related to the vitamin D receptor (VDR). Critically important to the body, the Vitamin D Receptor (VDR) controls the innate immune system – the body’s first line of defense against infection. It’s also responsible for turning on/off a wide array of genes and chemical pathways. One of the VDR’s myriad jobs is to control expression of several families of antimicrobial peptides (AMPs), proteins that kill bacteria, viruses and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

Although casually referred to as a vitamin by some members of the medical community, molecular biologists have long realized that the precursor form of vitamin D (25-D) is really a secosteroid.  Elevated levels of 25-D can bind and inactivate the VDR, which subsequently shuts down the innate immune system.

Certain species of bacteria also produce substances that can bind and inactivate the VDR in a manner similar to 25-D. Consequently, people who are infected with the Th1 pathogens and consuming vitamin D are no longer able to produce the AMPs or turn on the innate immune response. This allows their bacteria to proliferate and spread.

When the innate immune system can no longer function, people have a very hard time keeping other pathogens under control. They often find that childhood viral infections reactivate, or that they acquire Candida (pathogenic yeast) and Mycoplasma as well.

Unlike its inactive counterpart, 25-D, that inactivates the VDR in healthy individuals, 1,25-D binds and activates the VDR. But in individuals who have 25-D and bacterial proteins blocking the VDR, 1,25-D is forced out of the receptor and into the surrounding environment. Causing 1,25-D to rise to an unnaturally high level.

The nuclear receptors affected by 1,25-D are receptors that regulate the body’s hormones – the glucocorticoid receptor, and the alpha and beta thyroid receptors, the adrenal receptors, and the progesterone receptors, among others.

This means that when 1,25-D is high, it competitively displaces cortisol, T3, and other metabolites from their target nuclear receptors, causing havoc on the body’s hormonal pathways. Thus, most people with chronic disease find they have difficulty tolerating stress, changes in temperature, and a variety of other hormone-related issues. Also, when levels of 1,25-D rise above 42 ng/ml, calcium begins to be leached from the bones, a process that results in osteoporosis and osteopenia.

When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop. This means that low levels of 25-D – the form of vitamin D measured by most doctors – is not a sign of vitamin D deficiency. Instead, low levels of 25-D are a result of the disease process.

The Treatment

Patients on the Marshall Protocol take a medication called olmesartan (Benicar), which is able to bind and activate the VDR by pushing 25-D and bacterial proteins out of the receptor. Patients also lower levels of 25-D in the body by avoiding the kinds of vitamin D present in various foods. These measures renew the body’s ability to turn on the innate immune system and produce the anti microbial peptides. The immune system is then able to kill the Th1 pathogens and is once again able to manage viral and other co-infections.

At the same time, MP patients take pulsed, low-dose antibiotics. Antibiotics taken in this manner are much more effective against bacteria in biofilms and are able to greatly weaken the Th1 pathogens so that the patient’s own immune system is then able to destroy them. The antibiotics weaken the bacteria by blocking their ribosomes, which they need to produce proteins that help them survive and reproduce. It’s important to understand that when the Th1 pathogens die, there is a temporary change in a patient’s immunopathology.

Immunopathology refers to the changes in the immune system that result from bacterial death (another term sometimes used is the Jarisch-Herxheimer or “Herx” reaction). Dying bacteria release toxins into the bloodstream, stimulate the production of inflammatory cytokines, and generate temporary hormonal imbalances. This means that once patients begin the MP, each dose of antibiotic will cause them to feel bad for the period of time it takes their immune system to deal with the consequences of bacterial die-off.

Before starting the MP, many people may feel that they have improved through consuming vitamin D and taking steroids such as prednisone. In reality, these compounds further inactivate the VDR, preventing the immune system from effectively killing the Th1 pathogens. Since it is the death of these forms of bacteria that generates an increase in painful symptoms, people may experience short-term relief when using vitamin D or prednisone as their immune system shuts down and fewer bacteria are killed. However, in reality, this situation allows the bacteria to spread more easily.

Applicable Illnesses

Patients on the MP have dozens of different medical conditions. As evidenced by members’ reported progress on the marshallprotocol.com website, nearly all experience a powerful immunopathological reaction after taking a dose of antibiotics.

Many patients report great improvement, while some are approaching complete recovery.

Some of the diseases patients are currently using the MP to treat include (but are not limited to):

Chronic Fatigue Syndrome

Fibromyalgia

Chronic Lyme disease

Rheumatoid Arthritis

Multiple Chemical Sensitivity (MCS)

Myasthenia gravis

Psoriasis

Osteoarthritis

Sarcoidosis

Hashimoto’s Thyroiditis

Uveitis

Apart from the symptoms or diagnosis indicating Th1 disease, the easiest way to find out if the Marshall Protocol may be applicable to your disease is to get a blood test and check the level of your D Metabolites. This test can detect the elevated level of 1,25-D often seen in patients with chronic disease, but must be done correctly in order to be of any value.

Patients can also use a therapeutic probe to determine whether the MP can be applied to their illness. A therapeutic probe refers to a trial period during which a person tests whether or not the taking the MP medications results in immunopathology or other symptom changes.

 

 

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SIJ dysfunction

Jon Trister , MD.
With this issue of the newsletter, I would like to bring our attention to sacroiliac joint problems and the interrelationship between such as Fascia, Osseous structures, Ligaments, Muscles, Tendons, Neuro-Vascular structures, and Visceral structures.

There are different degrees of sacroiliac joint pathologies-from SIJ dysfunction to SIJ dislocation. What units them is the common element of instability of the supportive structures and a resulting lack of tensegrity. I will focus on the mechanical aspect of SIJ pathology. We will discuss other SIJ problems such as Infectious, Rheumatologic and Malignancy in the future newsletters.

Realizing the difference between dysfunction and dislocation I see similarities between them as well. Different factors and combinations of factors cause Sacroiliac Joint Dysfunction: Connective tissue insufficiency, Ligament laxity, and Muscular imbalance. All of these factors lead to abnormal Sacroiliac movement (hyper or hypo-mobility), joint locking and muscular imbalance.

There are many of variations of SIJ mechanical problems: Up-slip and down-slip are good examples. They develop as a result of acute or chronic injury. They are extreme manifestations of the Sacroiliac Joint instability. Very often underlying mechanism of these injuries are connective tissue insufficiency and ligamental laxity involving multiple ligamentous and musculotendinous structures.

Fryette originally described up-slip in 1914. This lesion (up-slip) is essentially a vertical shear between the sacrum and ilium and most commonly occurs on the left side. This injury shortens the distance between the sacroccygeal attachments of the Sacrotuberous ligament to the ischial tuberosity attachment.  Control of Nutation (forward flexion of the base of the sacrum) becomes insufficient. Secondary stabilizers, such as the Piriformis, Gemellus Superior & Inferior, Quadratus femoris , and Obturator internus muscles are activated to mainatain stability. Significant effort is required on the part of the muscles involved to keep the SI joint stable. Due to this extreme exertion and unnatural forces neuro-muscular pathology eventually evolves such as Piriformis syndrome, Posterior hip pain, buttocks pain, sciatica, peripheral nerve entrapment syndromes and so on.

What happens to the posterior Long and Short Sacroiliac Ligaments? Their orientation and tension will change in response to the structural and functional tensions present, this is turn will affect their control over Counter-nutation (backward movement of the base of the sacrum).  Losing control over nutation and counter-nutation will bring into action Gluteal muscles, Thoracodorsal Fascia, Quadratus Lumborum, the Hamstrings in the immediate area and have far reaching consequences through fascial planes and connections.

