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New Treatment for Crohn’s and Ulcerative Colitis with Safer & Greater Efficacy


Crohn’s disease and ulcerative colitis, otherwise known as inflammatory bowel disease (IBD) are two diseases that I am most passionate about treating because of my mother’s experience with Crohn’s disease.  Seeing my mother suffer from her illness opened my eyes to the extent to which inflammatory bowel disease can affect every aspect of daily life.

The current model for IBD treatment focuses solely on crisis management and neglects to treat what actually causes the disease to develop and exist i.e. a genetic defect causing serotonin and dopamine imbalance.  The treatment approach that will be discussed below does not replace acute/emergency management but rather is designed to fix the cause of the disease to support healing.  Through this new treatment people with IBD may have an opportunity to be completely healed.


The brain and nervous system use signaling molecules to transmit messages from one place to another. The group of signaling molecules called monoamine neurotransmitters (serotonin, dopamine, epinephrine, norepinephrine) is important for digestive health and brain function.  The digestive system and brain must have the proper balance and sufficient levels of these signaling molecules in order to be healthy and function normally.


There is a known genetic defect of neurotransmitter transporters (OCTN1/OCTN2) in the gastrointestinal tract of IBD patients.1 OCTN1 and OCTN2 are responsible for the transport of dopamine and serotonin. Because these transporters are defective, serotonin levels are too high causing serotonin toxicity, tissue damage, and the generation of symptoms.2,3


The imbalance between serotonin and dopamine in the digestive system has been shown to be the primary cause of inflammation that leads to tissue destruction in the intestines.4  The high serotonin level in the GI tract is what initiates the inflammatory process and perpetuates tissue damage.  Therefore, unless this genetic defect is addressed and treated, the disease process will continue to progress.

It should be noted that people with IBD often have associated anxiety and/or depression symptoms.  This could be the result of the previously discussed imbalance between serotonin and dopamine, both of which are vital for mood, cognition, and general psychiatric health.

Genetic Defect and IBD- Flow Chart

Genetic Defect in OCT1/OCT2 transporters — Serotonin/Dopamine imbalance — Immune Activation — Chronic inflammation – Intestinal wall damage = disease (IBD)

THE SOLUTION – New Treatment Approach

A group of medical doctors developed a cutting-edge treatment protocol using 17 years of clinical research. This nutritional approach balances the serotonin and dopamine neurotransmitters in the brain and gastrointestinal system. When these two neurotransmitters are BALANCED, excessive serotonin will no longer trigger the inflammatory process and intestinal tissue can begin to heal.5

This approach bypasses the genetically defective neurotransmitter transporter, and thereby achieves balance and restoration of normal function.  Treatment includes physician administration of serotonin and dopamine amino acid precursors using organic cation transporter(OCTN1/2) analysis testing.

Benefits of this approach:

  • Treats and bypasses the main genetic defect that perpetuates these diseases
  • Non-drug approach with proven efficacy
  • Only documented treatment to achieve full disease resolution = no symptoms and complete tissue healing5,6
  • Often time’s patients will experience relief of anxiety and depression symptoms through balancing serotonin and dopamine.

Delaying this approach:

  • Continues intestinal and other bodily damage through chronic inflammation
  • Continues exposure to powerful drugs their potential harmful side effects that suppress the immune system
  • Increases the likelihood of surgery and disease progression
  • Some may view their disease as mild and manageable but in reality Crohn’s disease and ulcerative colitis are like a walking time bomb, at any moment disaster can happen leading to unexpected surgery or death.

Note: There are other genetic defects seen in IBD patients but the previously discussed defect is among the most important for treatment.  Other aspects of comprehensive integrative medicine IBD care include: treatment of identified nutritional deficiencies, optimizing digestion and assimilation of food/nutrients, optimizing gut microbes, patient specific nutritional regimen, and intestinal lining repair.  Treating the neurotransmitter genetic defect is the seen to be one of the most important factors for complete remission of inflammatory bowel disease.


