Graves disease can be scary. It often starts off with terrible symptoms like a racing heart and a sensation of panic. All too often people who have it go on for some time before getting answers.

The core message I’d like to share is that Graves’ disease is treatable. Most people who have it can have the condition cured within 18-24 months by including natural treatments.

When they do get a final diagnosis, people often feel rushed into treatments that have permanent consequences. The natural question is whether there is some way to treat Graves’ disease without destroying the thyroid. Many wish to find a natural way to slow their thyroid without making them depend on long-term medications.

This article will explain what Graves’ disease is, how it is typically treated, and when natural treatments might be an option. Read More: https://www.drchristianson.com/how-to-treat-graves-disease-naturally/

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People with thyroid disease need better options. Because you can feel better. You deserve nothing less. The Thyroid Reset Diet gives you a step-by-step plan to reset your thyroid—and restore it to good function. The goal? Up to 70% of people feel significantly better and reverse their thyroid disease. Receive Special Gifts When You Order Your Copy Today: https://www.drchristianson.com/thyroidresetdiet/

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In this week’s episode of Thyroid Thursday with oculoplastic surgeon, Dr. Raymond Douglas, learn about the best methods to control the symptoms of Graves’ disease.

LEARN MORE – https://raymonddouglasmd.com/orbit/thyroid-eye-disease/

Graves’ disease is an autoimmune condition that can attack a number of organs, including the thyroid. Despite the fact that there is no official way to cure this disease, there are several ways to manage the symptoms.

Whether it’s taking thyroid medication, natural remedies like diet and exercise, or having your thyroid removed, Dr. Douglas and his team will guide you towards a better quality of life.

For more information regarding Graves’ eye disease, please contact our office! As a leading expert in his field, Dr. Douglas offers in-office consultations or Skype consultations for our out-of-town patients.

-CONTACT DR. DOUGLAS-
Call – 310.657.4302
Email – info@raymonddouglasmd.com
Website – https://raymonddouglasmd.com/
Facebook – https://www.facebook.com/thyroideyediseaseawareness
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Women are more at risk than men, with one in eight women developing thyroid problems in her lifetime, especially after pregnancy and menopause.
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Hey guys, here’s an update on how I am feeling taking no medication but healing my temple naturally! God is so good!

Here are some of the supplements that I take, I am only consistent with a few. 🙏🏽

Promise of God (Our Church)
https://www.youtube.com/channel/UCzGDvIQM1WcAH0IUkXMvfJg

HAIR on Faiths Oven

Here are some videos I enjoyed about FASTING

Fasting: The Full Movie (All You Need To Know)
https://youtu.be/A5sA18TzHM0

The Science of Fasting
https://youtu.be/t1b08X-GvRs

Other videos related to my Journey

My favorite green mango smoothie

Thyroid Juice | What Helps Me | Graves Disease
https://youtu.be/d_nhgqSLKuI

Hyperthyroidism – Graves Disease | MyStory – Sympthoms – How I’m healing naturally

Hyperthyroid part 3. How I am Healing Naturally/ Vitamins I take to Help Symptoms / Plant Based Diet
https://youtu.be/8eW9tPZEPas

Update – My Hyperthyroidism | Graves Disease | How I’m Healing Naturally – Part 2
https://youtu.be/iCZ3eEV2Tao

RECIPES ON FAITHS OVEN

How to make Stir Fry with Noodles Recipe

Oregano Oil and Elderberry Syrup Homemade | Cold & Flu Season| How to make and their benefits

Day #4 Plant Based Breakfast Ideas | Smoothie

How to make the BEST Home Made Alfredo Sauce | The Remix| From Scratch | Simple | Easy

How to make Potato Curry | Plant Based | vegan

The Best Meatless Chili – How to make Vegan/Vegetarian

Tortilla soup – How to make – Recipe

The Best Overnight French Toast Bake| Casserole | How to make and Cook | Souffle Recipe

How to Make Sweet Potato Casserole Recipe | Thanksgiving Fall

ow to make Apple Sauce (no sugar)

How to make the BEST Red Enchilada Sauce

How to make Skillet Pot Pie (plant based) vegan

How to make Roasted Rosemary, Lemon, Garlic Chicken, easy recipe

How to Make Cinnamon Roll Bundt Cake

BEST Apple Pie How to make in skillet – Recipe | Only 7 ingredients

my email address: faithrocksjesus@gmail.com
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Wendy Sax was tired, experiencing hair loss, and simply not feeling like herself when she was diagnosed with hyperthyroidism. Hear about how eating a plant-based diet changed that!