Superior displacement of the ilium (up-slip) will shorten the Ligaments running from the transverse processes of L4 and L5 to anterior ilium – the Ilio-Lumbar ligaments. Instability of these ligaments will increase shearing forces on L4-L5-S1 discs and lead to annulus tears, disc protrusion and eventually disc herniation. These forces will also activate contraction of the Quadratus Lumborum, Multifidus muscles, Psoas, Latissimus Dorsi  muscles.

Inferior displacement of the ilium (down-slip)- is a rare condition. To differentiate between the up-slip and the down-slip the physician utilizes thorough clinical examination and Standing x-rays. Sometimes the Iliac crest on the side of the down-slip can be perceived as superior due to activation of the Ipsilateral Quadratus lumborum, which pulls pelvis up and tilts the pelvis to the opposite side.

The pubic symphysis has no strong intrinsic stabilizing structures. Without the stabilizing actions of these muscles: transverse abd. m, oblique abd.  m., rectus abdominis m. and adductor longus m., the pubic symphysis would permit 5-10mm of vertical shear.

Any discussion of Sacrum and pelvis would not be complete without mention of the role of the Psoas muscle.  This muscle is always involved in lumbo-pelvic instability. Having arisen from the sides of the lumbar vertebrae and anterior aspects of the transverse processes, it connects to the respiratory and pelvic diaphragms. It plays an important role in general body support, maintaining body structure and the body’s functional relationships through it’s support of the autonomic lumbar plexus. It exerts it’s major impact through the viscera innervated by this plexus, it can well exert a vital influence on visceral function and bodily well-being.

Therefore, treatment of Sacroiliac Joint Mechanical Pathology should include many of the following treatment options: Osteopathic Manipulative Therapy-to restore normal structural relationships; Regenerative therapy utilizing Prolotherapy, Platelet-Rich Plasma, Stem Cell therapy-to restore structural integrity;  Neural therapy, Neuro-fascial injection therapy-to restore neurologic and autonomic function; Physical therapy-to restore proper biomechanics and neuromuscular re-education; Nutritional and Hormonal treatment-to provide critical elements for healing and repair.

The  following structures should be considered for treatments: Sacroiliac Joint(s), Sacroiliac Ligaments, Sacrotuberous Ligaments, Ilio-Lumbar ligaments, Thoracodorsal Fascia, Thoraco-Lumbar junction, Facets joints, Inter- and Supra-spinous ligaments, Multifidus, Quadratus Lumborum, Piriformis, Psoas muscles and in some cases distal attachments of the hamstrings.

Most cases will require diagnostic imaging studies, such as X-Ray , Ultrasound or MRI.

All of these modalities require a intensive study, reading, and education. Skill does not come after one or two conferences or workshops. The learning of Orthopaedic Medicine is a lifetime affair.

Be patient and persistent. Success will come.

Jon Trister MD

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Procedure in Orthopaedic medicine practice

Orthopaedic medicine has a long history and many tools with which to help the patient with musculoskeletal pain. In this Issue I would like to review basic principles regarding Prolotherapy for the benefit of physicians who are developing skills in Prolotherapy (Regenerative Injection Therapy )and PRP and as a review for those already practicing these skills.  In order to achieve the greatest success, the procedure should be performed correctly enhancing safe practices and limiting risk for the patients. Several important elements need attention: practice management (consent, documentation, billing and coding issues), assessment and identification of appropriate candidates for the procedure and safe performance of the procedure itself.

Knowledge of the pathology behind the patient’s complaint.

Identify the problem based on history, physical examination and imaging studies. Look for local tender points, as well as distal referral points. Remember, the initial presentation of pain could be referred pain and not necessarily where the problem is. Learn common patterns of referred pain. Become familiar with the diagnosis of instability of joints based on the clinical symptoms and exam findings. Make the correlation between clinical findings and imaging studies. Remember: Imaging studies do not always correlate with clinical findings and vice versa.

Knowledge of anatomy and function. Do your homework before treating the patient. Read anatomy, so you will know what are you are doing. Proficient prolotherapists are perpetual students of anatomy. Have diagrams, posters and anatomical illustrations readily available in your exam rooms. Show your patients where the problem is and how you will treat it.

Informed Consent

Inform the patient about the procedure in detail. Give them realistic expectations of the treatment and prognosis. Explain to the patient that prolotherapy is a PROCESS and requires multiple treatments and time to see results. Give the patient an option to review other possible treatments: Physical therapy, Surgery, OMT, and especially the options offered as standard of care for their particular diagnosis. Informed consent requires that the patient be presented the standard of care alternatives for their diagnosis.

Documentation of Informed Consent is just as important as the signature. Have the patient sign a detailed consent form, explaining all possible side effects and  complications. The potential side effects and complications should be discussed and outlined to the patient and documented on the consent form. You may wish to have your forms reviewed by your malpractice carrier to be certain they meet the standards. Encourage the patient to contact you before the scheduled procedure and to ask  questions. When examining elderly patients advise them to come with close relatives or friends so that all questions will be answered and not missed. Informed consent must list the standard medical options the patient was informed of and chose not to pursue.

Have the patient sign all medical and financial documents with the co-signature of a witness-your nurse or other office assistant.

Medical Practice/Procedure

Know important medical information pertinent to safe performance of an invasive procedure: Medical history, Medications list, Previous surgeries, Allergies, Presence of prosthesis, hardware, screws and plates. Discuss with referring physician the procedure you are going to perform. If you advise the patient to stop any medications ask the PCP for permission to do so. Do not discontinue  medications ordered by other doctors without consulting with them first. Do not criticize other physicians or previous treatments. You also may not be the last doctor. Strive to create a professional and healing atmosphere in your treatment room.

Never use old solutions. All solutions must be mixed on the day of the procedure. Aseptic technique must be taken very seriously. In some cases you may consider prophylactic antibiotics.  Proper positioning of the patient is very important. It must be safe for the patient and comfortable for physician performing the procedure. Consider IV line and VS monitoring in some cases. Make sure you are ready for medical emergencies. If you chose to use conscious sedation or pre-medicate your patients be sure they have a driver and that you meet the regulations of your state and malpractice carrier for conscious sedation or premedication.

Prepare skin for procedure. If the skin is inflamed in the area the injections are to be performed it is better to postpone the treatment. Again, know your anatomy and be very careful while injecting:

Midline of the vertebrae: direct needle caudate

Avoid cranial direction.

Be careful injecting midline below L3–Interspinal ligaments could be absent and risk for dural perforation is high.

Always touch the bone.

In some cases, aspirate before injecting, especially the transverse processes of cervical spine.

Be very careful around chest/rib/thoracic injections and lower cervical spine – risk for pneumothorax.

 

Check the function of the treated area after the procedure: ROM, pulsation, lungs sounds and vital signs.

 

Post Procedure: Offer patients fluids and snacks if necessary. Some patients will be light headed or vasovagal from the sympathetic stimulation of the injections. Give patients time for full recovery. All patients must be instructed to come with a designated driver. Make sure that you will be readily available to the patient after the procedure – give them you mobile phone number. It is a very beneficial practice to call your patient the next morning, especially after the first injection session. This is reassuring to the patient and allows you to evaluate their response to the treatment.

 

Documentation is a necessary part of the job of the physician. Make it simple, but detailed. Forms with diagrams, flow sheets with check boxes or items to circle can ease the documentation process for procedures. The following should always be present:

General information about Prolotherapy for patients as well as their physicians.

Detailed consent form

Medicare waiver

Financial disclosure and agreement

Preparation for Prolotherapy

Procedure protocols

Patient Response to the procedure

Post-procedure instructions

 

Taking the time to review these processes and implement safe processes and procedures as you introduce new techniques into your practice will facilitate safe practices for you and good outcomes for your patients.

