Eating Fish May Reduce Multiple Sclerosis Risk

Eating Fish May Reduce Multiple Sclerosis Risk

Summary: A new study reveals eating fish regularly and taking daily fish oil supplements may reduce the risk of developing multiple sclerosis. Researchers report high fish intake is associated with a 45% reduced risk of developing MS.

Source: AAN.

Eating fish at least once a week or eating fish one to three times per month in addition to taking daily fish oil supplements may be associated with a reduced risk of multiple sclerosis (MS), according to a preliminary study released today that will be presented at the American Academy of Neurology’s 70th Annual Meeting in Los Angeles, April 21 to 27, 2018. These findings suggest that the omega-3 fatty acids found in fish may be associated with lowering the risk of developing MS.

Multiple sclerosis is a disease of the central nervous system that affects communication between the brain and other parts of the body. With MS, the body’s immune system attacks myelin, the fatty white substance that insulates and protects the nerves. This disrupts the signals between the brain and the rest of the body. Symptoms of MS may include fatigue, numbness, tingling or difficulty walking. The first episode of MS symptoms, lasting at least 24 hours, is known as clinically isolated syndrome. There is no cure for MS.

“Consuming fish that contain omega-3 fatty acids has been shown to have a variety of health benefits, so we wanted to see if this simple lifestyle modification, regularly eating fish and taking fish oil supplements, could reduce the risk of MS,” said study author Annette Langer-Gould, MD, PhD, of Kaiser Permanente Southern California in Pasadena, Calif., and a member of the American Academy of Neurology.

For this study, researchers examined the diets of 1,153 people with an average age of 36 from a variety of backgrounds, about half of whom had been diagnosed with MS or clinically isolated syndrome.

Participants were asked about how much fish they regularly ate. High fish intake was defined as either eating one serving of fish per week or eating one to three servings per month in addition to taking daily fish oil supplements. Low intake was defined as less than one serving of fish per month and no fish oil supplements. Examples of fish consumed by study participants include shrimp, salmon and tuna.

salmon

The study found that high fish intake was associated with a 45 percent reduced risk of MS or clinically isolated syndrome when compared with those who ate fish less than once a month and did not take fish oil supplements. A total of 180 of those with MS had high fish intake compared to 251 of the healthy controls.

The study also looked at 13 genetic variations in a human gene cluster that regulates fatty acid levels. Researchers found two of the 13 genetic variations examined were associated with a lower risk of MS, even after accounting for the higher fish intake. This may mean that some people may have a genetic advantage when it comes to regulating fatty acid levels.

While the study suggests that omega-3 fatty acids, and how they are processed by the body, may play an important role in reducing MS risk, Langer-Gould emphasizes that it simply shows an association and not cause and effect. More research is needed to confirm the findings and to examine how omega-3 fatty acids may affect inflammation, metabolism and nerve function.

Fish such as salmon, sardines, lake trout and albacore tuna are generally recommended as good sources of omega-3 fatty acids.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study was supported by the National Institute of Neurological Disorders and Stroke.

Source: Renee Tessman – AAN
Publisher: Organized by NeuroscienceNews.com.

$64K per year Multiple sclerosis drug or a holistic healing option

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MS and Sphingomyelin in blood for early detection

Sphingomyelin

Abnormalities and associated diseases

Sphingomyelin can accumulate in a rare hereditary disease called Niemann–Pick disease, types A and B. It is a genetically-inherited disease caused by a deficiency in the lysosomal enzyme acid sphingomyelinase, which causes the accumulation of sphingomyelin in spleenliverlungsbone marrow, and brain, causing irreversible neurological damage. Of the two types involving sphingomyelinase, type A occurs in infants. It is characterized by jaundice, an enlarged liver, and profound braindamage. Children with this type rarely live beyond 18 months. Type B involves an enlarged liver and spleen, which usually occurs in the pre-teen years. The brain is not affected. Most patients present with <1% normal levels of the enzyme in comparison to normal levels.

As a result of the autoimmune disease multiple sclerosis (MS), the myelin sheath of neuronal cells in the brain and spinal cord is degraded, resulting in loss of signal transduction capability. MS patients exhibit upregulation of certain cytokines in the cerebrospinal fluid, particularly tumor necrosis factor alpha. This activates sphingomyelinase, an enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide; sphingomyelinase activity has been observed in conjunction with cellular apoptosis.[17]

An excess of sphingomyelin in the red blood cell membrane (as in abetalipoproteinemia) causes excess lipid accumulation in the outer leaflet of the red blood cellplasma membrane. This results in abnormally shaped red cells called acanthocytes.

