Coffee For MS – Wonderful!
If you’ve ever wondered why roughly three times as many women than men, are diagnosed with MS each year, looking at the ways sugary coffee promotes thyroid energy function, and shields against the development of this and other metabolic stress conditions, can be very illuminating.
“Compared with those who reported no coffee consumption, the risk of MS was substantially reduced among those who reported a high consumption of coffee exceeding 900 mL daily…we observed a significant association between high consumption of coffee and decreased risk of developing MS.” (Hedström AK, et al., 2016)
Multiple sclerosis (MS) is known to arise, at least in part, because of an inflammatory process – damaging and interfering with the proper myelination of nerve cells – however, there are a number of explanations as to why this might occur, and why women are more likely to get it. Some of the reasons seem more logical than others. Officially there is no known cure, and popular treatment approaches have had limited success.
Although it’s probably true that what causes a disease, is never entirely black and white, one thing that is reasonably clear, is that the metabolic promoters of stress and inflammation (such as serotonin, nitric oxide, prolactin, cortisol, and the polyunsaturated fats (PUFAs) and their breakdown products), have a tendency to be significantly raised in cases of MS.
“Clinical studies have shown that…multiple sclerosis (MS) patients exhibit a chronically activated hypothalamo-pituitary-adrenal (HPA) axis…(MS) patients…who exhibited stronger HPA reactivity at baseline were significantly more likely to experience progression…” (Gold SM, et al., 2005)
“…NO [nitric oxide] produced by iNOS-positive inflammatory cells may cause demyelination by destroying oligodendrocytes and/or damaging myelin…NO levels are abnormally high in…MS lesions…” (Chuman H, 2006)
“Serotonin-induced platelet aggregation was increased in 40% of the MS patients…6 were suffering from an acute exacerbation of the disease at the time of measurement…serotonin-induced platelet aggregation was increased in all 6 of these patients…” (Neu IS, et al., 1982)
“The findings of our study confirm previous studies that have found mild to moderate hyperprolactinemia in MS cohorts…we observed higher prolactin levels in MS patients during relapse…Prolactin levels might thus serve as potential predictors of MS…” (Türkoğlu R, et al., 2016)
“Oxidative stress in general and isoprostanes and other lipid peroxidation products…may contribute to the pathogenesis of MS by a variety of mechanisms…Isoprostanes and other lipid peroxidation products can initiate signaling cascades to regulate cell viability and toxicity…Lipid peroxidation can also lead to changes in neurotransmission and signaling…” (Fozia Mir, et al., 2014)
Susceptibility to stress is a central factor encouraging a rise in the inflammatory things, associated with MS. Ongoing exposure to excess stress, tends to promote the kind of energy metabolism suppressed, low thyroid, high estrogen state (more prevalent in women), well known to aggravate systemic inflammation and disease.
“We found that thyroid disorders were at least three times more common in women with MS than in female controls. This was accounted for mainly by the prevalence of hypothyroidism among the female MS patients.” (Karni A, Abramsky O., 1999)
“Patients with high estradiol and low progesterone levels had a significantly greater number of…lesions…Patients with a high estrogen to progesterone ratio had a significantly greater number of active…lesions than those with a low ratio…Estradiol and progesterone may influence disease activity in MS.” (Bansil S, et al., 1999)
“It has been shown that 20-25% of untreated MS patients have autoimmune thyroiditis (AIT) and/or subclinical hypothyroidism…These facts emphasize the significance of systematic thyroid assessment in patients with MS…” (Bagir’ LV, et al., 2009)
Unfortunately, the idea that an ‘estrogen deficiency’ makes women more at risk of MS, is still popular, and it’s not uncommon for estrogen supplements to be suggested as a treatment. On top of that, glucocorticoids, immune suppressant drugs, and immunotherapy (disease modifying therapy), get promoted.
In order to justify the use of the highly profitable (yet often ineffective, potentially very harmful) treatments, biologically contradictory theories, get heavy support. And physiologically sound principles, that would help to make things clearer, get twisted and misrepresented, or disregarded.
For starters estrogen (instead of progesterone) has for decades, been referred to as the female/pregnancy hormone. This is despite the obvious pregnancy ending role that increased exposure to estrogen plays, as a form of birth control. Also conflicting with pro-estrogen dogma, is the known impact of rising estrogen levels, in the promotion of breast (and other) cancer. The failure to consider high tissue levels of estrogen, is significant with cancer, as well as likely in relation to MS susceptibility.
The upside-down theory, that if something rises under stress, exposure to even more of that thing, must also be helpful, seems to help keep alive false beliefs about the impact of estrogen on metabolism. The same principle, confuses ideas about rising levels of other stress substances (like serotonin, nitric oxide, cortisol, lactate, and breakdown products of PUFAs), interconnected with high estrogen and metabolic disease.
Some products (aside from estrogen), which rely on cognitive dissonance to make huge profits, include ‘anti-depressants’, cholesterol lowering drugs, polyunsaturated seed and fish oils, iron supplements, and even nitric oxide increasing drugs like Viagra and Cialis. All have been shown to be involved with the promotion of neurodegenerative conditions.
The ‘health world’ relies on short term results, to frame estrogen (and other things) as protective against neurodegeneration and MS. But what often gets ignored, are the many rising indicators of systemic stress, inflammation, and metabolic dysfunction, which go hand in hand with (and promote) high estrogen levels (including in tissue), fueling long term issues, and MS progression.