 

 

 

 

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Natural Support for Neurologic Health: A Multiple Pathway Approach

Article summary   Renata Trister DO

Advances in medicine, science and hygiene have allowed modern man to become the longest living humans in history. As life expectancy lengthened, disorders of the nervous system in the aging population are seen more frequently. Dementia, cerebrovascular disease as well as progressive disorders such as peripheral neuropathy and Alzheimer’s are a growing concern for the aging patient.  Diseases of the nervous system are being diagnosed in record numbers in the United States: up to 6.8 million suffer from dementia; approximately 4 million have Alzheimer’s disease (AD), and roughly 1.5 million may suffer from Parkinson’s disease (PD), with 50,000 newly diagnosed patients every year. These numbers are projected to continue to increase.  Dysfunction in older patients should not be assumed to be the result of the aging process.  Although progressive decline in neurologic functioning is a normal aging process, progression to a neurologic disease is not inevitable.  Early intervention may prevent and delay the deterioration in these disorders.

Research suggests that a cumulative effect of imbalanced biochemical pathways can greatly impact neurologic cellular decline. Four major biochemical pathways are thought to mediate both aging and premature neurologic decline. By maintaining adequate function in these pathways, it may be possible to achieve optimal neurologic health and brain function.

Environmental factors such as poor diet, toxins and oxidative damage can stress biochemical pathways in the body and accelerate the biological aging of tissue.

Four Biochemical Pathways Implicated in Nervous System Decline

I.  Chronic Inflammation—Research suggests that chronic inflammation is a possible mechanism in aging associated neuro-degeneration. Multiple aspects of the inflammatory pathway are capable of propagating premature aging and neuron cell death. Chronic inflammation beyond its protective role, can cause harm to tissue.  Epidemiological evidence indicates that populations taking anti-inflammatory drugs for other conditions have a reduced risk of neurodegenerative conditions.  Inflammation and oxidation are closely linked.  Oxidants serve as signaling agents for the pro-inflammatory factors.  Several natural substances offer safe and effective alternatives to anti-inflammatory drugs, which are known to cause various adverse side effects.

II. Mitochondrial Dysfunction—Tissues with a high-energy requirement, such as the brain and heart, have a greater density of mitochondria—the cell’s energy-producers. Since the brain depends so highly on mitochondrial energy supply, dysfunction of mitochondria can affect the central nervous system (CNS) more severely than other tissues.  Research suggests two methods of supporting mitochondrial health and function: 1) promoting healthy mitochondrial energy production, and 2) combating free radical production and damage by increasing mitochondrial antioxidants.

 

III. Endocrine Imbalance—Aging is associated with a reduced ability to adapt to stress and chronic elevations of stress hormones called glucocorticoids (e.g., cortisol).Animal and human data suggest that high levels of glucocorticoids can be particularly detrimental to the hippocampus (the brain structure involved in learning and memory). In addition, changes in glucose and insulin handling during the aging process can lead to neuronal degeneration due to negative effects on nerve cell structure and function. Proper diet, exercise, and nutritional interventions may help reduce glucocorticoid levels, enhance the body’s ability to cope with stress, and improve glucose and insulin metabolism.

IV. Hypomethylation—Methylation, the transfer of a methyl group (CH3) from one molecule to another, is required for numerous biochemical reactions vital to good health. However, insufficient levels of folate and vitamins B6 and B12 can cause reduced methylation, or hypomethylation, which in turn can produce elevated levels of the amino acid homocysteine (Hcy). Elevated Hcy levels are strongly linked to cognitive decline and irreversible dementia.  See tables below.

Nutritional Modulation of the Four Pathways

Fortunately, interventions begun in the initial stages of the disease process may prevent or delay the course of neurologic deterioration, resulting in an overall improvement.  The following nutrients may help prevent and interrupt the damaging cascade that contributes to neurologic decline.

Niacinamide—Niacinamide, a form of the B vitamin niacin, is a potent inhibitor of inflammatory cascade.  In animal models, administration of niacinamide resulted in reduced brain damage and reduced neurologic functional losses.

Essential Fatty Acids—Fish oils, which contain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are well known for their anti-inflammatory activity. Furthermore, DHA is required for normal brain function in adults. Decreases in brain DHA content are associated with age-related cognitive decline, dementia, and AD.

Resveratrol—Resveratrol is a polyphenol found in the skins of red grapes and various other plants. In vitro, animal, and epidemiologic research suggests that resveratrol may protect against inflammation and CNS disorders.  It is also a potent antioxidant.

N-Acetylcysteine (NAC)—The protective effect of NAC is likely related its restoration of brain glutathione (GSH) levels.GSH is central to antioxidant defenses in the brain and cellular detoxification of free radicals. In addition, NAC has been shown to support proper mitochondrial function.

Alpha-Lipoic Acid (ALA)—ALA is a cofactor in the synthesis of ATP (energy required for tissue function) and improves overall mitochondrial function. ALA is also an excellent antioxidant agent in neurodegenerative diseases due to the fact that it can interrupt free radical damage at several points. Animal research has shown that ALA supplementation elevates antioxidants in various brain regions and improves memory in aged mice.In addition, ALA supports healthy blood glucose levels and insulin activity.

Acetyl-L-Carnitine (ALC)—ALC is a vitamin-like substance that may improve energy production within brain cells via its effect on mitochondria.An analysis of studies reports that persons with dementia given 1.5 to 3 grams of ALC daily have shown improvement in numerous clinical measures of cognitive function such as memory, depression, and mental deterioration.

Magnesium & Thiamin—Magnesium plays an important role in maintaining the integrity and permeability of the mitochondrial membrane as well as assisting in energy-producing machinery of the mitochondria. Thiamin is a cofactor needed for mitochondrial energy production.

Coenzyme Q10 (CoQ10)—CoQ10 is a mitochondrial antioxidant cofactor that has been shown to be neuro-protective. In addition to being a potent free radical scavenger, CoQ10 is also critical for energy production by the mitochondria. CoQ10 supplementation has proven effective in a wide variety of age-related conditions.

Vitamin E—Vitamin E is the primary antioxidant found in all tissues. Low vitamin E levels are consistently associated with an increased risk and occurrence of neurologic disease, including AD and Parkinson’s. In a study of patients with AD, treatment with 2000 IU of vitamin E per day for 2 years was beneficial in delaying the primary outcome (time to the occurrence of death, institutionalization, loss of ability to perform activities of daily living, and severe dementia) of disease progression.

Ginkgo (Ginkgo biloba)—Ginkgo biloba extract (GBE) is an approved treatment for dementia in Germany, and it is the only nonprescription substance considered a treatment for dementia in Canada. Many clinical studies have demonstrated the effectiveness of GBE in the treatment of patients with dementia, AD, and age-associated memory and cognitive impairment. In addition, GBE may also prevent changes in mitochondrial structure and function associated with aging of the brain.

Adaptogenic herbsAdaptogens are plants that help to decrease cellular sensitivity to stress. Herbs with adaptogenic properties may be beneficial in ameliorating the decreased ability to handle stress and the increased levels of glucocorticoids associated with aging and neurodegeneration. Ayurvedic herbs such as ashwagandha (Withania somnifera), holy basil (Ocimum sanctum), and brahmi (Bacopa monniera) have a positive influence on stress response, mental function, and cognition.

Mixed Carotenoids—Carotenoids are a class of naturally occurring plant pigments that provide the bright red, orange, and yellow colors of fruits and vegetables. A balanced intake of mixed carotenoids, as found in a healthy diet, provides the best protection against oxidative damage. In addition, the carotenoids lutein and zeaxanthin are found concentrated in the retina of the eye where they offer protection from conditions such as age-related macular degeneration.