From Wikipedia, the free encyclopedia

General structures of sphingolipids

Sphingomyelin (SPH, ˌsfɪŋɡoˈmaɪəlɪn) is a type of sphingolipidfound in animal cell membranes, especially in the membranous myelin sheath that surrounds some nerve cellaxons. It usually consists of phosphocholine and ceramide, or a phosphoethanolamine head group; therefore, sphingomyelins can also be classified as sphingophospholipids.[1] In humans, SPH represents ~85% of all sphingolipids, and typically make up 10–20 mol % of plasma membrane lipids.

Sphingomyelins contain phosphocholine or phosphoethanolamine as their polar head group and are therefore classified along with glycerophospholipids as phospholipids. Indeed, sphingomyelins resemble phosphatidylcholines in their general properties and three-dimensional structure, and in having no net charge on their head groups . Sphingomyelins are present in the plasma membranes of animal cells and are especially prominent in myelin, a membranous sheath that surrounds and insulates the axons of some neurons—thus the name “sphingomyelins”.[1]

Sphingomyelin was first isolated by GermanchemistJohann L.W. Thudicum in the 1880s.[2] The structure of sphingomyelin was first reported in 1927 as N-acyl-sphingosine-1-phosphorylcholine.[2] Sphingomyelin content in mammals ranges from 2 to 15% in most tissues, with higher concentrations found in nerve tissues, red blood cells, and the ocular lenses. Sphingomyelin has significant structural and functional roles in the cell. It is a plasma membrane component and participates in many signaling pathways. The metabolism of sphingomyelin creates many products that play significant roles in the cell.[2]

Physical characteristics

Sphingomyelin
Black:Sphingosine
Red:Phosphocholine
Blue:Fatty acid

Top-down view of sphingomyelin, demonstrating its nearly cylindrical shape

Composition

Sphingomyelin consists of a phosphocholine head group, a sphingosine, and a fatty acid. It is one of the few membrane phospholipids not synthesized from glycerol. The sphingosine and fatty acid can collectively be categorized as a ceramide. This composition allows sphingomyelin to play significant roles in signaling pathways: the degradation and synthesis of sphingomyelin produce important second messengers for signal transduction.

Sphingomyelin obtained from natural sources, such as eggs or bovine brain, contains fatty acids of various chain length. Sphingomyelin with set chain length, such as palmitoylsphingomyelin with a saturated 16 acyl chain, is available commercially.[3]

Properties

Ideally, sphingomyelin molecules are shaped like a cylinder, however many molecules of sphingomyelin have a significant chain mismatch (the lengths of the two hydrophobic chains are significantly different).[4] The hydrophobic chains of sphingomyelin tend to be much more saturated than other phospholipids. The main transition phase temperature of sphingomyelins is also higher compared to the phase transition temperature of similar phospholipids, near 37 C. This can introduce lateral heterogeneity in the membrane, generating domains in the membrane bilayer.[4]

Sphingomyelin undergoes significant interactions with cholesterol. Cholesterol has the ability to eliminate the liquid to solid phase transition in phospholipids. Due to sphingomyelin transition temperature being within physiological temperature ranges, cholesterol can play a significant role in the phase of sphingomyelin. Sphingomyelin are also more prone to intermolecular hydrogen bonding than other phospholipids.[5]

Location[edit]

Sphingomyelin is synthesized at the endoplasmic reticulum (ER), where it can be found in low amounts, and at the trans Golgi. It is enriched at the plasma membrane with a greater concentration on the outer than the inner leaflet.[6] The Golgi complex represents an intermediate between the ER and plasma membrane, with slightly higher concentrations towards the trans side.[7]

Metabolism

Synthesis

The synthesis of sphingomyelin involves the enzymatic transfer of a phosphocholine from phosphatidylcholine to a ceramide. The first committed step of sphingomyelin synthesis involves the condensation of L-serine and palmitoyl-CoA. This reaction is catalyzed by serine palmitoyltransferase. The product of this reaction is reduced, yielding dihydrosphingosine. The dihydrosphingosine undergoes N-acylation followed by desaturation to yield a ceramide. Each one of these reactions occurs at the cytosolic surface of the endoplasmic reticulum. The ceramide is transported to the Golgi apparatus where it can be converted to sphingomyelin. Sphingomyelin synthase is responsible for the production of sphingomyelin from ceramide. Diacylglycerol is produced as a byproduct when the phosphocholine is transferred.[8]

Sphingomyelin de novo synthesis pathway

Degradation

Sphingomyelin breakdown is responsible for initiating many universal signaling pathways. It is hydrolyzed by sphingomyelinases (sphingomyelin specific type-C phospholipases).[6] The phosphocholine head group is released into the aqueous environment while the ceramide diffuses through the membrane.