A well functioning thyroid energy metabolism, helps protect against increasing (and excessive) levels of estrogen in circulation, and trapped in tissue, and limits exposure to many of the inflammatory (potentially neurodegenerative) substances of stress.
Improvements in thyroid function and energy metabolism, assist in the production of highly protective, anti-inflammatory substances (such as pregnenolone, progesterone and testosterone), which also have anti-estrogen effects, and help protect against the onset and worsening of MS symptoms. Women are generally more susceptible to thyroid dysfunction, in part because of naturally higher levels of estrogen, and slower livers.
“Observations…obtained in experimental autoimmune encephalomyelitis (EAE) have revealed the promising neuroprotective effects exerted by progesterone (PROG)…results indicate that PROG is effective in reducing the severity of chronic EAE and, consequently, may have potential with respect to MS treatment.” (Giatti S, et al., 2012)
When energy production is suppressed and stress is high, digestive and liver function tends to be less effective, and this can lead to the development of bacterial issues. Increased exposure to bacterial toxins like endotoxin (LPS), promotes inflammation and rising levels of both serotonin and estrogen, helping to drive a self-feeding, immune system dysregulated state of stress, increasing MS and arthritis risk. Women are more likely than men to suffer from arthritis, as well as gastrointestinal disorders like IBS, known to be driven by issues with inflammation, endotoxin, serotonin and estrogen.
“Besides inflammatory bowel diseases…inflammatory diseases with remote tissues affected seem to be modulated by the gut environment; for example, in rheumatoid arthritis and type 1 diabetes mellitus……findings are of direct relevance to multiple sclerosis…” (Kerstin Berer, et al., 2011)
“LPS [endotoxin] regulates the expression of inflammatory proteins associated with inflammatory diseases…data…show that LPS levels systemically increased by 118.31 % in 2 patients with MS compared with the control group…data…back up the important role played by oxidative stress in the establishment, course, and evolution of neuroinflammatory processes like MS.” (Begoña M. Escribano, et al., 2017)
Endotoxin powerfully suppresses thyroid energy system function, and increases cortisol and prolactin levels, and both of these stress substances have been shown to rise under inflammatory conditions, and can promote MS. Prolactin blood levels are known to be an accurate measure of tissue levels of estrogen, and excessive prolactin exposure is probably also part of the reason why women are at greater risk of MS and related issues.
“516 articles were obtained after searching databases, and 8 studies with 426 MS patients and 296 controls…our meta-analysis revealed a significantly higher PRL level in MS patients than healthy controls…” (Wei Wei et al., 2017)
Interference with mitochondrial energy production and thyroid performance, encourages the production of lactate, and lactate is another thing which rises with the progression of MS, as well as many other diseases associated with inflammation, thyroid dysfunction, and increased estrogen, including breast cancer. As women are more prone to thyroid and estrogen issues, and have lower liver function, it makes sense that lactate exposure will also be higher.
“In patients with MS serum lactate was three times higher than that of healthy controls…mitochondrial dysfunction is an important feature in MS and of particular relevance to the neurodegenerative phase of the disease.” (Amorini AM, et al., 2014)
Now is as good a time as any, for ideas about regular consumption of coffee – in combination with sufficient quantities of sugar – to enter into the story.
Numerous studies have shown the protective effects of coffee (and caffeine), and it isn’t mere coincidence that the positive impact of coffee (encouraging efficient metabolic function, helping to inhibit stress, inflammation and excessive estrogen exposure), can also help to protect against MS.
“This study reveals that increasing coffee consumption is associated with significantly smaller invasive breast tumor sizes, a lower proportion of ER+ tumors, and improved disease-free survival…predominantly caffeine, but also caffeic acid, mimics the actions of antiestrogens…” (
“…caffeine exerts a neuroprotective effect against EAE…provides a neurobiological basis for…investigation into the…relationship between caffeine consumption and…multiple sclerosis in humans.” (Chen GQ, et al., 2010)
Apart from having progesterone-like actions (guarding against inflammation and excess estrogen and serotonin), caffeine is known to act somewhat similarly to thyroid, boosting mitochondrial energy production. All this protects against stress and lowers MS risk.
“Myelin destruction due to inflammatory damage…is one of the major…hallmarks of multiple sclerosis (MS)…TH can alleviate MS by promoting remyelination…TH (thyroid hormone) may be an ideal compound that can…impede MS progression.” (Zhang M, et al., 2016)
“…caffeine…increased oxidative metabolism…caffeine heightens metabolic rate…caffeine stimulates metabolism and favorable mitochondrial production…findings support the advertised metabolic benefits of caffeine…” (Vaughan RA, et al., 2012)
Improved thyroid metabolism means more effective digestive and liver function, lowering the potential for bacterial toxins to enter into the main system, where they also promote systemic inflammation and metabolic disease, and can help cause neurodegeneration.
Regular coffee consumption improves liver health, increasing detoxification potential, and leads to lower levels of estrogen and other inflammatory things, circulating throughout the system.
“There is emerging evidence for a hepatoprotective effect of coffee in a wide range of liver conditions of different severity ranging from elevation of liver enzymes to fibrosis and hepatocellular carcinoma.” (Alexander Hodge, et al., 2017)
Improved liver function allows for better conversion of the inactive thyroid hormone (T4), into the active thyroid hormone (T3), and this is a central issue underlying sub-optimal thyroid function in women, and it is also a common problem associated with MS.