Folate, Vitamin B6, and Vitamin B12—Folate and vitamins B6 and B12 are needed for proper methylation and to keep Hcy within a normal range.Insufficiencies of these nutrients may result in forgetfulness, memory loss, confusion, depression, dementia, and mood and sensory changes.

Conclusion

Healthcare professionals and their patients must take a preventative stance against neurologic decline. Due to the great deal of interest and research in this area, information about appropriate nutritional supplementation is constantly evolving. By looking for early warning signs and providing nutritional guidance that simultaneously addresses chronic inflammation, mitochondrial dysfunction, endocrine imbalance, and hypomethylation, perhaps more people can live out their most rewarding years with mind and body intact.

 

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Nutritional Influences on Estrogen Metabolism

Article Summary

Renata Trister DO

Estrogens affect the growth, differentiation, and function in various organs and tissues.  Although commonly known as the “female hormone”, estrogen plays an important role in bone health, protects the cardiovascular system, and influences behavior and mood. Estrogen also affects male organs such as prostate and testes. While appropriate levels of estrogens are essential for good health, excessive estrogen exposure can lead to health problems such as premenstrual syndrome (PMS), endometriosis, fibrocystic breasts and breast cancer.

Lifestyle and environmental factors can greatly influence estrogen production, metabolism, and balance. These factors include poor diet, obesity, excess alcohol consumption, high insulin levels, medications such as hormone replacement therapy and birth control pills, overexposure to chemicals found in pesticides and industrial chemicals, and agricultural hormones in animal products consumed by humans.

Nutritional Support of Optimum Estrogen Metabolism

Diet and nutrition play an important role in influencing estrogen metabolism and detoxification. Incorporating dietary changes with the addition of beneficial nutrients and herbs can profoundly affect estrogen balance.

Dietary modulation of estrogen metabolism

Consumption of cruciferous vegetables like cabbage and broccoli, and foods such as soy can significantly increase the 2-hydroxylation of estrogen. Dietary fiber intake can promote the excretion of estrogen by binding estrogens in the digestive tract and also increases sex hormone binding globulin (SHBG), thus reducing levels of free estradiol. Complex carbohydrates, such as those found in vegetables and whole grains, are more effective in optimizing estrogen metabolism than simple carbohydrates, which can raise blood glucose and insulin levels, resulting in secondary adverse influences on sex hormone balance.

 

Phytoestrogens — These plant compounds are similar in shape to the estrogen molecule and can bind to estrogen receptors (ERs). They are much weaker than endogenous estrogens and, through competitive inhibition, have been shown to prevent the receptor binding of “stronger”, more stimulating estrogens. Phytoestrogens are currently under extensive investigation as a potential alternative therapy for a range of conditions associated with estrogen imbalance, including menopausal symptoms, PMS, endometriosis, prevention of breast and prostate cancer, and protection against heart disease and osteoporosis.

 

 

 

The two main classes of phytoestrogens are isoflavones and lignans. Soy is perhaps the most common food source of isoflavones, but other excellent sources include legumes, clover, and kudzu root. Higher intakes of soy products and isoflavones, such as consumed in traditional Japanese diets, are associated with low rates of hormone-dependent cancers. Lignans are compounds found in fiber-rich foods such as flaxseeds, whole grains, legumes, and vegetables. Lignans stimulate the production of SHBG in the liver, and therefore reduce the levels of free estrogen in circulation. They also inhibit aromatase, an enzyme that synthesizes estrogen.

 

Vitamin E and Magnesium — Low serum vitamin E is associated with elevated estrogen levels, and may negatively affect estrogen detoxification. Women with PMS have experienced improvements of their symptoms when given supplemental vitamin E. Magnesium promotes estrogen detoxification by promoting methylation and glucuronidation, key estrogen detoxification pathways. Ovarian hormones influence magnesium levels, triggering decreases at certain times during the menstrual cycle as well as altering the calcium to magnesium ratio. These cyclical changes can produce many of the well-known symptoms of PMS in women who are deficient in magnesium and/or calcium.

 

Indole-3-Carbinol (I3C) – I3C is a naturally occurring compound derived from cruciferous vegetables that actively promotes the breakdown of estrogen via the beneficial 2-OH pathway. Therefore, I3C is protective to estrogen-sensitive tissues and may be beneficial to those with health issues related to excessive estrogen. Not only does I3C promote healthier estrogen metabolism, it may also act as a “weak” or anti-estrogen in a similar fashion to isoflavones.

 

B Vitamins — B12, B6 and folate function as important cofactors for enzymes involved in estrogen detoxification; thus, decreased levels of B vitamins can lead to increased levels of circulating estrogens. Vitamin B6 can also modulate the effects of estrogen by decreasing the cell’s response when estrogen binds to the estrogen receptor. B vitamins are also important for DNA synthesis and repair.

Beneficial Phytonutrients and Herbs

Many other compounds can promote healthy estrogen metabolism.  Curcumin, a compound found in the herb turmeric (Curcuma longa) increases the phase II detoxification of estrogens; chrysin, a bioflavonoid that inhibits aromatase activity, thus reducing the synthesis of estrogen; D-limonene from citrus fruits promotes the detoxification of estrogen and shows promise in the prevention and treatment of breast and other cancers. Antioxidants can reduce the oxidation of the 2-OH and 4-OH estrogen metabolites. Antioxidants include vitamin C, N-acetyl cysteine, selenium, and green tea.  Traditional medicines from many cultures have relied on a variety of hormone-modulating herbs in treating women’s health conditions. These include black cohosh, chaste berry, ginseng, dong quai, and licorice.

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Prolotherapy

Renewed Treatment for Low Back Pain

Prolotherapy has been introduced for the treatment of chronic pain arising from problems with ligaments. A previous form of treatment to strengthen ligaments and form scar tissue was popular in the last century for the repair of hernias. With the advent of modern surgery, sclerotherapy, as it was called, has been reserved for varicose veins and the like. Earl Gedney, as osteopath from Philadelphia was the first to use an injection to strengthen sacroiliac ligaments. George Hackett, an industrial surgeon from Canton Ohio, active in the late fifties, correlated pain patterns from stained ligament with instability He treated thousands of patients with ligament strengthening injections which he renamed prolotherapy and reported a 90% improvement.

 

Though prolotherapy has not been popular in the last thirty years because of complications reported in five cases in the early sixties, a resurgence in its use is taking place.

What is Prolotherapy?

The word comes from proles – to stimulate growth (in Latin). It has been found over the last 150 years that a variety of agents can stimulate the growth and regrowth of ligament tissue. In many instances, it is thought, the stimulation for the growth is from an internal bruise, or hematoma which induces the natural healing process. Fibroblasts are the cells responsible for creating the ‘stings’ and ‘ropes’ which join the bones, crossing the joints. They are particularly important in the spine. The spine can be described as analogous to a pile of bricks bound together in a mobile column by the ligaments which tie each vertebra to its neighbor, creating from this pile a mobile strong and flexible support for the body. It is not surprising that a combination of mobility and support occasionally fails. With use, the normally perfect and smooth movements can become ‘kinky’. We speak of somatic dysfunction to describe the areas where movement is stiff or absent. Ligaments are also thought to store elastic energy, a little like a spring, this being their second function. The springiness of ligaments improves body motion and when they deteriorate the elasticity fails.

Stretched ligaments

It was Dr. Hackett who introduced the term relaxation of ligaments. It is plain that in certain instances the ligaments are frayed and even torn from injuries. But it is now thought, particularly in connection with the spine, that the ligaments become relaxed in part because of the shrinkage of the vertebrae and the intervertebral discs and only in part from direct stretching and damage to the ligaments themselves. Probably both mechanisms are active in certain situations.