Function

Membranes

The membranous myelin sheath that surrounds and electrically insulates many nerve cell axons is particularly rich in sphingomyelin, suggesting its role as an insulator of nerve fibers.[1] The plasma membrane of other cells is also abundant in sphingomyelin, though it is largely to be found in the exoplasmic leaflet of the cell membrane. There is, however, some evidence that there may also be a sphingomyelin pool in the inner leaflet of the membrane.[9][10] Moreover, neutral sphingomyelinase-2 – an enzyme that breaks down sphingomyelin into ceramide – has been found to localise exclusively to the inner leaflet, further suggesting that there may be sphingomyelin present there.[11]

Signal transduction

The function of sphingomyelin remained unclear until it was found to have a role in signal transduction.[12] It has been discovered that sphingomyelin plays a significant role in cell signaling pathways. The synthesis of sphingomyelin at the plasma membrane by sphingomyelin synthase 2 produces diacylglycerol, which is a lipid-soluble second messenger that can pass along a signal cascade. In addition, the degradation of sphingomyelin can produce ceramide which is involved in the apoptotic signaling pathway.

Apoptosis

Sphingomyelin has been found to have a role in cell apoptosis by hydrolyzing into ceramide. Studies in the late 1990s had found that ceramide was produced in a variety of conditions leading to apoptosis.[13] It was then hypothesized that sphingomyelin hydrolysis and ceramide signaling were essential in the decision of whether a cell dies. In the early 2000s new studies emerged that defined a new role for sphingomyelin hydrolysis in apoptosis, determining not only when a cell dies but how.[13]After more experimentation it has been shown that if sphingomyelin hydrolysis happens at a sufficiently early point in the pathway the production of ceramide may influence either the rate and form of cell death or work to release blocks on downstream events.[13]

Lipid rafts

Sphingomyelin, as well as other sphingolipids, are associated with lipid microdomains in the plasma membrane known as lipid rafts. Lipid rafts are characterized by the lipid molecules being in the lipid ordered phase, offering more structure and rigidity compared to the rest of the plasma membrane. In the rafts, the acyl chains have low chain motion but the molecules have high lateral mobility. This order is in part due to the higher transition temperature of sphingolipids as well as the interactions of these lipids with cholesterol. Cholesterol is a relatively small, nonpolar molecule that can fill the space between the sphingolipids that is a result of the large acyl chains. Lipid rafts are thought to be involved in many cell processes, such as membrane sorting and trafficking, signal transduction, and cell polarization.[14] Excessive sphingomyelin in lipid rafts may lead to insulin resistance.[15]

Due to the specific types of lipids in these microdomains, lipid rafts can accumulate certain types of proteins associated with them, thereby increasing the special functions they possess. Lipid rafts have been speculated to be involved in the cascade of cell apoptosis.[16]


Connie’s comments: Toxic substances  (metals, chemicals,etc) for the liver can destroy the myelin sheath that covers our neurons.

$86000 per year MS drug or go natural from whole foods to supplements

Multiple sclerosis

For 23 years, Diane Whitcraft injected herself every other day with Betaseron, a drug that helps prevent flare-ups from multiple sclerosis. The drug worked well, drastically reducing Whitcraft’s trips to the hospital. But as her 65th birthday approached last September, she made a scary decision: to halt the medication altogether.

With health insurance through her job, Whitcraft had paid a $50 or $100 monthly co-pay for the drug; she hadn’t even realized that the price of Betaseron had soared to more than $86,000 a year. Shopping around for drug coverage through Medicare, the out-of-pocket costs were mind-boggling: close to $7,000 annually.

“I was just feeling really bad that my disease was going to affect our retirement budget,” Whitcraft said. “You’re retired; you’re on a fixed income. And it just really was bothersome to me. I was doing this to us. This disease was doing this to us.”


By Dr Axe

Multiple sclerosis is an autoimmune disease of the central nervous system that can develop at any age.

Multiple sclerosis (MS) affects women more than men.

The disorder is most commonly diagnosed between ages 20 and 40, but can be seen at any age.

MS affects 2.5 million people worldwide and around 400,000 people in the United States.

Multiple Sclerosis Causes

MS is caused by damage to the myelin sheath, the protective covering that surrounds nerve cells. When this nerve covering is damaged, nerve signals slow down or stop.

The nerve damage is caused by Inflammation which occurs when the body’s own immune cells attack the nervous system. This damage can happen anywhere in the brain or spinal cord.

