Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the auto-immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Tuesday, September 22, 2015

Melatonin and MS

New research shows the connection between low levels of melatonin, known as the sleep hormone, and MS relapses.

Melatonin is the hormone which helps encourage our sleep state.   It is made by the pineal gland in our brains, and it needs the visual cue of darkness in order to begin production.  We naturally produce more melatonin in the fall and winter months, because darkness is more prevelant.  This is why we might find ourselves sleepier and more likely to want to hibernate during these darker months, because our brain is cranking out melatonin.

New research is linking this lower level of melatonin found in spring and summer to seasonal relapses in MS.

It appears that in humans with MS, the lower levels of melatonin found in their blood during the sunnier months might be linked to MS progression and relapse rate.  That is, there is a correlation between seasonal low melatonin levels and clinical relapses.  (It's always important to make the distinction between correlation and causation---  the researchers are just noticing that in people with lower levels of melatonin, there were more frequent relapses...but, if you read this whole post, I hope I'll explain why this might be.)  Don't go out and buy melatonin just yet!

The researchers who are studying melatonin weren't quite sure why it is so helpful to people with MS.   So, they go to the EAE model of MS in mice and studying t-cell modulation.  ARGHHH!!!!   Why???

We don't need to look at EAE in mice---we already have a correlation of melatonin levels in brain health for HUMANS.

When we look at MS as a disease like stroke in humans, where hypoxic injury and reperfusion injury damage the endothelial layer of the brain's blood vessels....it all makes sense.

Because melatonin protects the brain's endothelial cells under hypoxic and oxidative stress conditions.

Melatonin has a cellular protective effect in cerebrovascular and neurodegenerative diseases. Protection of brain endothelial cells against hypoxia and oxidative stress is important for treatment of central nervous system (CNS) diseases, since brain endothelial cells constitute the blood brain barrier (BBB). In the present study, we investigated the protective effect of melatonin against oxygen-glucose deprivation, followed by reperfusion- (OGD/R-) induced injury, in bEnd.3 cells. The effect of melatonin was examined by western blot analysis, cell viability assays, measurement of intracellular reactive oxygen species (ROS), and immunocytochemistry (ICC). Our results showed that treatment with melatonin prevents cell death and degradation of tight junction protein in the setting of OGD/R-induced injury. In response to OGD/R injury of bEnd.3 cells, melatonin activates Akt, which promotes cell survival, and attenuates phosphorylation of JNK, which triggers apoptosis. Thus, melatonin protects bEnd.3 cells against OGD/R-induced injury.

Now in plain English---melatonin protects the endothelial cells of the blood brain barrier, and keeps those endothelial cells alive during times of of low oxygen and low glucose delivery--- so they can protect the brain.  Melatonin is a known anti-oxidant.  Just like fruits and vegetables.  

Another connection could be that people with MS who have lower levels of melatonin just aren't getting enough good sleep---and that could be the connection to higher relapse rates.  Especially now that we understand how the brain's lymphatic cleansing system works only when we sleep.

To complicate and confuse matters---melatonin has an inverse relationship with vitamin D.  In research in people with MS, it was shown that people taking higher Vitamin D supplementation had lower levels of melatonin. 

But we also know that lower vitamin D rates are correlated with MS relapses.  So, what's a human with MS to do?  Take melatonin???  Bump up vitamin D?  Do both?  How much?  When?  How...?  Light?  Dark?  

Bottom line:  Both melatonin and vitamin D are hormones which are also anti-oxidants, decrease inflammation and address oxidative stress. 

Long-time readers of this blog will know that it's never about one pill or supplement, it's about living a complete lifestyle which encourages endothelial health.   It's all about balance. And there are many ways to accomplish this.  

It's difficult to double-blind and research a complete lifestyle----which is why researchers will pick one aspect at a time---like Vitamin D levels, or melatonin levels, or cholesterol levels.  You get the picture.  