The spine as a column of vertebrae

When the ligaments do not hold the vertebrae in perfect alignment there is a tendency for one or more vertebra to be slightly displaced or rotated. It is thought that the sacrum is particularly prone to minor displacements between the two pelvic (iliac) bones. Chiropractors use the terminology of a displacement in the sacroiliac joint to describe this. According to official medical dogma this phenomenon does not occur, but many patients who have the experience of ‘putting my back out’ and having it corrected with a chiropractic manipulation have firsthand experience of something moving. The cause for this abnormal movement is ligament relaxation.

How to correct ligament relaxation

Since it is possible with prolotherapy to stimulate ligaments to become stronger, and probably more elastic, it is quite easy to understand that prolotherapy is the treatment of choice when chronic pain is due to ligament relaxation.

The diagnosis

The symptoms of ligament relaxation are multiple and the site of the patient’s pain depends on which ligament is strained. It is usual for pain to move from place to place in the body due to the phenomenon of referred pain as well as to mechanical causes. It is the doctor’s job to make the diagnosis. A number of physicians who have trained in orthopedic medicine in modern times have made it their business to study these problems. The diagnosis is made first of all, by learning from the patient about his pain and where it is, and secondly, by sophisticated clinical examination. The diagnosis depends only a very little bit on special tests, such as x-rays. These are obtained mainly in order to exclude other conditions.

The modern use of prolotherapy

It is almost too simple to need stating that if something is out of place it should first be put back and then kept in place_ It is however amazing, how this simple concept has been battered by disbelief and institutionalized dogma.

Milne J. Ongley, a New Zealand physician integrated Hackett’s understanding of ligament relaxation with the existing British style of systemadc clinical evaluation in the musculoskeletal system, called by it initiator, James Cyriax, orthopedic medicine. He also developed Clinical techniques which ensure safety. Indeed in the last 30 years his methods have been used in many thousands of cases without important complications.

The routine for low back treatment

In cases of chronic low back pain, when the orthopedic physician has made the diagnosis of ligamentous insufficiency, usually in association with a displacement of the sacrum or one of the lower lumbar vertebrae, the following routine is undertaken: 1) the use of local anesthesia, 2) manipulation to restore normal alignment of the sacrum and spine, 3) prolotherapy injections, usually weekly for six week. 4) exercises to ensure healing in the presence of movement. It is sometimes advisable to reduce the inflammation at sites of strain (but not in mechanically important ligaments) with an injection of a steroid (modern cortisone) into an inflamed and painful part. The steroids are used occasionally and sparingly.

Other parts of the body

The principles discussed here are useful in the management of pain and instability of any part of the musculoskeletal system (Perhaps it would be better called the ligamentous and fascia] system?) The routine for low back treatment, which is the best known can be applied very effectively to other parts of the spine. Chronic neck pain and headaches are usually relieved, even after many years of trouble, with prolotherapy.

The solution

The proliferant in use at present consists of three common substances:

1) Dextrose, which is a type of sugar. It is used in a concentrated form. It produces an inflammatory response and is perfectly safe, even in patients with diabetes, because the total amount used is small.

2) Glycerine, is found naturally in the body as a component of some of the fats. It causes the tissues injected to swell temporarily (you will notice how puffy your back feels after the shots) and helps coagulate any blood which may form in the tissues and provides a framework or matrix on which new fibroblast cells can grow. It has recently been used for certain kinds of nerve ram (trigeminal neuralgia) where it abolishes the pain without upsetting the function o F the nerves.

3) Phenol, is used in most injectable medications as a preservative since it prevents the growth of bacteria. It also induces the growth of new collagen in connective tissue. It has been used for many years in face peels by plastic surgeons since it is known to induce healthy collagen and elastic tissue which removes wrinkles. It also has sortie properties of a long lasting anesthetic.

These three ingredients have been used together since 1948 in Britain, where they were first introduced in the treatment of varicose veins and overall it is estimated more than one million injections have been administered, all over the body, though mostly for low back pain without any permanent or serious reactions.

The United States Food and Drug Administration (FDA) has not officially approved (or disapproved) this mixture for use, but all of its constituents are in common use since before the advent of the FDA and are regarded, therefore, as standard preparations.

Safety of the solution

In the sixties there were five serious complications from intraspinal injections of proliferants. The solution used then was of different materials. The present solution is thought to be safe. Four times the concentration of phenol and glycerine has been placed intentionally into the spinal canal to relieve pain in cancer patients without dangerous effect. The needle placement used when following Ongley’s teaching is such that a high degree of safety is assured. In difficult cases x-ray control with fluoroscopy is used.

Exercise

In order to stimulate the new growth of collagen the proliferant is injected, but in order to align the new collagen correctly with the existing ligament tissues it is very important for the structures to heal in the presence of movement. This will protect the ligament from forming adhesions to neighboring structures and increase longitudinal alignment of the new collagen. You will receive written and. verbal instructions for the correct exercises. These movements, which we have named exercises, are essential. Repetition of the movements ensures proper healing. As the healing process goes on for several months, it is recommended that patients continue with the exercises for at least three months after the last injection.

Disc disease

Chronic back, leg and arm pain is sometimes due to disc disease. When this is so, an operation can relieve pressure on nerve. Only a physician can make a determination if an. operation is necessary. Disc disease itself is due to ligament relaxation in the first place. It is the abnormal range of movement caused by the relaxed ligaments which allows for most of the abnormal strain o: the discs. Therefore, ligament strengthening is usually recommended before or after surgery, when it is necessary.

Referred pain

There are instances when the patient feels pain at a site. remote From the injured ligament. This is called referred pain Referred pain From ligaments can mimic sciatica and neuritis. It is often confused with pain due to pressure on a nerve root from an abnormal disc in the spine. Differentiating between these is not always easy, but it is exactly this that the orthopedic physician prides himself on doing best.

Selecting treatment

Each branch of medicine and chiropractic, etc., promotes its own methods. Patients are often stranded without a ‘shoppers guide’. It is the recognition of this problem which is bringing the orthopedic physician back into popularity. He combines the use of medicine, exercises, injections, manipulation and the select recommendation for surgery to the patients’ best advantage. It should be understood that the presence of disc degeneration is the rule in cases of chronic back pain and is often found is similar individuals without pain. Disc problems are, however, not always, or even very often, the cause of pain. In any case disc displacement can often be managed with manipulation. Most cases of back pain, suitably ‘diagnosed, improve with treatment with prolotherapy.

Surgery for discs

There are cases where surgery is essential and sometimes urgent. Most surgeons will agree, however, that in the majority of instances a trial of conservative means is best first. Surgeons should, however, recognize that if an operation is needed after prolotherapy Has been used, there is an increase in the thickness of the ligaments, so the dissection can take longer to reach the deeper structures (the nerves arid dura).

Success

Hackett reported about 90% success. Contemporary research shows similar results. In a double blind trial of Ongley’s method performed in Santa Barbara an 1986 in 81 patients 88% reported more than 50% improvement in their back pain over the six months the trial was ‘blinded’, and at a year the improvement was the same. A similar rate of success is reported from several doctors’ offices where circumstances allow the treatment to be offered to a larger variety of patients. Several additional scientific papers have been published on a number of aspects of prolotherapy, many by Dr. Dorman_ Recurrent pain can develop, but is usually less severe, and more easily treated, often with a single visit to the doctor and perhaps one injection_ Patients who are treated are, however, not immune to injury, there are no bionic backs in this business.

Side effects

Soreness and bruising at the injection site and temporary stiffness are normal. Patients often report a numbness over the injection site and tingling or itching. It always passes. Triamcinalone (the steroid) sometimes causes a flushing in the face for a few days. Palpitations, insomnia, irritability and increased urination are reported rarely. There are no long term bad effects from it. Women who have a uterus may experience unusual menstruation or uterine bleeding, like a period; for up to three months after the steroid injection, which is usually used on the first day of treatment. There is no permanent. harm from this.