All medications are continued at the initiation of this treatment approach.  Only until complete stabilization has been reached and upon the supervision and direction of a gastroenterologist are medications to be changed or altered.

This blog is for general informational purposes only and does not constitute the practice of professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this blog or materials linked from this blog is at the user’s own risk. The content of this blog is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard, or delay in obtaining, medical advice for any medical condition they may have, and should seek the assistance of their health care professionals for any such conditions.


  1. Sartor RB. Mechanisms of disease: pathogenesis of Crohn’s disease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol. 2006;3(7): 390–407.
  2. Itta M. Minderhoud, Bas Oldenburg, Marguerite E.I. Schipper, Jose – J.M. ter Linde, Melvin Samson. Serotonin Synthesis and Uptake in Symptomatic Patients with Crohn’s Disease in Remission. Clinical Gastroenterology and Hepatology. June 2007
  3. R. Spiller. Recent advances in understanding the role of sertonin in gastrointestinal motility in functional bowel disorders: alterations in 5-HT signaling and metabolism in human disease. Neurogastroenterology and Motility. Jul. 2007
  4. Jean-Eric Ghia, Nan Li, Huaqing Wang et al. Serotonin has a key role in pathogenesis of experimental colitis. Gastroenterology. Nov 2009
  5. Stein, A., Hinz, M., & Uncini, T. (2010). Amino acid-responsive Crohn’s disease: a case study. Clinical and experimental gastroenterology, 3, 171.
  6. Hinz, M., Stein, A., & Uncini, T. (2012). Relative nutritional deficiencies associated with centrally acting monoamines. Int J Gen Med, 5, 413-430.
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Hair Loss in Women

Why you’re losing hair: 8 Common Causes for women hair loss in women – And what to do about it

  • Hypothyroidism: = underactive thyroid
  • Thyroid disorders are the most common cause of hair loss in women, with 90% of cases being Hashimoto’s thyroiditis. This is a disease that causes the immune system to attack and destroy thyroid tissue, lowering hormone levels.  The standard of care is to replace the depleted thyroid hormone to hopefully relieve symptoms.  This approach while often necessary, fails to address the multiple factors causing the immune system to destroy the thyroid.
  • SOLUTION: Functional medicine can treat the underlying problem, stop the damage to the organ, and in most cases restore healthy function of the thyroid, and thereby fixes the hair loss problem. (Hashimoto’s Thyroiditis article upcoming in the future)
  • Anemia: Approximately 1 out 10 women suffers from anemia caused by iron deficiency. – Associated symptoms include fatigue, cold hands and feet, headache, and dizziness.
  • SOLUTION: Your doctor can order a simple blood test to see whether you have this type of anemia. In most cases additional iron intake either through food or medicine is necessary.  Caution- supplementation without doctor supervision can be dangerous because excessive iron can initiate inflammation throughout the body.
  • Telogen Effluvium: hair growth temporarily stops and becomes dormant
  • Potential causes include the flu, stress, pregnancy, or stopping birth control pills.2,3
  • SOLUTION: Depending on the cause hormone balancing treatment, stress management, and/or immune system support may be indicated.
  • Trichotillomania: Psychological disorder causing a strong impulse to pull out hair. Most commonly affecting younger girls.
  • SOLUTION: Monoamine amino acid therapy has been shown to yield successful results.

