Coffee For MS – Wonderful!

Wonderul If you have ever wondered why roughly three times as many women than men, are diagnosed with MS every year, looking at the ways that sugary coffee shields from the development of this (and other related conditions), can be 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.”

Multiple sclerosis (MS) is known to arise 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 some of them are more logical than others. Officially there is no known cure, and popular treatment approaches have had limited success.

Although it’s probably true that nothing is ever entirely black and white, one thing that does seem clear, is that the promoters of 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 multiple sclerosis (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…”

“…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…”

“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…”

“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…”

“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…”

Susceptibility to stress is a central factor encouraging a rise in the inflammatory things associated with the development of MS. Ongoing exposure to stress promotes the kind of energy metabolism suppressed, low thyroid, high estrogen, state (more prevalent in women), well known to aggravate 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.”

“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.”

“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…”

Unfortunately, popular medical theories continue to push the idea that an ‘estrogen deficiency’ makes women more susceptible to MS, and it is not uncommon for estrogen supplements to be suggested as treatment. Other popular treatments include glucocorticoids, immune suppressant drugs and immunotherapy, also called disease modifying therapy.

When it comes to justifying ineffective (although highly profitable) treatments, many scientifically contradictory or misleading belief systems need to be maintained, and to do so, a number of physiologically sound principles need to be twisted, or completely disregarded.

In particular, misrepresentations labeling estrogen (instead of progesterone) as the female/pregnancy hormone, confusion over the function of estrogen for ‘birth control’, and constant downplaying of the role of estrogen in the development of breast (and other) cancer, prevent better understanding.

Tied in with biologically unsound theories regarding estrogen, are many popularly endorsed, erroneous ideas relating to the role of the inflammatory stress promoting things (like serotonin, nitric oxide, cortisol and the PUFAs), helping to allow confusion to reign, to optimize the sale of pharmaceutical products, and to prevent the whole belief structure from crumbling because of the truth.

Some products which require a level of cognitive dissonance in order for them to stay on the market, include many ‘anti-depressants’, estrogen drugs, cholesterol lowering drugs, polyunsaturated oils, as well as nitric oxide raising drugs like Viagra and Cialis. Many of these have been shown to have a role in promoting the neurodegenerative conditions.

Although popular science attempts to frame estrogen as something which protects against neurodegeneration and MS (arguing that low levels of estrogen in the blood are proof of this), what is largely ignored, are the many indicators of stress and inflammation which rise with MS progression, and which are well known to promote estrogen levels, in particular inside tissue, where it is more harmful and rarely tested.

A well functioning thyroid energy metabolism, protects against increasing (and excessive) levels of estrogen in tissue, and restrains the rise in many of the inflammatory (potentially neurodegenerative) substances of stress.

Improvements in thyroid function and metabolic performance in general, assist in the production of numerous highly protective and genuinely anti-inflammatory hormones (such as pregnenolone, progesterone), which are known to have anti-estrogenic effects, and to protect against the onset and worsening of MS symptoms. Women are generally more susceptible to thyroid dysfunction, and this is in part because of increased exposure to estrogen.

“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.”

When energy metabolism is suppressed and stress is high, digestion and liver function is less effective, and this can lead to the development of bacterial issues. Increased exposure to bacterial toxins like endotoxin (LPS), promote inflammation, as well as rising levels of both serotonin and estrogen, helping to drive a self-feeding, immune system dysregulated state of stress, increasing the risk of MS.

“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…”

“…we hypothesize that gut microbiota contribute to creating a sustained proinflammatory environment…and suggests a potentially causal role for the gut microbiota in MS.”

“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.”

Endotoxin powerfully suppresses thyroid energy function, and increases cortisol and prolactin levels, and both of these substances have been shown to rise under inflammatory stressful conditions, and promote MS. Prolactin blood results are known to be an accurate measure of tissue levels of estrogen.