Pain from the injections

The injections themselves are painful, particularly in the First two to three visits.  For that reason we advise mild opioids to be taken prior to injections.

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Nutritional Influences on Estrogen Metabolism

Article Summary

Renata Trister DO

Estrogens affect the growth, differentiation, and function in various organs and tissues.  Although commonly known as the “female hormone”, estrogen plays an important role in bone health, protects the cardiovascular system, and influences behavior and mood. Estrogen also affects male organs such as prostate and testes. While appropriate levels of estrogens are essential for good health, excessive estrogen exposure can lead to health problems such as premenstrual syndrome (PMS), endometriosis, fibrocystic breasts and breast cancer.

Lifestyle and environmental factors can greatly influence estrogen production, metabolism, and balance. These factors include poor diet, obesity, excess alcohol consumption, high insulin levels, medications such as hormone replacement therapy and birth control pills, overexposure to chemicals found in pesticides and industrial chemicals, and agricultural hormones in animal products consumed by humans.

Nutritional Support of Optimum Estrogen Metabolism

Diet and nutrition play an important role in influencing estrogen metabolism and detoxification. Incorporating dietary changes with the addition of beneficial nutrients and herbs can profoundly affect estrogen balance.

Dietary modulation of estrogen metabolism

Consumption of cruciferous vegetables like cabbage and broccoli, and foods such as soy can significantly increase the 2-hydroxylation of estrogen. Dietary fiber intake can promote the excretion of estrogen by binding estrogens in the digestive tract and also increases sex hormone binding globulin (SHBG), thus reducing levels of free estradiol. Complex carbohydrates, such as those found in vegetables and whole grains, are more effective in optimizing estrogen metabolism than simple carbohydrates, which can raise blood glucose and insulin levels, resulting in secondary adverse influences on sex hormone balance.

Phytoestrogens — These plant compounds are similar in shape to the estrogen molecule and can bind to estrogen receptors (ERs). They are much weaker than endogenous estrogens and, through competitive inhibition, have been shown to prevent the receptor binding of “stronger”, more stimulating estrogens. Phytoestrogens are currently under extensive investigation as a potential alternative therapy for a range of conditions associated with estrogen imbalance, including menopausal symptoms, PMS, endometriosis, prevention of breast and prostate cancer, and protection against heart disease and osteoporosis.

The two main classes of phytoestrogens are isoflavones and lignans. Soy is perhaps the most common food source of isoflavones, but other excellent sources include legumes, clover, and kudzu root. Higher intakes of soy products and isoflavones, such as consumed in traditional Japanese diets, are associated with low rates of hormone-dependent cancers. Lignans are compounds found in fiber-rich foods such as flaxseeds, whole grains, legumes, and vegetables. Lignans stimulate the production of SHBG in the liver, and therefore reduce the levels of free estrogen in circulation. They also inhibit aromatase, an enzyme that synthesizes estrogen.

Vitamin E and Magnesium — Low serum vitamin E is associated with elevated estrogen levels, and may negatively affect estrogen detoxification. Women with PMS have experienced improvements of their symptoms when given supplemental vitamin E. Magnesium promotes estrogen detoxification by promoting methylation and glucuronidation, key estrogen detoxification pathways. Ovarian hormones influence magnesium levels, triggering decreases at certain times during the menstrual cycle as well as altering the calcium to magnesium ratio. These cyclical changes can produce many of the well-known symptoms of PMS in women who are deficient in magnesium and/or calcium.

Indole-3-Carbinol (I3C) – I3C is a naturally occurring compound derived from cruciferous vegetables that actively promotes the breakdown of estrogen via the beneficial 2-OH pathway. Therefore, I3C is protective to estrogen-sensitive tissues and may be beneficial to those with health issues related to excessive estrogen. Not only does I3C promote healthier estrogen metabolism, it may also act as a “weak” or anti-estrogen in a similar fashion to isoflavones.

B Vitamins — B12, B6 and folate function as important cofactors for enzymes involved in estrogen detoxification; thus, decreased levels of B vitamins can lead to increased levels of circulating estrogens. Vitamin B6 can also modulate the effects of estrogen by decreasing the cell’s response when estrogen binds to the estrogen receptor. B vitamins are also important for DNA synthesis and repair.

Beneficial Phytonutrients and Herbs

Many other compounds can promote healthy estrogen metabolism.  Curcumin, a compound found in the herb turmeric (Curcuma longa) increases the phase II detoxification of estrogens; chrysin, a bioflavonoid that inhibits aromatase activity, thus reducing the synthesis of estrogen; D-limonene from citrus fruits promotes the detoxification of estrogen and shows promise in the prevention and treatment of breast and other cancers. Antioxidants can reduce the oxidation of the 2-OH and 4-OH estrogen metabolites. Antioxidants include vitamin C, N-acetyl cysteine, selenium, and green tea.  Traditional medicines from many cultures have relied on a variety of hormone-modulating herbs in treating women’s health conditions. These include black cohosh, chaste berry, ginseng, dong quai, and licorice.

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Hypothyroidism

Dr. Renata Trister DO

The thyroid gland is a butterfly-shaped endocrine gland that is located in the lower front of the neck. The thyroid gland is an important organ of the endocrine system. The thyroid’s job is to make thyroid hormones, which are secreted into the blood and then carried to every tissue in the body. Thyroid hormone helps the body use energy, stay warm and keep the brain, heart, muscles, and other organs working properly. The thyroid makes hormones that control the way every cell in the body uses energy. This process is called metabolism.

Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn’t produce enough of certain important hormones. An underactive thyroid is most common in women and patients over 50.

HOW DOES THE THYROID GLAND FUNCTION?

The major thyroid hormone secreted by the thyroid gland is thyroxine, also called T4 because it contains four iodine atoms. T4 is converted to triiodothyronine (T3) by the removal of an iodine atom. T3 is the active form of thyroid hormone. This occurs mainly in the liver and in the brain. The amount of T4 produced by the thyroid gland is controlled by another hormone, which is made in the pituitary gland located at the base of the brain, called thyroid-stimulating hormone (abbreviated TSH). The amount of TSH that the pituitary sends into the blood stream depends on the amount of T4 that the pituitary sees. If the pituitary sees very little T4, then it produces more TSH to tell the thyroid gland to produce more T4. Once the T4 in the blood stream goes above a certain level, the pituitary’s production of TSH is shut off. In fact, the thyroid and pituitary act in many ways like a heater and a thermostat. When the heater is off and it becomes cold, the thermostat reads the temperature and turns on the heater. When the heat rises to an appropriate level, the thermostat senses this and turns off the heater.

TSH and T4:

The best way to initially test thyroid function is to measure the TSH level in a blood sample. A high TSH level indicates that the thyroid gland is failing because of a problem that is directly affecting the thyroid (primary hypothyroidism). (Low TSH levels usually indicate that the person has an overactive thyroid that is producing too much thyroid hormone.) Occasionally, a low TSH may result from an abnormality in the pituitary gland, which prevents it from making enough TSH to stimulate the thyroid (secondary hypothyroidism).

T4 circulates in the blood in two forms: 1) T4 bound to proteins that prevent the T4 from entering the various tissues that need thyroid hormone and 2) free T4, which does enter the various target tissues to exert its effects. The free T4 fraction is the most important to determine how the thyroid is functioning, and tests to measure this are called the Free T4 (FT4) and the Free T4 Index (FT4I or FTI). Individuals who have hyperthyroidism will have an elevated FT4 or FTI, whereas patients with hypothyroidism will have a low level of FT4 or FTI. Combining the TSH test with the FT4 or FTI accurately determines how the thyroid gland is functioning. The finding of an elevated TSH and low FT4 or FTI indicates primary hypothyroidism due to disease in the thyroid gland. A low TSH and low FT4 or FTI indicates hypothyroidism due to a problem involving the pituitary gland. A low TSH with an elevated FT4 or FTI is found in individuals who have hyperthyroidism.