“…MS patients had significantly increased T4 levels whereas T3 and T.S.H. were found to be significantly lower…results suggest that in MS the T4/T3 conversion might be reduced…” (Kiessling WR, et al., 1980)
“Both men and women suffering from multiple sclerosis manifested low serum T3 concentrations coexisting with normal T4 levels which may indicate changed peripheral conversion pathway of thyroid hormones.” (Zych-Twardowska E, Wajgt A., 2001)
By improving overall metabolism and energy system function, coffee consumption helps protect against some of the harm done by excessive exposure to polyunsaturated fats (PUFAs). The PUFAs interfere with digestion, liver function, and thyroid hormone conversion and effectiveness. High stress and suppressed metabolism, increases the release of PUFAs out of storage as free fatty acids.
The PUFAs promote inflammation and oxidative stress, and directly increase tissue levels of estrogen, thereby playing what appears to be a central role in the development of MS, and neurodegenerative disease in general.
“The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines, which contribute to the development and progression of multiple sclerosis…Oxidative stress precedes the inflammatory response in the multiple sclerosis patients.” (Wang P, et al., 2014)
The breakdown products of PUFAs interfere with cholesterol production, and cholesterol is crucial for proper nervous system development and protection. PUFAs damage circulating cholesterol, which can harm nervous system and brain function, and can impede progesterone and testosterone production.
“Cholesterol availability is a prerequisite for myelination…remyelination failure in MS reflects, at least partially, the inability to locally increase the cholesterol content in demyelinated lesions.” (Stefan A. Berghoff, et al., 2017)
When cholesterol metabolism is sub-optimal, a high estrogen, high cortisol, inflammatory state, more sensitive to stress, can develop. Rising cholesterol is also a sign of stress, and cholesterol helps protect against endotoxin, inflammation, and MS. Using PUFAs or statin drugs, to force cholesterol levels down, is not the same as limiting stress or using up cholesterol rapidly, and has also been associated with neurodegeneration.
Sugar lowers stress and helps with cholesterol production, and sugar also promotes conversion of cholesterol into the protective steroids, stimulating thyroid energy metabolism, and limiting stress and inflammation. Sugar lowers exposure to the inflammatory, oxidative stress promoting breakdown products of the polyunsaturated free fatty acids, associated with MS development.
“Oxidative stress plays a crucial role in the pathogenesis of multiple sclerosis (MS)…results showed that…MDA (a byproduct of PUFA breakdown)…levels were significantly higher in patients with MS than those in control…” (Yousefi B, et al., 2014)
“…examined levels of MDA…in…patients…They found that the increase in OS markers preceded inflammatory response in MS patients…Oxidative stress processes participate in both inflammatory and neurodegenerative pathophysiological components of MS.” (Adamczyk B, Adamczyk-Sowa M., 2016)
It’s not popular to say this, but it makes sense to see sugar (and coffee) as very important for the protection against stress and inflammation, as well as probably any rational anti-MS strategy.
Blood sugar dysregulation has been associated with the progression of MS. Sugar restriction (to the degree that it causes thyroid dysfunction, and rising cortisol, estrogen, lactate, endotoxin, serotonin and free fatty acid release), interferes with the ability of the cell to properly use sugar, encourages insulin resistance, and promotes hypometabolic conditions connected to the onset of MS and diabetes. Sugar consumption per se, is not the cause of blood sugar dysregulation. Coffee is protective against insulin and blood sugar issues.
“…observations…especially those referred with mitochondrial aberrations and impaired glucose metabolism in MS, pointed to a relationship between glucose metabolism and MS disease pathogenesis…” (Mathur D, et al., 2014)
“The severity of cerebral hypometabolism was also related to the number of relapses…results suggest that measurement of cerebral metabolism in MS has the potential to be an objective marker for monitoring disease activity and to provide prognostic information.” (Sun X, et al., 1998)
Coffee is protective against inflammation and oxidative stress, and increased coffee intake has also been demonstrated to protect against obesity. Obesity is becoming more and more prevalent in women, and is a major risk factor for diabetes, cancer and MS.
When thyroid metabolism is suppressed, liver function is impaired, and estrogen and cortisol levels are raised, sensitivity to coffee can be exacerbated, and might at first encourage a stress response.
Sugar helps to increase thyroid function and lower stress, and can help to protect against some of the potential stress promoting effects of coffee. Coffee increases the need for fuel, and lack of sugar with coffee can be stressful. Sugar also helps with the production of the anti-stress and anti-inflammatory hormones (such as pregnenolone, progesterone, testosterone and DHEA), which protect against the development of MS.
“While current medication reduces relapses and inflammatory activity, it has only a modest effect on long-term disability and gray matter atrophy…during testosterone treatment, gray matter loss was no longer evident…these observations may reflect the potential of testosterone treatment to reverse gray matter atrophy associated with MS…” (Kurth F, et al., 2014)
“…progesterone and its derivatives might play a role in the control of the synthesis of the two major proteins of the peripheral nervous system (PNS): the glycoprotein Po (Po) and peripheral myelin protein…” (Martini L, et al., 2003)
If you think about what really protects against stress, inflammation, and thyroid dysfunction (things that also encourage liver and digestive function, and keep cortisol and estrogen levels under control), it seems illogical to suggest estrogen (and other anti-metabolic things), for MS.