Read Wendy’s full story and learn more about how foods affect our hormones in Dr. Barnard’s new book, Your Body in Balance: The New Science of Food, Hormones, and Health, which debuts on Feb. 4, 2020. https://bit.ly/36LK0J2

Get your copy today!
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May is Huntington’s disease awareness month. We in the European Huntington Association would therefore like to draw attention to the disease. (For more information go to www.eurohuntington.org)

Did you know that Huntington’s Disease was recognized as an inherited disorder in 1872? A 22-year-old American doctor, George Huntington, wrote a paper on the disease – giving it its name “Huntington’s chorea”.

‘Chorea’ means “to dance”. The name comes from the involuntary movements that often follows with the disease.

Today, we simply call it ‘Huntington’s disease’, because there are more to it than just movements.

In many countries, the situation for people with Huntington’s disease is gradually improving. However, it often comes with stigma. Many family members don’t talk about the disease and hide the illness.

Unfortunately, there is still no known cure for the disease, but brilliant scientists work around the clock to develop treatments.

Scientists will probably find the answer to the puzzle of Huntington’s one day. Until then we will work to spread knowledge, raise awareness and break down stigma.
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A whiteboard animation describing the Huntington’s Disease. Brought to you by the HOPES team at Stanford.
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Huntington’s disease (HD), also known as Huntington’s chorea, is a neurodegenerative disease that is mostly inherited.[7] The earliest symptoms are often subtle problems with mood or mental abilities.[1] A general lack of coordination and an unsteady gait often follow.[2] It is also a basal ganglia disease causing a hyperkinetic movement disorder known as chorea.[8][9] As the disease advances, uncoordinated, involuntary body movements of chorea become more apparent.[1] Physical abilities gradually worsen until coordinated movement becomes difficult and the person is unable to talk.[1][2] Mental abilities generally decline into dementia.[3] The specific symptoms vary somewhat between people.[1] Symptoms usually begin between 30 and 50 years of age but can start at any age.[3][4] The disease may develop earlier in each successive generation.[1] About eight percent of cases start before the age of 20 years, and are known as juvenile HD, which typically present with the slow movement symptoms of Parkinson’s disease rather than those of chorea.[3]

HD is typically inherited from an affected parent, who carries a mutation in the huntingtin gene (HTT).[4] However, up to 10% of cases are due to a new mutation.[1] The huntingtin gene provides the genetic information for huntingtin protein (Htt).[1] Expansion of CAG repeats of cytosine-adenine-guanine (known as a trinucleotide repeat expansion) in the gene coding for the huntingtin protein results in an abnormal mutant protein (mHtt), which gradually damages brain cells through a number of possible mechanisms.[7][10] Diagnosis is by genetic testing, which can be carried out at any time, regardless of whether or not symptoms are present.[5] This fact raises several ethical debates: the age at which an individual is considered mature enough to choose testing; whether parents have the right to have their children tested; and managing confidentiality and disclosure of test results.[2]

No cure for HD is known, and full-time care is required in the later stages.[2] Treatments can relieve some symptoms, and in some, improve quality of life.[3] The best evidence for treatment of the movement problems is with tetrabenazine.[3] HD affects about 4 to 15 in 100,000 people of European descent.[1][3] It is rare among Japanese, while the occurrence rate in Africa is unknown.[3] The disease affects men and women equally.[3] Complications such as pneumonia, heart disease, and physical injury from falls reduce life expectancy.[3] Suicide is the cause of death in about 9% of cases.[3] Death typically occurs 15–20 years from when the disease was first detected.[4]

The earliest known description of the disease was in 1841 by American physician Charles Oscar Waters.[11] The condition was described in further detail in 1872 by American physician George Huntington.[11] The genetic basis was discovered in 1993 by an international collaborative effort led by the Hereditary Disease Foundation.[12][13] Research and support organizations began forming in the late 1960s to increase public awareness, provide support for individuals and their families and promote research.[13][14] Research directions include determining the exact mechanism of the disease, improving animal models to aid with research, testing of medications and their delivery to treat symptoms or slow the progression of the disease, and studying procedures such as stem-cell therapy with the goal of replacing damaged or lost neurons.[12]

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Neurology – Topic 17 Huntingtons disease – patient
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Huntington’s disease: Genetics, Neurology & Clinical Aspects, Diagnosis and Treatments
Huntington disease is a rare genetic disease that can give rise to involuntary movements like Huntington chorea.
**UPDATE: How Close are We to Curing Huntington Disease? Read my article on our Blog here: https://tinymedicine.org/?p=56