The most common cause of hypothyroidism is thyroiditis. Swelling and inflammation damage the thyroid gland’s cells.

Thyroiditis is caused by:

The immune system attacking the thyroid gland

Viral infections (common cold) or other respiratory infections

Pregnancy (often called postpartum thyroiditis)

Other causes of hypothyroidism include:

Certain medicines, such as lithium and amiodarone

Congenital (birth) defects

Radiation treatments to the neck or brain to treat different cancers

Radioactive iodine used to treat an overactive thyroid gland

Surgical removal of part or all of the thyroid gland

SYMPTOMS:

Constipation

Increased sensitivity to cold temperature

Fatigue or feeling slowed down

Heavier and irregular menstrual periods

Joint or muscle pain

Paleness or dry skin

Sadness or depression

Thin, brittle hair or fingernails

Weakness

Weight gain

If untreated:

Decreased taste and smell

Hoarseness

Puffy face, hands, and feet

Slow speech

Thickening of the skin

Thinning of eyebrows

TREATMENT:

Treatment is aimed at replacing the thyroid hormone that you are lacking.

Levothyroxine (also called Synthroid) is the most commonly used medication:

You will be prescribed the lowest dose possible that relieves your symptoms and brings your blood hormone levels back to normal.

Most people with an underactive thyroid will need to take this medicine for life.

When starting your medicine, your dosage may need adjustment and your hormone levels may need to be monitored for 2 to 3 months. Once your hormone levels stabilize, your thyroid hormone levels will be monitored at least once every year.

When you are taking thyroid medicine, be aware of the following:

Do not stop taking the medicine when you feel better. Continue taking it exactly as your doctor prescribed.

If you change brands of thyroid medicine, let your doctor know. Your levels may need to be checked.

Thyroid medicine works best on an empty stomach and when taken 1 hour before any other medications.

Wait at least 4 hours after taking thyroid hormone before you take fiber supplements, calcium, iron, multivitamins, aluminum hydroxide antacids, colestipol, or medicines that bind bile acids.

While you are taking thyroid replacement therapy, tell your doctor if you have any symptoms that suggest your dose is too high, such as:

Palpitations

Rapid weight loss

Restlessness or shakiness

Sweating

DIETARY DEFENSE:

Making dietary changes can be very helpful to your overall health and in addressing hypothyroidism. Many people with hypothyroidism experience crippling fatigue and brain fog, which prompts reaching for non-nutritional forms of energy like sugar and caffeine.

1. Decrease Sugars: Greatly reduce or eliminate caffeine and sugar, including refined carbohydrates like flour, which the body treats like sugar. Reduce grain-based carbohydrates and focus on eating non-starchy vegetables.

2. Add Healthy Proteins: Proteins include nuts and nut butters; quinoa; hormone- and antibiotic-free animal products (organic, grass-fed meats, eggs, and sustainably-farmed fish); and legumes.

3. Good fats: Fat is your friend and cholesterol is the precursor to hormonal pathways; if you’re getting insufficient fat and cholesterol, you could be exacerbating hormonal imbalance, which includes thyroid hormones. Natural, healthful fats include olive oil; ghee; avocados; flax seeds; fish; nuts and nut butters; hormone- and antibiotic-free full fat cheese, yogurt, and cottage cheese (yes, full fat, not skim); and coconut milk products.

3. Nutrients: While nutritional deficiencies may not be the cause of hypothyroidism, not having enough of these micronutrients and minerals can aggravate symptoms: vitamin D, iron, omega-3 fatty acids, selenium, zinc, copper, vitamin A, the B vitamins, and iodine.

It’s commonly believed that hypothyroidism is due to insufficient iodine, but this is not always true true.  Rather than supplements, primary sources of iodine include sea vegetables and seafood. Secondary sources: eggs, asparagus, lima beans, mushrooms, spinach, sesame seeds, summer squash, Swiss chard, and garlic.

Omega-3s, found in fish, grass-fed animal products, flaxseeds, and walnuts, are the building blocks for hormones that control immune function and cell growth, are critical to thyroid function, and improve the ability to respond to thyroid hormones.

4. Address underlying food sensitivities. Just like the body’s attack on the thyroid in the presence of Hashimoto’s thyroditis, the body will also see offending or inflammatory foods as an invader and can induce or exacerbate the autoimmune response. There is much association with gluten sensitivity and various autoimmune disorders. Eating gluten can increase the autoimmune attack on your thyroid. Trying a gluten free diet may be helpful.

5. Do a gut check. A whopping 20 percent of thyroid function depends on a sufficient supply of healthy gut bacteria, so it’s best to supplement with probiotics (friendly intestinal bacteria).

6. Address silent inflammation with whole foods nutrition. Systemic inflammation and autoimmunity often go hand-in-hand.

7. Look at your stressors and practice relaxation. The thyroid is a very sensitive gland and is exceptionally reactive to the stress response.

PROGNOSIS:

In most cases, thyroid hormone levels  and symptoms will return to normal with proper treatment. You will likely take a thyroid hormone medicine for the rest of your life.

 

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Hormone Replacement Therapy

Also called: ERT, Estrogen replacement therapy, HRT, Menopausal hormone therapy 

 Renata Trister DO

Menopause is a normal life event that usually occurs between ages 40 and 55. It is defined as 12 months without a menstrual period. Surgical removal of the uterus and ovaries, chemotherapy or other medical interventions and/or trauma can lead to early menopause (younger than 40).

Each woman will experience menopause in her own unique way. Some women may not experience any symptoms at all. For many women, however, the most common symptoms are hot flashes, night sweats, and vaginal dryness. The most effective treatment for these symptoms is hormone replacement therapy (HRT), although other treatments are also available.

HRT commonly refers to two different options:

     If you have a uterus, you may be prescribed combination estrogen plus progestin therapy (EPT). The progestin is added to protect your uterus from cancer that can occur when estrogen is used alone. If you are prescribed a low‐dose vaginal estrogen for treatment of vaginal dryness, you probably will not be prescribed a progestin.

     If you do not have a uterus, you will need only one hormone, estrogen (ET). There are many HRT options available by prescription from your doctor:

     A pill taken by mouth  a patch, cream, gel, or spray that can be applied to your skin  a cream, suppository, tablet, or ring that can be used within the vagina.

Many doses are available to meet your needs. Each of these options has different pros and cons that you can discuss with your healthcare provider.

Bioidentical hormones, which are similar to the hormones naturally made by the ovaries, are available in well‐tested, government‐approved products that can be prescribed by your doctor. Bioidentical hormones are a good option for many women.

In 2002, a large study called the Women’s Health Initiative (WHI) reported an increased risk of breast cancer, heart disease, stroke, and blood clots with the use of HRT. In the ten years since the reporting of those results, we have learned that the type of HRT (Estrogen versus estrogen-progestin therapy), how it is taken, and the timing of starting this treatment (early versus late after menopause) produce different benefits and side effects. The risk of side effects (such as heart attack, stroke, blood clot, or breast cancer) with HRT in healthy women ages 50 to 59 is low. In contrast, using HRT for a long time or starting HRT when you are a number of years beyond menopause is associated with a higher risk of these side effects.

Evaluating the benefits and risks of HRT for you personally is an important discussion for you to have with your physician. Treatment options should be tailored to your needs and your concerns.

HRT remains the most effective treatment available for menopausal symptoms, including hot flashes and night sweats that can interrupt sleep and impair quality of life. Many women can use these therapies safely.