Although estrogen and cortisol (and also serotonin, nitric oxide, and PUFAs) can potentially suppress stress and immune system related symptoms in the short term, evidence shows they don’t do so in a way which promotes long term metabolic health and regeneration. Instead, ongoing exposure to increased levels of these substances, damages metabolism, and encourages stress, chronic inflammation, and immune system dysregulation and disease.
“…chronic administration of E2…increases the expression of numerous inflammatory cytokines and NO by these cells in response to LPS activation ex vivo…the experimental results obtained with a short-term E2 treatment in vitro are not predictive of the effect of a long-term exposure to estrogens in vivo…physiological endogenous estrogens levels as well as exogenous E2 promote the inflammatory status of macrophages and thus the ability to mount inflammatory and immune responses…” (Bertrand Calippe, et al., 2010)
Excess estrogen in particular, has been shown to be involved with many conditions (effecting both women and men), associated with stress, inflammation, and thyroid dysfunction. MS risk is reduced when optimal metabolism is maintained, and when the stress, inflammation, and thyroid interfering things are kept low. High levels of progesterone in the third trimester of pregnancy, coincides with a significant reduction in symptoms of MS. For men, low testosterone is a predictor of MS severity, and this is likely to coincide with stress, inflammation, suppressed energy metabolism, as well as increasing estrogen exposure.
Women are about twice as likely than men to suffer from depression, and depression has been shown to be promoted by chronic stress, systemic inflammation, suppressed thyroid energy metabolism, blood sugar dysregulation, as well as excess estrogen, cortisol, serotonin, and nitric oxide. People diagnosed with MS suffer from depression at a very high rate.
“Multiple sclerosis is a,,,disease affecting one million people worldwide, with a significant burden of psychiatric comorbidity. Depression is the commonest psychiatric manifestation but still remains largely underdiagnosed and undertreated.” (Skokou M, et al., 2012)
Excess iron building up in tissue is another thing which is known to be involved with inflammatory metabolic disease. Estrogen, endotoxin, and the PUFAs, promote iron dysregulation issues, now known to play a role in the development and progression of neurodegeneration and MS. It is common for women to suffer from anemia, usually a symptom of thyroid dysregulation, and highly reactive and inflammatory iron supplements are very often prescribed. Women get Alzheimer’s more than men, and endotoxin, tissue buidup of iron, and PUFAs, are directly involved. Coffee is protective against all kinds of dementia.
“…iron-positive microglia and macrophages in chronic active MS lesions constitute a distinct, previously unappreciated inflammatory compartment that may be a significant contributor to tissue damage, disease severity, and/or progression.” (Gillen KM, et al., 2018)
I’m not scientist or a doctor of any kind, and none of this is intended as medical/health/dietary advice, but I’m starting to see a pattern here, and hopefully you are too.
“High coffee consumption is associated with reduced odds of MS. Caffeine has neuroprotective properties and seems to suppress the production of proinflammatory cytokines, which may be mechanisms that explain the observed association.” (Ellen Mowry, et al., 2015)
A diet protecting against the inflammatory effects of stress and low metabolism, avoiding the PUFAs, and including plenty of sweet coffee, enough protein from milk, cheese, or gelatin, and lots of sugar from sweet ripe fruits, fruit juice, honey, and white sugar, makes sense to me, for the reasons given, to be highly protective.
Some other things which have been shown to help with MS, include thiamine, biotin, aspirin, Minocycline, niacinamide, activated charcoal, methylene blue, vitamin E, cyproheptadine and some other antihistamines, red light, and regular bag breathing.
“…high-dose biotin is exerting a therapeutic effect in patients with progressive MS through two different and complementary mechanisms: by promoting axonal remyelination by enhancing myelin production and by reducing axonal hypoxia through enhanced energy production.” (Sedel F, et al., 2016)
“…this trial showed that the risk of conversion from a clinically isolated syndrome to multiple sclerosis at 6 months was significantly lower with minocycline than with placebo…” (Luanne M. Metz, M.D., et al., 2017)
“…NAD+[able to be increased with niacinamide supplementation]…reverses disease progression by restoring tissue integrity via remyelination and neuroregeneration…NAD+ may be the ideal molecule to treat autoimmune diseases such as MS, type 1 diabetes and inflammatory bowel disease…” (Stefan G. Tullius, et al., 2014)
The answers can’t all be found in one study, and the biological conditions responsible for MS are not the result of just one isolated, biochemical change. Multiple changes occur together as part of one physiology, and make sense holistically. When you look at the details, it’s important to keep the big picture in mind, or else it becomes easier to be fooled into thinking, something harmful is helpful, and vice versa.
See more here
J Neurol Neurosurg Psychiatry. 2016 May;87(5):454-60. High consumption of coffee is associated with decreased multiple sclerosis risk; results from two independent studies. Hedström AK, Mowry EM, Gianfrancesco MA, Shao X, Schaefer CA, Shen L, Olsson T, Barcellos LF, Alfredsson L.
Biochim Biophys Acta. 2014 Jul;1842(7):1137-43. Serum lactate as a novel potential biomarker in multiple sclerosis. Amorini AM, Nociti V, Petzold A, Gasperini C, Quartuccio E, Lazzarino G, Di Pietro V, Belli A, Signoretti S, Vagnozzi R, Lazzarino G, Tavazzi B.