Interference with mitochondrial energy production and thyroid performance, encourages the production of lactate, and lactate is another thing which is known to rise with the progression of MS, as well as other diseases associated with inflammation, thyroid dysfunction and increased estrogen, such as breast cancer.

“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.”

This can be where the regular consumption of coffee – in combination with sufficient quantities of sugar – can enter into the story.

Many studies show the protective effects of coffee (and caffeine), and it isn’t mere coincidence that coffee’s effects (encouraging efficient metabolic function, and inhibiting excessive estrogen levels) help protect against MS.

“…study shows that 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.”

Apart from having progesterone-like actions (protecting against damaging effects of estrogen and serotonin), caffeine acts somewhat similarly to thyroid, and helps to boost mitochondrial energy systems, reducing 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.”

“…caffeine…increased oxidative metabolism…caffeine heightens metabolic rate…caffeine stimulates metabolism and favorable mitochondrial production…findings support the advertised metabolic benefits of caffeine…”

Improved thyroid metabolism means less exposure to estrogen and more effective digestive and liver function, reducing the potential for bacterial endotoxin to enter into the main system, where it can promote systemic inflammation and help cause neurodegeneration.

Regular coffee consumption improves liver health, increasing detoxification potential, leading to lower levels of estrogen 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.”

Improved liver function leads to better conversion of inactive thyroid hormone (T4) into active thyroid hormone (T3), and this is a central issue underlying sub-optimal thyroid function in women, and 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…”

“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.”

By improving overall metabolism and energy system function, coffee consumption can help to protect against some of the harm done by excessive exposure to polyunsaturated fats. The polyunsaturated fats (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.

PUFAs promote inflammation and oxidative stress, and directly increase tissue levels of estrogen, thereby playing an important part 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.”

The breakdown products of PUFAs interfere with cholesterol metabolism, impeding progesterone production, pushing things in the direction towards more estrogen and more cortisol, increased inflammation and greater sensitivity to any exposure to stress. Cholesterol is protective against MS.

“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.”

Sugar promotes the production of cholesterol, increases conversion of cholesterol into the protective steroids, stimulating thyroid metabolism, and suppressing stress and inflammation. Sugar lowers exposure to the inflammatory oxidative stress promoting breakdown products of the polyunsaturated free fatty acids, associated with MS.

“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…”

“…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.”

Sugar can be understood to be a very important ingredient in protection against stress and inflammation, as well as 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 worsens hypometabolic conditions connected to the onset of MS and diabetes. Sugar consumption is not the cause of 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…”

“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.”

Coffee has been shown to be protective against inflammation and oxidative stress and increased coffee intake has been demonstrated to protect against other inflammatory conditions aside from MS, including diabetes.

When thyroid metabolism is suppressed, liver function is impaired, and estrogen and cortisol levels are raised, sensitivity to coffee can be high and might at first encourage a stress response.

Sugar helps to increase thyroid function and lower stress, and can help to protect against potential stress promoting effects of coffee. Sugar also helps with the production of the anti-stress and anti-inflammatory hormones (pregnenolone, progesterone, testosterone and DHEA) protecting 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…”

“…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…”

When you think about the things that protect against stress, inflammation and thyroid dysfunction (things that are also known to encourage liver and digestive function, and help to keep cortisol and estrogen levels under control), and promote pregnenolone, testosterone and progesterone production, it makes little sense to suggest estrogen supplementation (and other stress promoting things) for the treatment of MS.

Although estrogen and cortisol (and other stress substances like serotonin and nitric oxide and PUFA) can suppress stress and immune system related symptoms in the short term, evidence shows that they do not do so in a manner which promotes long term metabolic health and regeneration. Instead, continuous exposure over time, 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…”

Excess estrogen in particular, has been shown to be involved with many conditions (which effect women more regularly) associated with stress, inflammation and thyroid dysfunction, and MS risk is reduced when optimal metabolism is maintained, and the stress, inflammation and thyroid interfering things are kept low. High levels of progesterone in the third trimester of pregnancy coincide with significant reduction in symptoms of MS.