 Medication Induced:

  • Medications: Cholesterol lowering drugs, Parkinson’s medications,4 antiulcer drugs,5 anticoagulants,6 anti-arthritics,7 drugs derived from vitamin A,8 anticonvulsants,9 beta-blockers,10 and anti-thyroid drugs.11
  • SOLUTION: It’s important to know what you’re taking and the risks/benefits of each medication. Potential side effects should be discussed with your doctor.
  • Nutritional Deficiencies/Therapies:
  • Biotin Deficiency: this is a water-soluble vitamin necessary for healthy hair growth and maintenance. Supplementing with 1mg/daily has been shown to improve hair loss (especially hair thinning) if biotin deficiency is present and the causative factor.12  Effects can be seen as soon as 1 week of consistent repletion.
  • L-arginine: is used to produce nitric oxide, a key factor in maintaining and promoting new hair growth.
  • Vitamin E: has potential to support youthful hair thickness and growth. Study with 30 people, nearly all subjects showed improvement in hair thickness and density.13  Note: It is important to only take pharmaceutical-grade mixed tocopherols for the best results and ensured safety.
  • Lack of Protein: If protein intake is low or the body is not able to digest and use protein efficiently the body will begin to shut down hair growth. Adult Recreational Exerciser: recommended 0.5-0.75 grams of protein per pound of weight.
  • Vitamin B Deficiency: Often seen in women who are dieting off and on for long periods of time, dramatic weight loss, or in those taking over-the-counter or prescription antacid medication. Antacids decrease stomach acid and will therefore hinder B vitamin absorption. It often necessary to identify the cause to truly fix the deficiency, as well as to increase vitamin B ingestion. For supplementation it is best to take a vitamin B complex, as this will increase the likelihood of balanced repletion.
  • Note: Chronic antacid use contributes to B vitamin deficiencies and B12 in particular because stomach acid is necessary for B12 absorption. Chronic B12 deficiency can cause nerve pain, depression symptoms, and/or fatigue.
  • Lupus: autoimmune disease
  • This is an autoimmune disease where the body’s immune system attacks and damages connective tissue as well as other organs including hair. If autoimmune disease is in your family history it may be important to see your doctor for testing.
  • SOLUTION: Lupus is a serious disease with many potential complications. Functional medicine can be used to identify and treat the specific factors that may be causing your immune system to attack your body so the best possible outcome can be achieved.
  • Polycystic Ovary Syndrome (PCOS): most common female hormone disorder
  • Symptoms of this disorder include excess facial hair, acne, weight gain, and infertility. Those affected commonly have insulin resistance and excess androgen production (testosterone) resulting in body hair, acne, and hair loss.
  • Most common cause of female infertility and is associated with developing type 2 diabetes.
  • SOLUTION: Underlying causes include insulin resistance and hormonal imbalance. Standard of care often neglects to treat insulin resistance through lifestyle and specific nutritional interventions.
  • Nutritional therapies proven to improve insulin resistance includes in PCOS:
  • Myo-inositol: improves insulin sensitivity; beneficially lowers testosterone, blood pressure, and triglycerides; promotes weight loss; and increases ovulation frequency.14,15,16,17,18
  • N-acetyl cysteine(NAC): improves insulin sensitivity in PCOS; can contribute to fertility restoration.19,20
  • Magnesium: These women tend to be magnesium deficient which can significantly contribute to insulin resistance and elevated blood glucose levels.21,22
  • Chromium: improves insulin sensitivity23
  • Lipoic Acid: can improve insulin sensitivity, promote weight loss, reduce blood pressure, improve cholesterol profile, and is a powerful antioxidant.24,25
  • Vitamin D: contributes to healthy insulin levels and normal menstrual cycle regulation26,27
  • Omega-3 Fatty Acids: can reduce liver fat content and improve cardiovascular health in women with PCOS.28
  • Cinnamon: can improve insulin resistance and can produce a 20-fold increase in sugar metabolism29,30,31

Note: It is important to seek the care of a dermatologist at first sign of hair loss to ascertain a proper diagnosis and appropriate treatment.