Clin Cancer Res. 2015 Apr 15;21(8):1877-87. Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer. Rosendahl AH, Perks CM, Zeng L, Markkula A, Simonsson M, Rose C, Ingvar C, Holly JM, Jernström H.
NMR Biomed. 2012 Nov;25(11):1271-9. Lactate and glycine-potential MR biomarkers of prognosis in estrogen receptor-positive breast cancers. Giskeødegård GF, Lundgren S, Sitter B, Fjøsne HE, Postma G, Buydens LM, Gribbestad IS, Bathen TF.
NFS Journal Volume 3, August 2016, Pages 1-7. Coffee and metabolic impairment: An updated review of epidemiological studies. Silvio Buscemia Stefano Marventano Mariagrazia Antoci Antonella Cagnetti Gabriele Castorina Fabio Galvano Marina Marranzano Antonio Mistretta.
Noro Psikiyatr Ars. 2016 Dec;53(4):353-356. Serum Prolactin Levels in Multiple Sclerosis, Neuromyelitis Optica, and Clinically Isolated Syndrome Patients. Türkoğlu R, Giriş M, Gencer M, Akcan U, Örçen A.
Neuroendocrinology. 2015;101(4):296-308. Dihydrotestosterone as a Protective Agent in Chronic Experimental Autoimmune Encephalomyelitis. Giatti S, Rigolio R, Romano S, Mitro N, Viviani B, Cavaletti G, Caruso D, Garcia-Segura LM, Melcangi RC.
Nature volume 479, pages538–541(2011). Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Kerstin Berer, Marsilius Mues, Michail Koutrolos, Zakeya Al Rasbi, Marina Boziki, Caroline Johner, Hartmut Wekerle & Gurumoorthy Krishnamoorthy.
Cell Mol Neurobiol. 1993 Jun;13(3):247-61. Chronic Caffeine Alters the Density of Adenosine, Adrenergic, Cholinergic, GABA, and Serotonin Receptors and Calcium Channels in Mouse Brain. Shi D, Nikodijević O, Jacobson KA, Daly JW.
Brain Res. 2010 Jan 14;1309:116-25. Chronic caffeine treatment attenuates experimental autoimmune encephalomyelitis induced by guinea pig spinal cord homogenates in Wistar rats. Chen GQ, Chen YY, Wang XS, Wu SZ, Yang HM, Xu HQ, He JC, Wang XT, Chen JF, Zheng RY.
PLoS One. 2014 Sep 3;9(9):e106335. Intestinal Barrier Dysfunction Develops at the Onset of Experimental Autoimmune Encephalomyelitis, and Can Be Induced by Adoptive Transfer of Auto-Reactive T Cells. Nouri M, Bredberg A, Weström B, Lavasani S.
Nutrients. 2017 Jan 10;9(1). pii: E56. Coffee Intake Is Associated with a Lower Liver Stiffness in Patients with Non-Alcoholic Fatty Liver Disease, Hepatitis C, and Hepatitis B. Hodge A, Lim S, Goh E, Wong O, Marsh P, Knight V, Sievert W, de Courten B.
The American Journal of Clinical Nutrition, Volume 109, Issue 3, March 2019, Pages 635–647. Coffee consumption and plasma biomarkers of metabolic and inflammatory pathways in US health professionals. Dong Hang, Ane Sørlie Kværner, Wenjie Ma, Yang Hu, Fred K Tabung, Hongmei Nan, Zhibin Hu, Hongbing Shen, Lorelei A Mucci, Andrew T Chan, Edward L Giovannucci, Mingyang Song.
Neuropharmacology. 2016 Nov;110(Pt B):644-653. Targeting demyelination and virtual hypoxia with high-dose biotin as a treatment for progressive multiple sclerosis. Sedel F, Bernard D, Mock DM, Tourbah A.
Neurology, April 06, 2015; 84 (14 Supplement). Greater Consumption of Coffee is Associated with Reduced Odds of Multiple Sclerosis. Ellen Mowry, Anna Hedstrom, Milena Gianfrancesco, Xiaorong Shao, Catherine Schaefer, Lisa Barcellos, Tomas Olsson, Lars Alfredsso.
Nature Communications volume 8, Article number: 14241 (2017). Dietary cholesterol promotes repair of demyelinated lesions in the adult brain. Stefan A. Berghoff, Nina Gerndt, Jan Winchenbach, Sina K. Stumpf, Leon Hosang, Francesca Odoardi, Torben Ruhwedel, Carolin Böhler, Benoit Barrette, Ruth Stassart, David Liebetanz, Payam Dibaj, Wiebke Möbius, Julia M. Edgar & Gesine Saher.
Mol Cell Endocrinol. 1982 Oct;28(2):199-209. Norepinephrine stimulates testosterone aromatization and inhibits 5 alpha reduction via beta-adrenoceptors in rat pineal gland. Cardinali DP, Ritta MN, Gejman PV.
J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):272-5. Sex hormones modulate brain damage in multiple sclerosis: MRI evidence. Tomassini V, Onesti E, Mainero C, Giugni E, Paolillo A, Salvetti M, Nicoletti F, Pozzilli C.