Today, we’ll explore the genetic basis of Huntington disease and the Neurological basis of chorea.
• This is the short arm of chromosome 4. It is the home of the Huntington gene which codes for the Huntington protein. All humans have two copies of this gene. It has a section called trinucleotide repeat, which is a sequence of three DNA bases, Cytosine, Adenine, and Guanine, repeated multiple times.
• A mutation in this gene can further increase the repeat count. If the repeat count is over 40, this will result in a very long Huntington protein called mutant Huntington protein. It can increase the decay of certain neurons in the brain.
• This gene is inherited as autosomal dominant. You get two copies of the gene from each parent. But since it’s dominant, one mutant copy is enough to give you the disease.
• The other important feature is its penetrance close to one hundred percent.
o It means that almost all the people with the mutant gene will develop the disease.
Symptoms typically arise after the age of 35-44. The age of onset depends on the number of the repeat count of the mutation. Symptoms may arise in the childhood itself if the repeat count is very high.
At first, they develop cognitive changes and mood changes like depression.
Later, the patients will develop speech and swallowing difficulty.
Finally, they will develop jerky, uncontrollable dancing like movements called chorea.
The brain learns and stores different motor patterns in the cerebral cortex. A structure called basal ganglia keeps these motor patterns switched off via a pathway called the indirect pathway. When you want to initiate a certain movement, the motor cortex signals the basal ganglia to activate the specific motor patterns. Activation occurs via a pathway called the direct pathway. In Huntington’s disease, neurons in the indirect pathway are decayed. Therefore the brain loses the ability to switch off the motor patterns. This results in uncontrollable movement such as chorea.
The presence of symptoms and positive family history is used to come to a clinical diagnosis. Genetic testing can confirm if an adult or an embryo carries the mutant Huntington Gene.
At the moment, there’s no cure for Huntington disease Drugs such as antipsychotics are given to control the movement. Supportive care includes occupational therapy, nutritional support and speech and language therapy. A new clinical trial tests a gene silencing drug to slow down the disease progression. But the hope for a complete cure is gene editing. Let’s hope the mankind will reach there soon.

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Huntington’s disease is an incurable and fatal neurodegenerative disorder characterized by movement problems and a variety of other symptoms. It is a rare example of a neurological disorder that can be traced back to a mutation in a single gene. In this video, I discuss the symptoms and pathology of Huntington’s disease.

For an article (on my website) that discusses Huntington’s disease more in-depth, click this link: https://neuroscientificallychallenged.com/posts/know-your-brain-huntingtons-disease

TRANSCRIPT:

Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss Huntington’s disease.

The symptoms of Huntington’s disease typically emerge during middle age and at first often involve subtle changes in personality, cognition, and movement. Eventually, the symptoms progress into substantial movement problems like chorea, which involves uncontrolled, spasmodic movements; impaired coordination and balance; muscle rigidity; and difficulty speaking and/or swallowing. Cognitive and psychiatric symptoms like dementia and depression occur as well. The disease is incurable and fatal.

These symptoms are associated with neurodegeneration, or the deterioration and death of neurons. A group of structures called the basal ganglia are strongly affected, but other regions of the brain experience neurodegeneration as well.

The pathology of Huntington’s disease can be traced back to a mutation in a single gene called huntingtin. The mutation that causes Huntington’s disease is a dominant mutation. Thus, if one parent has the disease, their child has a 50% chance of developing it, too. The huntingtin gene contains a DNA sequence that consists of three nucleotides (cytosine, adenine, and guanine) in repetition—a pattern known as a trinucleotide repeat. When the gene is mutated, an excess number of repeats can occur, and a mutated form of huntingtin protein is created. The higher the number of repeats, the greater the risk of disease, and all people with 40 or more repeats in the huntingtin gene will develop Huntington’s disease. Mutated huntingtin proteins have a tendency to group together, forming clusters within neurons that are not easily removed by brain enzymes. It has been hypothesized these clusters may play a role in the neurodegeneration seen in Huntington’s disease, for their accumulation in the brain is associated with increased neurodegeneration.

Reference:

Walker FO. Huntington’s disease. Lancet. 2007 Jan 20;369(9557):218-28.
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For more information and resources, please visit www.HDSA.org.

The Huntington’s Disease Society of America is the premier nonprofit organization dedicated to improving the lives of everyone affected by Huntington’s disease. From community services and education to advocacy and research, HDSA is the world’s leader in providing help for today, hope for tomorrow for people with Huntington’s disease and their families. In the battle against Huntington’s disease no one fights alone. At HDSA, family is everything.

#HuntingtonsDisease #LetsTalkAboutHD #HDSAFamily #HDSA #Huntingtons #Disease #Brain #HD
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