  • Hibino T, Nishiyama T. Role of TGF-beta2 in the human hair cycle. J Dermatol Sci. 2004 Jun;35(1):9-18.
  • Whiting DA. Chronic telogen effluvium. Dermatol Clin. 1996 Oct;14(4):723-31.
  • Hadshiew IM, Foitzik K et al. Burden of hair loss: stress and the underestimated psychosocial impact of telogen effluvium and androgenetic alopecia. J Invest Dermatol. 2004 Sep;123(3):455-7
  • Yamada K, Goto S. Bilateral subthalamic nucleus stimulation results in reversal of alopecia in Parkinson’s disease. Parkinsonism Relat Disord. 2004 Aug;10(6):353-5.
  • Borum ML, Cannava M. Diffuse alopecia associated with omeprazole. Am J Gastroenterol. 1997 Sep;92(9):1576.
  • Sarris E, Tsele E et al. Diffuse alopecia in a hemodialysis patient caused by a low-molecular-weight heparin, tinzaparin. Am J Kidney Dis. 2003 May;41(5):E15
  • Ettefagh L, Nedorost S et al. Alopecia areata in a patient using infliximab: new insights into the role of tumor necrosis factor on human hair follicles. Arch Dermatol. 2004 Aug;140(8):1012.
  • Chave TA, Mortimer NJ et al. Agranulocytosis and total scalp alopecia following acitretin. Br J Dermatol. 2003 May;148(5):1063-4
  • Kohno Y, Ishii A et al. [A case of hair loss induced by carbamazepine]. Rinsho Shinkeigaku. 2004 Jun;44(6):379-81.
  • Gautam M. Alopecia due to psychotropic medications. Ann Pharmacother. 1999 May;33(5):631-7
  • Shelley ED, Shelley WB. Alopecia and drug eruption of the scalp associated with a new beta-blocker, nadolol. Cutis. 1985 Feb;35(2):148-9.
  • Tosti A, Piraccini BM, Sisti A, Duqu-Estrada B. Hair loss in women. Minerva Ginecol. 2009 Oct;61(5):445-52.
  • Yuen Kah Hay, B. Randomized clinical trial of tocotrienols supplementation vs. placebo for androgenetic alopecia. School of Pharmaceutical Sciences, Universiti Sains, Malaysia.
  • Costantino D et al. Metabolic and hormonal effects of myo-inositol in women with polycystic ovary syndrome: a double-blind trial. Eur Rev Med Pharmacol Sci. 2009 Mar-Apr;13(2):105-10
  • Genazzani AD, Lanzoni C, Ricchieri F, JasonniVM. Myo-inositol administration positively affects hyperinsulinemia and hormonal parameters in overweight patients with polycystic ovary syndrome. GynecolEndocrinol. 2008 Mar;24(3):139-44.
  • Gerli S et al. Randomized, double blind placebo-controlled trial: effects of myo-inositol on ovarian function and metabolic factors in women with PCOS. Eur Rev Med Pharmacol Sci. 2007 Sep-Oct;11(5):347-54
  • Papaleo E, Unfer V, Baillargeon JP, Chiu TT. Contribution of myo-inositol to reproduction. Eur J ObstetGynecolReprod Biol. 2009 Dec;147(2):120-3
  • Zacchè MM, Caputo L, Filippis S, et al. Efficacy of myo-inositol in the treatment of cutaneous disorders in young women with polycystic ovary syndrome. GynecolEndocrinol. 2009 Aug;25(8):508-13