Neuroendocrinology. 2015;101(4):296-308. Dihydrotestosterone as a Protective Agent in Chronic Experimental Autoimmune Encephalomyelitis. Giatti S, Rigolio R, Romano S, Mitro N, Viviani B, Cavaletti G, Caruso D, Garcia-Segura LM, Melcangi RC.
Neurosci Lett. 2001 Jul 27;308(1):25-8. Caffeine inhibits exercise-induced increase in tryptophan hydroxylase expression in dorsal and median raphe of Sprague-Dawley rats. Lim BV, Jang MH, Shin MC, Kim HB, Kim YJ, Kim YP, Chung JH, Kim H, Shin MS, Kim SS, Kim EH, Kim CJ.
Mult Scler Relat Disord. 2015 Mar;4(2):159-69. High doses of biotin in chronic progressive multiple sclerosis: a pilot study. Sedel F, Papeix C, Bellanger A, Touitou V, Lebrun-Frenay C, Galanaud D, Gout O, Lyon-Caen O, Tourbah A.
BMC Neurology volume 18, Article number: 86 (2018). Environmental exposures and the risk of multiple sclerosis in Saudi Arabia. Osama Al Wutayd, Ashri Gad Mohamed, Jameelah Saeedi, Hessa Al Otaibi & Mohammed Al Jumah.
. Association between low testosterone and brain atrophy in men multiple sclerosis. (S38.006). Riley Bove, Brian Healy, Svetlana Egorova, Bonnie Glanz, Rohit Bakshi, Philip De Jager, Karen Miller, Charles Guttmann, Tanuja Chitnis.
Arch Neurol. 2005 Feb;62(2):277-80. Fatigue and regulation of the hypothalamo-pituitary-adrenal axis in multiple sclerosis. Gottschalk M, Kümpfel T, Flachenecker P, Uhr M, Trenkwalder C, Holsboer F, Weber F.
17β-Estradiol Promotes TLR4-Triggered Proinflammatory Mediator Production through Direct Estrogen Receptor α Signaling in Macrophages In Vivo. Bertrand Calippe, Victorine Douin-Echinard, Laurent Delpy, Muriel Laffargue, Karine Lélu, Andrée Krust, Bernard Pipy, Francis Bayard, Jean-François Arnal, Jean-Charles Guéry and Pierre Gourdy.
Psychoneuroendocrinology. 2011 Nov;36(10):1505-12. Circadian cortisol, depressive symptoms and neurological impairment in early multiple sclerosis. Kern S, Schultheiss T, Schneider H, Schrempf W, Reichmann H, Ziemssen T.
J Neurol. 2003 Jun;250(6):672-5. Prevalence of autoimmune thyroiditis and non-immune thyroid disease in multiple sclerosis. Niederwieser G, Buchinger W, Bonelli RM, Berghold A, Reisecker F, Költringer P, Archelos JJ.
Neurotherapeutics, January 2017, Volume 14, Issue 1, pp 199–211. Lipopolysaccharide Binding Protein and Oxidative Stress in a Multiple Sclerosis Model. Begoña M. EscribanoFrancisco J. Medina-FernándezMacarena Aguilar-LuqueEduardo AgüeraMontserrat FeijooFe I. Garcia-MaceiraRafael LilloPatricia Vieyra-ReyesAna I. GiraldoEvelio LuqueRené Drucker-ColínIsaac Túnez.
Nature Communications volume 5, Article number: 5101 (2014). NAD+ protects against EAE by regulating CD4+ T-cell differentiation. Stefan G. Tullius, Hector Rodriguez Cetina Biefer, Suyan Li, Alexander J. Trachtenberg, Karoline Edtinger, Markus Quante, Felix Krenzien, Hirofumi Uehara, Xiaoyong Yang, Haydn T. Kissick, Winston P. Kuo, Ionita Ghiran, Miguel A. de la Fuente, Mohamed S. Arredouani, Virginia Camacho, John C. Tigges, Vasilis Toxavidis, Rachid El Fatimy, Brian D. Smith, Anju Vasudevan & Abdallah ElKh.
J Neuroimmunol. 2005 Aug;165(1-2):186-91. Hypothalamo-pituitary-adrenal axis activity predicts disease progression in multiple sclerosis. Gold SM, Raji A, Huitinga I, Wiedemann K, Schulz KH, Heesen C.
Hormones (Athens). 2005 Oct-Dec;4(4):226-30. A unique case of a benign adrenocortical tumor with triple secretion of cortisol, androgens, and aldosterone: development of multiple sclerosis after surgical removal of the tumor. Markou A, Tsigou K, Papadogias D, Kossyvakis K, Vamvakidis K, Kounadi T, Piaditis G.
Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models. Egle Cekanaviciute, Bryan B. Yoo, Tessel F. Runia, Justine W. Debelius, Sneha Singh, Charlotte A. Nelson, Rachel Kanner, Yadira Bencosme, Yun Kyung Lee, Stephen L. Hauser, Elizabeth Crabtree-Hartman, Ilana Katz Sand, Mar Gacias, Yunjiao Zhu, Patrizia Casaccia, Bruce A. C. Cree, Rob Knight, Sarkis K. Mazmanian, and View ORCID ProfileSergio E. Baranzini
Mult Scler. 2006 Aug;12(4):487-94. Fatigue in progressive multiple sclerosis is associated with low levels of dehydroepiandrosterone. Téllez N, Comabella M, Julià E, Río J, Tintoré M, Brieva L, Nos C, Montalban X.