Having a history of blood clots, heart disease, stroke, or breast cancer, make HRT risky, and is only used in special situations.

     The length of time is different for EPT (estrogen-progestin) and ET(estrogen only). For EPT, the time is limited by the increased risk of breast cancer that is seen with more than 3 to 5 years of use. For ET, no sign of an increased risk of breast cancer was seen during an average of 7 years of treatment, a finding that allows more choice in how long you choose to use ET.

     Healthy women under age 60, do not increase risk of heart disease with HRT. The risks of stroke and blood clots in the lungs do increase, averaging to 1 in every 1000 women per year.

     ET delivered through the skin (by patch, cream, gel, or spray) and low‐dose oral estrogen may have lower risks of blood clots and stroke than standard doses of oral estrogen, but all the evidence is not yet available. Research will continue to bring valuable information to help women with their decision about HRT.

 

 

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Gut Dysfunction and Chronic Disease: “4R GI Restoration Program”

Summary Article Review.

Renata Trister DO

Gastrointestinal (GI) symptoms are one of the leading causes for visits to the primary care physician and the emergency room.  Over 70 million Americans are suffering from some form of serious GI disorder.  Assessment and proper support of the gastrointestinal (GI) system may provide benefit for patients with a variety of chronic ailments.   There is an association between impaired GI function and some chronic conditions, such as gastritis, peptic ulcers, colon cancer, inflammatory bowel disease, irritable bowel syndrome, rheumatoid arthritis, asthma, eczema, metabolic bone disease, allergies, nutrient malabsorption, and esophageal reflux (GERD). Many factors are associated with impaired GI function including food allergies, excessive stress, and the use of non-steroidal anti-inflammatory (NSAIDS) drugs and corticosteroids.  Fortunately, the constant renewal of intestinal cells provides a great opportunity for healing.

Recent work has been compiled in order to define a systematic approach for the support and optimization GI function. Based on the concepts of Remove, Replace, Reinoculate, and Regenerate, the 4R GI Restoration Program promotes overall GI health by removing unhealthy bacteria from the intestinal tract and allergenic foods from the diet, replacing supportive stomach acids and digestive enzymes, reinoculating the intestine with healthy bacteria (probiotics), and regenerating the intestinal lining with targeted nutritional support.

GI Restoration and the 4R Program

Remove focuses on eliminating harmful bacteria, viruses, fungi, parasites, and other environmentally derived toxic substances from the GI tract. An oligoantigenic or “elimination” diet is important to this step of the 4R GI Restoration Program, since foods to which a patient is intolerant or allergic can worsen GI dysfunction and stimulate negative immune and inflammatory responses.

It is important to keep in mind that even a healthy GI tract may permit pathogens, food proteins and environmental toxins to reach the circulation system. Therefore, removal of offending substances and microorganisms is a critical component in GI restoration.

Replace refers to the replacement of enzymes and other digestive factors lacking or in limited supply in an individual’s GI environment. These include digestive enzymes, such as pepsin, proteases, lipases, and saccharidases, as well as hydrochloric acid (HCl) and intrinsic factor.

HCl is particularly important to consider, especially in individuals older than 60, since inadequate levels (hypochlorhydria) are often associated with GI dysfunction. HCl is necessary for proper digestion, nutrient absorption, and the breakdown of protein for further digestion in the small intestine. HCl has been shown to effectively kill harmful organisms in the GI tract—which results in the decreased likelihood and severity of certain bacterial and parasitic intestinal infections.

Nutritional deficiencies can also impact GI function, protection, and health. Extensive evidence suggests a strong association between Helicobactor pylori infection and vitamin C deficiency. H. pylori is a bacteria that can cause peptic ulcers and stomach inflammation (chronic gastritis). Since vitamin C may help eradicate H. pylori, this deficiency, when coupled with poor intake of vitamin C, may increase both the colonization of H. pylori and the threat to the GI tract. In addition, zinc deficiency is known to worsen inflammatory bowel disease, delay GI restoration, and cause a variety of functional problems, including interruption of protein synthesis and reduced cell-mediated immunity.

Reinoculate refers to the reintroduction of desirable bacteria (or probiotics) into the intestine to restore the balance of the GI tract. Probiotics are “friendly” bacteria that serve a variety of functions in the GI tract.  For example, they prevent colonization by harmful bacteria and help break down toxins. Lactobacillus acidophilus and Bifidobacterium lactis are examples of probiotics.

Prebiotics may also be useful in supporting a healthy bacterial balance. Prebiotics are non-digestible food ingredients that selectively stimulate the growth of friendly bacteria without supporting pathogenic flora. Some prebiotics include fructooligosaccharides, soluble rice fibers, some soy fibers, and arabinogalactans.

Regenerate refers to providing support for the healing and growth of the GI mucosa. Part of the support for healing comes from promoting healthy microflora and removing impediments that continually re-injure or irritate the mucosa. In addition, appropriate nutritional support is crucial to overall health and responsible for reversing GI dysfunction and eliminating the chronic diseases associated with it. Important nutrients for support of GI regeneration include vitamins C and E and the carotenoids, for their antioxidant effects, and zinc and vitamin B5 (pantothenic acid), due to their roles in supporting the healing mechanisms. In addition, the following dietary factors are particularly helpful for the healing and regeneration of the GI tract.

Plantain Fruits The mucus coating in the GI system is important in protecting the body from microbes such as H. pylori and other ulcer causing substances (NSAIDS, alcohol) Plantains contain botanical phytonutrients that support the upper GI mucus layer.  Plantains contain lectins and flavonoids, which promote mucus thickening and protect the gastric layer from damage by exogenous agents. For these reasons plantains can be used therapeutically.

Phosphatidylcholine Recent studies show that consumption of phosphatidylcholine (lecithin) with potential ulcer-causing substances like aspirin or bile salts protects the gastric layer from damage and promotes healing.

L-Glutamine The amino acid glutamine is considered a preferred fuel for the rapidly replicating cells of the GI mucosa. Glutamine may promote production of glutathione (an important antioxidant) in the GI cells, which supports healing and provides additional protection from free radical damage during inflammation. Dietary glutamine is important for maintenance of GI mucosa during stress, injury, inflammation, and sepsis—a serious, severe illness caused by infection of the bloodstream. Furthermore, glutamine deficiencies are often associated with degenerative changes in the small intestine following intestinal injury, infection, surgery, or radiation.

Lactoferrin and Lactoperoxidase These proteins are found in milk and other secretions and play important roles in the intestinal immune system. They have have antimicrobial and antiviral properties, stimulate the immune system, and promote healing of the GI tract.

Arabinogalactans are non-starch polysaccharides found in many vegetables and grains. They are considered a fiber, but also have prebiotic functions that promote healthy intestinal bacteria, and can support the immune system.

Summary of the 4R GI Restoration program:

1. Remove any of the factors that may be causing GI dysfunction. Pathogens include “bad” bacteria, viruses, fungi and parasites.  Identify and remove foods to which the individual is sensitive.

Clinical approaches may include:

Elimination diet

Botanical antimicrobials and phytonutrients

1. Replace digestive enzymes and restore normal pH of the stomach.

2. Reinoculate with “good” bacteria or probiotics along with prebiotics.

3. Regenerate by providing nutritional support for healing and growth of normal GI mucosaMicronutrients especially important for GI support include

Vitamin C, Vitamin E and carotenoids for their antioxidant abilities

Zinc and Vitamin B5 for their roles in healing.

The key to successful regeneration is providing the nutrients necessary for the mucosal epithelial cells to proliferate.  A diet that is high in nutritional value and low antigenicity provides a basis for the regeneration of the GI tract.

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