Have your vitamin D levels tested.  If they are low, supplement and get some UV ray therapy.  If you have trouble sleeping, or are jet-lagged,  talk to your doctor about possibly adding melatonin to your regimen.  But remember to move, and eat whole and colorful foods, and laugh, and reduce stress, and get good sleep.  It's a complete lifestyle, and no one pill or supplement can replace that.

Be well!


  1. Thank you Joan.
    You make these scientific things so understandable!!!

    1. you're more than welcome, Shirley! I try to stay on top of the research, to keep Jeff healthy----and this story piqued my interest, so I wanted to dig deeper. Glad it can be of service. xo

  2. This article is excellent information but I must ask if it is not more pragmatic to refer to DEMYALNATION and not keep reinforcing th irrational and illogical notion that MS is a ' conditon that basically ' causes itself' ... like some sort of idiopathic disorder - MS mean manykesions and when er==we ask the Neduc=s what causes the lesions we are to MS ... i.e. the lesions cause the lesions.
    Also is it not true that Charcot , father of Neurology who actualy categorised Medicine, himself 'literally' DREW' in gat detail the evidence connecting mylin breakdown w=tio ' engorged blood vessels' some 100 years before Rindfleisch.
    soewhat pedantic I know and apologise but when Dcotors themselves either domt KNOW the history of their profesion or , worse, REFUSE to apply that knowledge we nust surely at least be precise in how we , as patients, go about promoting our cause to have our health issues addresed.
    MS ( many lseions) is NOT a ' condition but collection of physiological phenomena that HAS a cause or rather myriad causes, e.g. B12 Deficiency.
    Professor of NEUROLOGY, david Hubbard, explains ( on YOU TUBE and elsewhere) in his discourse ' a Solution in SIx Minutes' how myelin, fragile LIPID breaks down as NORMAL and the immune system sends in Macrophaeges to ' CLEAN UP' as it does in all cases of physioliocal assault ... MS is NOT an autoimmune disorder - the Immune system is behaving in perfectly order as it is MENAT TO.
    We must stop reinforcing this mistakeb referral practice and its not a hard thing to do in this day and aghe when we routinely adopt and reject Custom abd practise without question: I cant recall evr witnesing as many theories and varied interventons with NO supporting evidence as I witness dailu on the web... people are happy to put their faith in everything from 'Hype..rbaric Oxygen' to 'STEROIDS' to 'Germ Theory' to 'God' without question so why so much resistance to ditch an obviously problematic and sefl-defeating use of such NON or even ANTI- medical terminology.

  3. Hi Kevin---I'm not sure I understand your point, even after reading your note a few times. I'll try to respond as best I can.

    MS is a multi-factorial disease, which has been defined by demyelinating lesions, those are the "many scars." But we now know that disability and progression are actually linked to gray matter loss, not white matter lesions. This is why MS progresses, even after white matter lesions and relapses stop.

    And I do agree with you, this means that MS is not a classic auto-immune disorder, but rather, a disease where immune activation may well be secondary to neurodegeneration.

    I try to write clearly to explain the vascular connection to MS. This includes how blood, cerebrospinal fluid and lymph flow affect the central nervous system. And I use published, peer-reveiwed research to establish scientific evidence. I believe there are many things that people with MS can do to help their health---and I stand behind this research, with my husband Jeff. Jeff is now 8 1/2 years past his MS diagnosis, with no disease progression, no gray matter loss, and remyelination of his lesions. He was treated with venoplasty 6 years ago, and has been on the Endothelial Health Program for 8 years. His healing is documented on MRI. I hope some of the ideas on this blog can help you, as well. Take care of yourself. All best, Joan

  4. Also---for clarification--Rindfleish and Charcot were contemporaries, and Rindfleisch published his drawings of the engourged vessels surrounding MS lesions in 1863, five years before before Charcot published on his findings.
    Rindfleisch (1863). Histologisches detail zu der grauen degeneration von gehirn und rueckenmark. Arch. Path. Anat. Physiol. Klin. Med. 26: 474.
    Charcot (1868) Histologie de la sclerose en plaques.Gaz Hopit Civils Milit. 41: 554-566.

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