European Journal of Clinical Nutrition volume 69, pages1220–1225(2015). The evaluation of inflammatory and oxidative stress biomarkers on coffee–diabetes association: results from the 10-year follow-up of the ATTICA Study (2002–2012). E Koloverou, D B Panagiotakos, C Pitsavos, C Chrysohoou, E N Georgousopoulou, A Laskaris & C Stefanadis.
Elife. 2015 Aug 11;4. A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model. Arima Y, Kamimura D, Atsumi T, Harada M, Kawamoto T, Nishikawa N, Stofkova A, Ohki T, Higuchi K, Morimoto Y, Wieghofer P, Okada Y, Mori Y, Sakoda S, Saika S, Yoshioka Y, Komuro I, Yamashita T, Hirano T, Prinz M, Murakami M.
Zh Nevrol Psikhiatr Im S S Korsakova. 2009;109(1):10-5. Pathology of the thyroid gland and multiple sclerosis: a possible influence on efficacy and tolerability of treatment. Bagir’ LV, Batysheva TT, Boĭko AN, Gusev EI.
Nature Communications volume 6, Article number: 8466 (2015). Structural and functional rejuvenation of the aged brain by an approved anti-asthmatic drug. Julia Marschallinger, Iris Schäffner, Barbara Klein, Renate Gelfert, Francisco J. Rivera, Sebastian Illes, Lukas Grassner, Maximilian Janssen, Peter Rotheneichner, Claudia Schmuckermair, Roland Coras, Marta Boccazzi, Mansoor Chishty, Florian B. Lagler, Marija Renic, Hans-Christian Bauer, Nicolas Singewald, Ingmar Blümcke, Ulrich Bogdahn, Sebastien Couillard-Despres, D. Chichung Lie, Maria P. Abbracchio & Ludwig Aigner.
Acta Neurol Belg. 2018 Jun;118(2):153-159. Thyroid disorders in alemtuzumab-treated multiple sclerosis patients: a Belgian consensus on diagnosis and management. Decallonne B, Bartholomé E, Delvaux V, D’haeseleer M, El Sankari S, Seeldrayers P, Van Wijmeersch B, Daumerie C.
Brain. 2013 Jan;136(Pt 1):132-46. The neural androgen receptor: a therapeutic target for myelin repair in chronic demyelination. Hussain R, Ghoumari AM, Bielecki B, Steibel J, Boehm N, Liere P, Macklin WB, Kumar N, Habert R, Mhaouty-Kodja S, Tronche F, Sitruk-Ware R, Schumacher M, Ghandour MS.
N Engl J Med. 2017 Jun 1;376(22):2122-2133. Trial of Minocycline in a Clinically Isolated Syndrome of Multiple Sclerosis. Metz LM, Li DKB, Traboulsee AL, Duquette P, Eliasziw M, Cerchiaro G, Greenfield J, Riddehough A, Yeung M, Kremenchutzky M, Vorobeychik G, Freedman MS, Bhan V, Blevins G, Marriott JJ, Grand’Maison F, Lee L, Thibault M, Hill MD, Yong VW;
Neuroscience. 2007 Feb 23;144(4):1293-304. Progesterone and its derivatives are neuroprotective agents in experimental diabetic neuropathy: a multimodal analysis. Leonelli E, Bianchi R, Cavaletti G, Caruso D, Crippa D, Garcia-Segura LM, Lauria G, Magnaghi V, Roglio I, Melcangi RC.
Crit Rev Food Sci Nutr. 2019;59(4):652-663. Consumption of coffee or caffeine and serum concentration of inflammatory markers: A systematic review. Paiva C, Beserra B, Reis C, Dorea JG, Da Costa T, Amato AA.
J Steroid Biochem Mol Biol. 2016 Apr;158:157-177. Preliminary evidence of altered steroidogenesis in women with Alzheimer’s disease: Have the patients “OLDER” adrenal zona reticularis? Vaňková M, Hill M, Velíková M, Včelák J, Vacínová G, Dvořáková K, Lukášová P, Vejražková D, Rusina R, Holmerová I, Jarolímová E, Vaňková H, Kancheva R, Bendlová B, Stárka L.
Eur J Phys Rehabil Med. 2015 Oct;51(5):557-68. Ventilatory function during exercise in multiple sclerosis and impact of training intervention: cross-sectional and randomized controlled trial. Hansen D, Wens I, Keytsman C, Verboven K, Dendale P, Eijnde BO.
J Magn Reson Imaging. 2017 Nov;46(5):1464-1473. Progressive iron accumulation across multiple sclerosis phenotypes revealed by sparse classification of deep gray matter. Elkady AM, Cobzas D, Sun H, Blevins G, Wilman AH.
Neuroimage Clin. 2014 Mar 6;4:454-60. Neuroprotective effects of testosterone treatment in men with multiple sclerosis. Kurth F, Luders E, Sicotte NL, Gaser C, Giesser BS, Swerdloff RS, Montag MJ, Voskuhl RR, Mackenzie-Graham A.
J Neuroendocrinol. 2012 Jun;24(6):851-61. Neuroprotective effects of progesterone in chronic experimental autoimmune encephalomyelitis. Giatti S, Caruso D, Boraso M, Abbiati F, Ballarini E, Calabrese D, Pesaresi M, Rigolio R, Santos-Galindo M, Viviani B, Cavaletti G, Garcia-Segura LM, Melcangi RC.