Although no specific cause is known, some possible causes include: infections, mold toxicity, emotional stress, hormonal imbalances, toxic exposure, vitamin D deficiency, food allergies, and immunizations.

Multiple Sclerosis Symptoms

Multiple sclerosis symptoms can vary widely but the most common symptoms include:

  • Blurred or double vision
  • Trouble thinking
  • Lack of coordination
  • Loss of balance
  • Numbness
  • Tingling
  • Weakness in an arm or leg

For everyone, MS symptoms can display differently.

You may have a single symptom, and then go months or years without any others. A problem can also happen just one time, go away, and never return. For some people, the symptoms become worse within weeks or months.

The good news is there are natural treatments for multiple sclerosis that are effective and in many instances the condition can be reversed or greatly improved.

 

 

Foods for Multiple Sclerosis Diet 

In order to help recover from this disease, following a multiple sclerosis diet that is high in healthy fats and nutrients is key:

Unprocessed foods – Choose whole, organic, unprocessed foods as often as possible.

Coconut Oil – Coconut oil contains large amounts of medium chain fatty acids (MCFA) that support the brain and nervous system.

Fresh fruits and vegetables – Aim for a variety of colors to provide antioxidants that can help prevent free radical damage.

Omega-3 fats – The EPA/DHA fats found in wild-caught fish can help reduce inflammation.

Cabbage and bean sprouts – Foods high in lecithin may help strengthen the nerves.

MS Diet Foods to Avoid

Processed foods – Reduce your exposure to chemicals and toxins by avoiding any foods that are processed.

Gluten – People with MS generally have a gluten-intolerance and gluten can make symptoms worse.

Potential food allergens – Allergens can make MS symptoms worse, avoid any foods you might be allergic to.

Sugar – Lowers the immune response and causes systemic inflammation and premature aging.

Alcohol – Increases inflammation and can create a toxic environment.

Top 5 Natural Treatments for Multiple Sclerosis 

#1 Fish Oil (2,000mg daily) can help reduce inflammation and promote better nerve functioning.

#2 High potency multi-vitamin Provides basic nutrients needed for immune function.

#3 Digestive enzymes (1-2 capsules with meals) May help with digestion and reduce autoimmune reactions to foods.

#4 Vitamin D3 (5000 IU daily) helps modulate the immune system and support brain and nervous system.

#5 Vitamin B12 (1000 mcg daily) helps with the formation of nerves.

Bonus Remedy Astaxanthin, a powerful carotenoid antioxidant found in wild caught salmon can support the brain and nervous system.  Take 2 mg 1-2x daily.

Essential Oils for Multiple Sclerosis 

Essential oils of frankincense and helichrysum support the neurological system.  Take 2 drops of frankincense internally 3x a day 3 weeks, then take 1 week off and repeat that cycle.

Rub 2 drops of helichrysum to temples and neck 2x daily. Also, basil oil and cypress oil can improve circulation and muscle tone and can help reduce MS symptoms.


From Connie:

Quality supplements, anti-inflammatory, try AGELOC and Likepak at:

http://www.clubalthea.pxproducts.com

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Fish oil, creatine and CQ10 protect your mitochondria

Your brain needs Vitamin B complex and sulfur to protect its myelin sheaths preventing MS.

Foods High in Creatine. Especially those contained in beef, salmon, and tuna. It is accounted that about one pound of beef consists of 5 grams of creatine monohydrate, and one pound of red meat contains 2 grams of creatine monohydrate. There is about 4.5 grams in one pound of salmon.

CQ10: Organ meats

top nutrients

Food plan:  3 cups of green leaves, 3 cups of seaweed (Iodine and Selenium), 3 cups of

Viewers comments:

T Skeen, I have secondary progressive MS, had it undiagnosed and untreated for 4 years that was through high school and my first year of university. I don’t believe much in medicine and that it can do much better than healthy eating can. I’m no doctor but after I was put on many different drugs and didn’t get any better I regulated my diet very similar to how she did and maintained my healthy lifestyle best I could. I can now run 100m in 11.9 seconds….Two years ago I was wheelchair bound. I’m living proof that what you just said is completely wrong.

Personally, I’ve had those anti-thyroid effects with lots of cruciferous vegetables but neutralized them by taking kelp caplets or eating nori or other algae.

Have just viewed this shocking video. A Doctor promoting health. What is she thinking? Is this not against some oath or other. I am a disgustingly healthy 71 yr old, still run, take no medication and have been eating this way for years. If I can’t kill it, pick it or dig it up I dont eat it. My mitochondria thank me.