  • Abu Hashim H, Anwar K, El-Fatah RA. N-acetyl cysteine plus clomiphene citrate versus metformin and clomiphene citrate in treatment of clomiphene-resistant polycystic ovary syndrome: a randomized controlled trial. J Womens Health (Larchmt). 2010 November; 19(11): 2043-8
  • Badawy A, State O, Abdelgawad S. N-Acetyl cysteine and clomiphene citrate for induction of ovulation in polycystic ovary syndrome: a cross-over trial. ActaObstetGynecol Scand. 2007;86(2):218-22
  • Kauffman RP, Tullar PE, Nipp RD, Castracane VD. Serum magnesium concentrations and metabolic variables in polycystic ovary syndrome. ActaObstetGynecol Scand. 2011 Jan 4
  • Mooren FC, Kruger K, Völker S, Golf W, Wadepuhl M, Kraus A. Oral magnesium supplementation reduces insulin resistance in non-diabetic subjects – a double-blind, placebo-controlled, randomized trial. Diabetes, Obesity and Metabolism. 2011 March; 13 (3): 281-84
  • Lucidi RS, et al. Effect of chromium supplementation on insulin resistance and ovarian and menstrual cyclicity in women with polycystic ovary syndrome. FertilSteril. 2005 December; 84(6):1755-7
  • Pershadsingh HA. Alpha-lipoic acid: physiologic mechanisms and indications for the treatment of metabolic syndrome. Expert OpinInvestig Drugs. 2007 Mar;16(3):291-302
  • Masharani U, Gjerde C, Evans JL, YoungrenJF, GoldfineID.Effects of controlled-release alpha lipoic acid in lean, nondiabetic patients with polycystic ovary syndrome. J Diabetes Sci Technol. 2010 Mar 1;4(2):359-64.
  • Wehr EB et al. Vitamin D-associated polymorphisms are related to insulin resistance and vitamin D deficiency in polycystic ovary syndrome. Eur J Endocrinol. 2011 Mar 9
  • Rashidi B et al. The effects of calcium-vitamin D and metformin on polycystic ovary syndrome: a pilot study. Taiwan J Obstet Gynecol. 2009 Jun;48(2):142-7.
  • Cussons AJ, et al. Omega-3 fatty acid supplementation decreases liver fat content in polycystic ovary syndrome: a randomized controlled trial employing proton magnetic resonance spectroscopy. J ClinEndocrinolMetab. 2009 October; 94(10):3842-8
  • Broadhurst L, Polansky MM, Anderson, RA. Insulin-like biological activity of culinary and medicinal plant aqueous extracts in vitro. J Agric Food Chem. 2000 Mar; 48(3):849–52
  • Cao H, Graves DJ, Anderson RA. Cinnamon extract regulates glucose transporter and insulin-signaling gene expression in mouse adipocytes. Phytomedicine. 2010 Nov;17(13):1027-32
  • Anderson RA, Broadhurst CL, Polansky MM, et al. Isolation and characterization of polyphenol type-A polymers from cinnamon with insulin-like biological activity. J Agric Food Chem. 2004 Jan 14;52(1):65-70
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New Treatment Provides Hope for Parkinson’s Disease