J R Soc Interface. 2016 Sep;13(122). pii: 20160539. Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide. Pretorius E, Mbotwe S, Bester J, Robinson CJ, Kell DB.
J Neuroimmunol. 2016 Oct 15;299:45-52. Methylene blue alleviates experimental autoimmune encephalomyelitis by modulating AMPK/SIRT1 signaling pathway and Th17/Treg immune response. Wang J, Zhao C, Kong P, Bian G, Sun Z, Sun Y, Guo L, Li B.
Neurol Res. 2012 Nov;34(9):854-8. Comparison of the effect of aspirin and amantadine for the treatment of fatigue in multiple sclerosis: a randomized, blinded, crossover study. Shaygannejad V, Janghorbani M, Ashtari F, Zakeri H.
Steroids. 2003 Nov;68(10-13):825-9. Review. Actions of progesterone and its 5alpha-reduced metabolites on the major proteins of the myelin of the peripheral nervous system. Martini L, Magnaghi V, Melcangi RC.
J Neurochem. 2014 Aug;130(4):591-7. Neuroactive steroid levels in plasma and cerebrospinal fluid of male multiple sclerosis patients. Caruso D, Melis M, Fenu G, Giatti S, Romano S, Grimoldi M, Crippa D, Marrosu MG, Cavaletti G, Melcangi RC.
J Neuropathol Exp Neurol. 2014 Feb;73(2):123-35. Gender differences in multiple sclerosis: induction of estrogen signaling in male and progesterone signaling in female lesions. Luchetti S, van Eden CG, Schuurman K, van Strien ME, Swaab DF, Huitinga I.
Oxid Med Cell Longev. 2017;2017:9625806. The Evaluation of Oxidative Stress Parameters in Serum Patients with Relapsing-Remitting Multiple Sclerosis Treated with II-Line Immunomodulatory Therapy. Adamczyk B, Wawrzyniak S, Kasperczyk S, Adamczyk-Sowa M.
J Endocrinol. 1994 Mar;140(3):349-55. Influence of thyroid hormone on androgen metabolism in peripuberal rat Sertoli cells. Panno ML, Beraldi E, Pezzi V, Salerno M, De Luca G, Lanzino M, Le Pera M, Sisci D, Prati M, Palmero S, Bolla E, Fugassa E, Andò S.
Journal of Neuroinflammation volume 9, Article number: 266 (2012). Endotoxin- and ATP-neutralizing activity of alkaline phosphatase as a strategy to limit neuroinflammation. Ruth Huizinga, Karim L Kreft, Sabina Onderwater, Joke G Boonstra, Ruud Brands, Rogier Q Hintzen & Jon D Laman.
Basic Clin Pharmacol Toxicol. 2008 Jun;102(6):543-51. Caffeine Inhibits the Proliferation of Liver Cancer Cells and Activates the MEK/ERK/EGFR Signalling Pathway. Okano J, Nagahara T, Matsumoto K, Murawaki Y.
Nutr Metab Insights. 2012 Sep 13;5:59-70. Effects of Caffeine on Metabolism and Mitochondria Biogenesis in Rhabdomyosarcoma Cells Compared with 2,4-Dinitrophenol. Vaughan RA, Garcia-Smith R, Bisoffi M, Trujillo KA, Conn CA.
PLoS One. 2012;7(1):e30655. Amelioration of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice by Photobiomodulation Induced by 670 nm Light. Muili KA, Gopalakrishnan S, Meyer SL, Eells JT, Lyons JA.
The Journal of Nutrition, Volume 136, Issue 1, January 2006, Pages 166–171, Consumption of Coffee, but Not Black Tea, Is Associated with Decreased Risk of Premenopausal Breast Cancer. Julie A. Baker, Gregory P. Beehler, Abhishek C. Sawant, Vijayvel Jayaprakash, Susan E. McCann, Kirsten B. Moysich.
Neurochemical Journal, July 2013, Volume 7, Issue 3, pp 226–229. Platelet serotonin in multiple sclerosis and its relationship with fatigue syndrome. T. V. BaidinaYu. V. AkintsevaEmail authorT. N. Trushnikova.
Open access peer-reviewed chapter, July 26th 2017, Serotonin in Neurological Diseases. By Jolanta Dorszewska, Jolanta Florczak-Wyspianska, Marta Kowalska, Marcin Stanski, Alicja Kowalewska and Wojciech Kozubski.
Scientific Reports volume 7, Article number: 43410 (2017). Relapsing-remitting multiple sclerosis patients display an altered lipoprotein profile with dysfunctional HDL. Winde Jorissen, Elien Wouters, Jeroen F. Bogie, Tim Vanmierlo, Jean-Paul Noben, Denis Sviridov, Niels Hellings, Veerle Somers, Roland Valcke, Bart Vanwijmeersch, Piet Stinissen, Monique T. Mulder, Alan T. Remaley & Jerome J. A. Hendriks.
Neurosci Lett. 2018 Nov 20;687:304-307. Cholesterol level correlate with disability score in patients with relapsing-remitting form of multiple sclerosis. Ďurfinová M, Procházková Ľ, Petrleničová D, Bystrická Z, Orešanská K, Kuračka Ľ, Líška B.