I know I’ve said before, that I’m no scientist and I’m certainly not a doctor of any kind, but I think I’m starting to see a pattern here, and I know I’m not the only one.

“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.”

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, is potentially highly protective.

Some other things which might help with MS include thiamine, biotin, aspirin, Minocycline, niacinamide, activated charcoal, methylene blue, vitamin E, cyproheptadine and some other antihistamines, red light and 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.”

“Methylene blue (MB) is an effective neuroprotectant in many neurological disorders…Our findings suggest that MB could be a promising reagent to treat…MS.”

“…experiments suggest…that photobiomodulation may be valuable as an adjunct therapy for the treatment of MS.”

“…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…”

“…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…”

The answers can’t all be found in just one study, and the biological conditions responsible for the onset of MS are generally not the result of the impact of just one isolated biochemical change. In reality, changes exist together in one physiology, and need to make sense as a whole. Unfortunately science and medicine has been fragmented into specialties, often promoting ideas which contradict overall biological function, and impede understanding of what causes and protects against disease.

See more here

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Serum lactate as a novel potential biomarker in multiple sclerosis.

Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer

Correlation between sex hormones and magnetic resonance imaging lesions in multiple sclerosis.

Multiple sclerosis is associated with alterations in hypothalamic-pituitary-adrenal axis function.

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Lactate and glycine-potential MR biomarkers of prognosis in estrogen receptor-positive breast cancers.

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Serum Prolactin Levels in Multiple Sclerosis, Neuromyelitis Optica, and Clinically Isolated Syndrome Patients

Prolactin secretion is increased in patients with multiple sclerosis.

Dihydrotestosterone as a Protective Agent in Chronic Experimental Autoimmune Encephalomyelitis.

Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination

Chronic Caffeine Alters the Density of Adenosine, Adrenergic, Cholinergic, GABA, and Serotonin Receptors and Calcium Channels in Mouse Brain

Chronic caffeine treatment attenuates experimental autoimmune encephalomyelitis induced by guinea pig spinal cord homogenates in Wistar rats.

Intestinal Barrier Dysfunction Develops at the Onset of Experimental Autoimmune Encephalomyelitis, and Can Be Induced by Adoptive Transfer of Auto-Reactive T Cells

Coffee Intake Is Associated with a Lower Liver Stiffness in Patients with Non-Alcoholic Fatty Liver Disease, Hepatitis C, and Hepatitis B

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Greater Consumption of Coffee is Associated with Reduced Odds of Multiple Sclerosis

Dietary cholesterol promotes repair of demyelinated lesions in the adult brain

Norepinephrine stimulates testosterone aromatization and inhibits 5 alpha reduction via beta-adrenoceptors in rat pineal gland.

Sex hormones modulate brain damage in multiple sclerosis: MRI evidence Free

Dihydrotestosterone as a Protective Agent in Chronic Experimental Autoimmune Encephalomyelitis.

Caffeine inhibits exercise-induced increase in tryptophan hydroxylase expression in dorsal and median raphe of Sprague-Dawley rats.

High dose thiamine improves fatigue in multiple sclerosis

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Salate derivatives found in sunscreens block experimental autoimmune encephalomyelitis in mice.

Environmental exposures and the risk of multiple sclerosis in Saudi Arabia

Involvement of CRH and hCG in the induction of aromatase by cortisol in human placental syncytiotrophoblasts.

Cortisol Awakening Response Is Linked to Disease Course and Progression in Multiple Sclerosis

Fatigue and regulation of the hypothalamo-pituitary-adrenal axis in multiple sclerosis.

17β-Estradiol Promotes TLR4-Triggered Proinflammatory Mediator Production through Direct Estrogen Receptor α Signaling in Macrophages In Vivo

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Thyroid Hormones, Oxidative Stress, and Inflammation

Beneficial effects of oral pure caffeine on oxidative stress

NAD+ protects against EAE by regulating CD4+ T-cell differentiation

Hypothalamo-pituitary-adrenal axis activity predicts disease progression in multiple sclerosis.