Huge Problem

Parkinson’s disease is a devastating illness and the rate of people dying from this condition continues to skyrocket.   We now know the reason WHY and what you can do about it.

Almost all of those with Parkinson’s are taking a medication that has recently been shown to increase symptoms and cause the disease to progress leading to premature death.1,2

328.7% increase in DEATH RATE


What’s happening in Parkinson’s Disease?

The nervous system works like electricity; there must be sufficient signaling in order for the body to function properly.  If there is damage to enough nerves also called neurons, then signaling and function will be disrupted causing symptoms and/or disease.  This is the primary disease process seen in Parkinson’s.

Parkinson’s disease is characterized by permanent damage of dopamine neurons in part of the brain called the substantia nigra.  These nerves that are responsible for fine motor control and damage to this part of the brain can lead to tremor and other movement abnormalities.


What’s the current treatment?

89% of all Parkinson’s patients take Sinemet, which is a combination of two medications- Carbiodopa and Levodopa (L-dopa).

The Problems with Current Therapy:

 (1.) Carbidopa: makes the disease worse

 Carbidopa has been proven to bind irreversibly to vitamin B6 (pyridoxal 5’-phosphate) and permanently deactivate and deplete the entire vitamin B6 reserve pool.2,3

Why is this a Big Deal?

  • Carbiodopa negatively affects every system in the body, which why it is the culprit for the increased death rates and rapid disease progression.2,4  Vitamin B6 is required for the function of over 300 enzymes and proteins.
  • It is estimated that it takes 5 or more years of chronic ingestion before complete vitamin B6 DEPLETION occurs leading to progressive deterioration.2  This is why rapid Parkinson’s deterioration is seen approximately 5 years after Carbidopa administration.
  • Carbiodopa has no therapeutic value. It is only used to combat nausea associated with L-dopa administration.
  • Recent research in 2014, implicated Carbidopa as the causative agent in the development of irreversible movement abnormalities e.g. tremor.4

Click here to see the full list of Carbidopa induced side effects

*** (attach Carbidopa side-effects sheet Carbidopa_Side_Effects(1)-2.pdf located in documents)

(2.) Continued Brain Damage/Nerve Death

Neurotoxins: #1 leading cause of brain damage in Parkinson’s

A neurotoxin is any substance that can cause damage to the nervous system.  The body’s best defense against these harmful substances is glutathione.  Glutathione is made within the body and allows us to neutralize dangerous compounds within the system so we can safely get rid of them.

Neurotoxins are responsible for continued destruction of nervous tissue and thus continued disease progression in Parkinson’s.In the current treatment model there is no strategy to prevent further damage to the brain by neurotoxins.  Therefore, the root cause of the disease is never addressed.

L-Dopa reduces protection from neurotoxins.

L-dopa administration causes sulfur amino acids to be depleted.  The body uses sulfur amino acids to make glutathione.  As sulfur amino acids are depleted so is the level of glutathione and also the body’s ability to neutralize toxins and their consequential damaging effects.  Therefore chronic L-dopa without replenishing the depleted sulfur amino acids actually accelerates brain damage due to neurotoxins.

L-dopa— depletes sulfur amino acids—– decreased glutathione production = increased susceptibility to nerve damage by neurotoxins

(3.) Causes Imbalances in the Body

 Relative Nutritional Deficiencies:

A relative nutritional deficiency (RND) occurs when the body’s requirement for a specific nutrient is higher than what can be met through normal or even optimal diet.  Numerous relative nutritional deficiencies (RND) exist in Parkinson’s disease.  See figure below.

L-dopa depletes:6

  • L-tyrosine: inadequate tyrosine levels will cause dopamine levels to fluctuate, which may result in increased symptoms such as movement abnormalities.  Tyrosine also important in thyroid hormones.
  • Sulfur-amino acids: leads to increased susceptibility to nerve damage by neurotoxins
  • Serotonin: causes severe depletion and may contribute to the development of depression
  • Tryptophan: precursor to serotonin
  • Epinephrine

 Carbidopa depletes:

  • Vitamin B6: DEPLETION– contributes to increasing death rate and disease progression.
  • Serotonin, dopamine, epinephrine, norepinephrine.7


 A Better Way-  THE SOLUTION

A group of medical doctors developed a cutting-edge treatment protocol using 17 years of clinical research. This nutritional approach replaces carbidopa while effectively addressing the nutritional deficiencies associated with Parkinson’s disease and L-dopa.  This has proven to be the first real advancement in L-dopa and Parkinson’s disease treatment in 50 years.

Physician Administration: L-dopa + amino acids

L-dopa Restores Brain Function: Parkinson’s disease patients do not have enough dopamine in their brains.  This causes the symptoms of Parkinson’s disease.  The only way for the brain to make enough dopamine is by taking L-dopa.  In all Parkinson’s disease patients a relative nutritional deficiency exists sense high enough levels of the nutrient L-dopa cannot be obtained from even an optimal diet.  Treatment with L-dopa is necessary as soon as possible to maintain or restore optimal brain function.

Balance to Restore Health: As previously discussed L-dopa is the best therapy for Parkinson’s; but administered without other neurotransmitter precursors can cause numerous side effects and multiple nutritional collapses in the body.  Therefore, in addition to L-dopa, other amino acid precursors and nutrients must be administered skillfully to balance the system.