 

Brain is connected to the immune system: strengthen your immune system to detox your brain

In a stunning discovery that overturns decades of textbook teaching, researchers at the University of Virginia School of Medicine have determined that the brain is directly connected to the immune system by vessels previously thought not to exist. That such vessels could have escaped detection when the lymphatic system has been so thoroughly mapped throughout the body is surprising on its own, but the true significance of the discovery lies in the effects it could have on the study and treatment of neurological diseases ranging from autism to Alzheimer’s disease to multiple sclerosis.

brain and immune system link

“Instead of asking, ‘How do we study the immune response of the brain?’ ‘Why do multiple sclerosis patients have the immune attacks?’ now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels,” said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA’s Center for Brain Immunology and Glia (BIG). “It changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can’t be studied. But now we can ask mechanistic questions.”

“We believe that for every neurological disease that has an immune component to it, these vessels may play a major role,” Kipnis said. “Hard to imagine that these vessels would not be involved in a [neurological] disease with an immune component.”

New Discovery in Human Body

Kevin Lee, PhD, chairman of the UVA Department of Neuroscience, described his reaction to the discovery by Kipnis’ lab: “The first time these guys showed me the basic result, I just said one sentence: ‘They’ll have to change the textbooks.’ There has never been a lymphatic system for the central nervous system, and it was very clear from that first singular observation — and they’ve done many studies since then to bolster the finding — that it will fundamentally change the way people look at the central nervous system’s relationship with the immune system.”

Even Kipnis was skeptical initially. “I really did not believe there are structures in the body that we are not aware of. I thought the body was mapped,” he said. “I thought that these discoveries ended somewhere around the middle of the last century. But apparently they have not.”

‘Very Well Hidden’

The discovery was made possible by the work of Antoine Louveau, PhD, a postdoctoral fellow in Kipnis’ lab. The vessels were detected after Louveau developed a method to mount a mouse’s meninges — the membranes covering the brain — on a single slide so that they could be examined as a whole. “It was fairly easy, actually,” he said. “There was one trick: We fixed the meninges within the skullcap, so that the tissue is secured in its physiological condition, and then we dissected it. If we had done it the other way around, it wouldn’t have worked.”

After noticing vessel-like patterns in the distribution of immune cells on his slides, he tested for lymphatic vessels and there they were. The impossible existed. The soft-spoken Louveau recalled the moment: “I called Jony [Kipnis] to the microscope and I said, ‘I think we have something.'”

As to how the brain’s lymphatic vessels managed to escape notice all this time, Kipnis described them as “very well hidden” and noted that they follow a major blood vessel down into the sinuses, an area difficult to image. “It’s so close to the blood vessel, you just miss it,” he said. “If you don’t know what you’re after, you just miss it.”

“Live imaging of these vessels was crucial to demonstrate their function, and it would not be possible without collaboration with Tajie Harris,” Kipnis noted. Harris, a PhD, is an assistant professor of neuroscience and a member of the BIG center. Kipnis also saluted the “phenomenal” surgical skills of Igor Smirnov, a research associate in the Kipnis lab whose work was critical to the imaging success of the study.

Alzheimer’s, Autism, MS and Beyond

The unexpected presence of the lymphatic vessels raises a tremendous number of questions that now need answers, both about the workings of the brain and the diseases that plague it. For example, take Alzheimer’s disease. “In Alzheimer’s, there are accumulations of big protein chunks in the brain,” Kipnis said. “We think they may be accumulating in the brain because they’re not being efficiently removed by these vessels.” He noted that the vessels look different with age, so the role they play in aging is another avenue to explore. And there’s an enormous array of other neurological diseases, from autism to multiple sclerosis, that must be reconsidered in light of the presence of something science insisted did not exist.


Story Source:

The above story is based on materials provided by University of Virginia Health System. Note: Materials may be edited for content and length.


Journal Reference:

  1. Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris, Jonathan Kipnis. Structural and functional features of central nervous system lymphatic vessels. Nature, 2015; DOI: 10.1038/nature14432

Cite This Page:

University of Virginia Health System. “Missing link found between brain, immune system; major disease implications.” ScienceDaily. ScienceDaily, 1 June 2015. <www.sciencedaily.com/releases/2015/06/150601122445.htm>.
Source: University of Virginia Health System
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Connie Dello Buono

Prevent vascular disease, manage inflammation, get GYV health caps to boost ATP cells performance and speedy repair of your body, email connie to get the caps and join in spreading the benefits with extra income for you at motherhealth@gmail.com and text 408-854-1883