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New Insights into the Role of Oxidative Stress Mechanisms in the Pathophysiology and Treatment of Multiple Sclerosis

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Fatigue in progressive multiple sclerosis is associated with low levels of dehydroepiandrosterone.

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A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model

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Structural and functional rejuvenation of the aged brain by an approved anti-asthmatic drug

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Nitric Oxide in Optic Neuritis and Multiple Sclerosis

Trial of Minocycline in a Clinically Isolated Syndrome of Multiple Sclerosis

Progesterone and its derivatives are neuroprotective agents in experimental diabetic neuropathy: a multimodal analysis.

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Preliminary evidence of altered steroidogenesis in women with Alzheimer’s disease: Have the patients “OLDER” adrenal zona reticularis?

Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity.

Ventilatory function during exercise in multiple sclerosis and impact of training intervention: cross-sectional and randomized controlled trial.

Blood levels of selected hormones in patients with multiple sclerosis.

Progressive iron accumulation across multiple sclerosis phenotypes revealed by sparse classification of deep gray matter.

Neuroprotective effects of testosterone treatment in men with multiple sclerosis

Neuroprotective effects of progesterone in chronic experimental autoimmune encephalomyelitis.

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Methylene blue alleviates experimental autoimmune encephalomyelitis by modulating AMPK/SIRT1 signaling pathway and Th17/Treg immune response.

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Prevalence of Thyroid Disease in a Multiple Sclerosis Clinic Cohort (P6.170)

Premenstrual Multiple Sclerosis Pseudoexacerbations

Actions of progesterone and its 5alpha-reduced metabolites on the major proteins of the myelin of the peripheral nervous system.

Association of MS with thyroid disorders.

Neuroactive steroid levels in plasma and cerebrospinal fluid of male multiple sclerosis patients.

Effects of aromatase inhibition and androgen activity on serotonin and behavior in male macaques.

Clinical significance of reduced cerebral metabolism in multiple sclerosis: a combined PET and MRI study.

Cortical deficits in multiple sclerosis on the basis of subcortical lesions.

Perturbed Glucose Metabolism: Insights into Multiple Sclerosis Pathogenesis

Thyroid Hormone Potentially Benefits Multiple Sclerosis via Facilitating Remyelination.

Serum arsenic and lipid peroxidation levels in patients with multiple sclerosis.

Gender differences in multiple sclerosis: induction of estrogen signaling in male and progesterone signaling in female lesions.

Oxidative stress induced by lipid peroxidation is related with inflammation of demyelination and neurodegeneration in multiple sclerosis.


Platelet aggregation and multiple sclerosis.

The Evaluation of Oxidative Stress Parameters in Serum Patients with Relapsing-Remitting Multiple Sclerosis Treated with II-Line Immunomodulatory Therapy

Influence of thyroid hormone on androgen metabolism in peripuberal rat Sertoli cells.

Effects of caffeine on anterior pituitary and thyroid function in the rat.

CSF isoprostane levels are a biomarker of oxidative stress in multiple sclerosis

Endotoxin- and ATP-neutralizing activity of alkaline phosphatase as a strategy to limit neuroinflammation

Caffeine Inhibits the Proliferation of Liver Cancer Cells and Activates the MEK/ERK/EGFR Signalling Pathway

Use of serotonin antagonists, particularly cyproheptadine, in the treatment of cancer, Alzheimer’s disease, AIDS and multiple sclerosis

The bacterial endotoxin lipopolysaccharide causes rapid inappropriate excitation in rat cortex.

Effects of Caffeine on Metabolism and Mitochondria Biogenesis in Rhabdomyosarcoma Cells Compared with 2,4-Dinitrophenol

Ondansetron, a 5-HT3 antagonist, improves cerebellar tremor.

Over-the-Counter Drug May Reverse Chronic Vision Damage Caused by Multiple Sclerosis

Amelioration of Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice by Photobiomodulation Induced by 670 nm Light




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