Eliminate Need for Carbidopa:  Properly administering serotonin precursors we can eliminate nausea associated with L-dopa ingestion and serotonin depletion.  Serotonin precursors are a superior and infinitely safer therapy than carbidopa.

 Protection from Toxic Damage:  Properly administering sulfur amino acids will prevent glutathione depletion by the disease process and L-dopa ingestion.  This approach enables the body’s defense against damaging neurotoxins.

 What are the expected outcomes of treatment?

For Parkinson’s disease patients who are early in the course of the disease, expectations should be complete restoration of function with few or no symptoms with slowed progression of the disease.   For patients who have had the diagnosis for many years; time, the disease, and drugs may have taken their toll.  While complete restoration of normal function may not be possible, the expectation should be to achieve the highest level of function possible without experiencing unmanageable L-dopa side effects.

What may happen if I delay treatment? Is it necessary?

Without this treatment approach, Parkinson’s patients experience significant nutritional deficiencies that cause the disease to get worse.  L-dopa can be the most effective therapy for Parkinson’s disease but is only successful long-term with this approach.  Delaying this type of treatment may prevent you from achieving complete symptom relief, as this is the only way to fix the real problem.  Each day without these relative nutritional deficiencies being treated, is another day that Parkinson’s disease progresses and permanent damage takes place.


  • 89% of all Parkinson’s patients are taking Sinemet- Carbidopa/L-dopa combination.
  • Carbidopa has been shown to cause severe vitamin B6 DEPLETION leading to nutritional collapse, increased symptoms, and disease progression- 328.7% increase in death rate in the past 38 years.
  • L-dopa can be the most effective treatment BUT unless it is balanced with other amino acids and nutrients it actually accelerates brain damage and is associated with numerous side effects. This is commonly seen with the current L-dopa approach to treatment.
  • Using cutting-edge mainstream medical research, we now have method to restore nerve and brain function, significantly reduce or eliminate symptoms, and protect against brain damage.
  • The current approach using carbidopa(Sinemet) is no longer medically and ethically responsible because the research strongly suggests it is causing a catastrophic nutritional collapse i.e. rapid disease progression.
  • This new approach is second to none for those with Parkinson’s disease because it addresses the underlying problems of the disease.


  • National Parkinson Foundation. The National Parkinson Foundation’s Help- line Speaks: Lessons from the 2011 Sinemet Shortage. Miami, FL: National Parkinson Foundation; 2012. Available from: Files/PDFs/NPF-Content-Documents/White-Papers/NPF466-_2011- Sinemet-Shortage_WhitePaper-_Full-art.
  • Hinz, M., Stein, A., & Cole, T. (2014). The Parkinson’s disease death rate: carbidopa and vitamin B6. Clinical pharmacology: advances and applications, 6, 161.
  • DaidoneF,MontioliR,PaiardiniA,etal.Identificationbyvirtualscreen- ing and in vitro testing of human DOPA decarboxylase inhibitors. PLoS One. 2012;7(2):e3161
  • Hinz, M., Stein, A., & Cole, T. (2014). Parkinson’s disease: carbidopa, nausea, and dyskinesia. Clinical pharmacology: advances and applications, 6, 189.
  • Zeevalk G, Manzino L, Sonsalla PK, Bernard LP. Characterization of intracellular elevation of glutathione (GSH) with glutathione monoethyl ester and GSH in brain and neuronal cultures: Relevance to Parkinson’s disease. Exp Neurol. 2007;203:512–520.
  • Hinz, M., Stein, A., & Uncini, T. (2011). Amino acid management of Parkinson’s disease: a case study. International journal of general medicine, 4, 165.
  • Hinz, M., Stein, A., & Uncini, T. (2012). Relative nutritional deficiencies associated with centrally acting monoamines. Int J Gen Med, 5, 413-430.
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