Physical Trauma and Multiple Sclerosis

Evidence, Pathophysiology, Management

At this moment I am co-managing two patients with multiple sclerosis. Both patients have a history of significant cervical spine/head trauma that occurred within a year of initiation of their multiple sclerosis symptoms. The primary symptoms that brought them to my care is spinal stiffness and pain. Both are experiencing significant improvement with spinal adjusting.

The concept of physical trauma causing or exacerbating the signs and symptoms of multiple sclerosis remains controversial (1). My initial introduction to the concept of physical trauma being potentially related to multiple sclerosis occurred in the mid-1980s. A local neurologist referred me a patient that he described as suffering from “trauma-related” multiple sclerosis. The patient, a 26 year old female, did well under our management. Her legal case went to trial, and both myself and the referring neurologist testified in court about the patient’s clinical status, prognosis, and causation. We lost the trial, primarily on causation issues. Since then, new information regarding multiple sclerosis and physical trauma has been published, some of which is reviewed here:

••••

In 1994, neurologist Charles Poser, MD, from the Department of Neurology at Harvard’s Medical School, published a study in the journal Clinical Neurology and Neurosurgery, titled (2):

The Role of Trauma in the Pathogenesis of Multiple Sclerosis:
A Review

The abstract from this article by Dr. Poser states:

The suggestion that an alteration of the blood-brain barrier (BBB) is an obligatory step in the pathogenesis of the multiple sclerosis (MS) lesion has been amply confirmed by innumerable magnetic resonance scans. There also exists a large body of clinical, neuropathologic, neuropsychologic, radiologic and experimental evidence that shows that trauma, in particular mild concussive injury to the head, neck or upper back, thus impinging on the brain and spinal cord, may result in an increase in BBB permeability. It is only logical therefore to infer that when such mild trauma to those parts of the body affects MS patients, the resulting alteration of the BBB leads to the formation of new lesions or the enlargement and activation of old ones. In such situations trauma acts as a facilitator of the postulated but still not fully understood pathogenetic mechanism of lesion formation. Because of the extremely poor correlation between site and size of the lesions and clinical manifestations of MS, one cannot expect that every episode of trauma will result in the appearance of new symptoms in an hitherto asymptomatic individual, or the recurrence of old symptoms in an MS patient. It is inappropriate to attempt to prove or disprove a causal relationship between physical trauma and MS exacerbations or clinical onset by means of epidemiologic studies. The unpredictability and variability of the clinical manifestations of the disease, the differences in the genetic and immunologic backgrounds of individuals, as well as in their degree of clinical and pathologic involvement and level of activity, render such investigations pointless.

••••

The November 16, 1996 issue of the British Medical Journal published a report titled (3):

Multiple Sclerosis Linked With Trauma in Court Case

The report notes that a former policeman was awarded $820,875.00 in damages by a court which accepted that he developed multiple sclerosis (MS) after sustaining whiplash injures in a road motor vehicle accident. The 49 year old man developed symptoms within a week of injuring his neck during a crash and overturn motor vehicle accident.

Neurologists who gave evidence on behalf of the officer told the court that they had seen people in which symptoms of MS developed within weeks of suffering whiplash injuries. One professor of neurology emphasized that such injuries could not cause MS by themselves but could bring on the condition in already susceptible individuals. He noted that the patient “might well have lived a normal life but for the injuries he sustained.” Dr. Charles Poser of the Harvard Medical School, said: “there were hundreds of such cases, too many to be caused by chance.”

The Judge (Lord) “accepted that the historical, anecdotal and experimental evidence supported the proposition that a causative factor in some cases” of MS, noting that the medical witnesses “had all themselves seen cases where they had accepted that the onset or recurrences of symptoms had been brought about by trauma, especially whiplash injury. In my opinion, these circumstances are far too strong to be put down to mere chance.”

At the time, this controversial judgment was expected to give rise to further legal action from patients with multiple sclerosis who suffered injuries before the onset of their symptoms.

••••

In July 2000, Harvard neurologist Charles Poser, MD, publishes another study pertaining to physical trauma and miultiple sclerosis. Published in the journal Archives of Neurology in a section titled Controversies in Neurology, and titled (4):

Trauma to the Central Nervous System May Result in Formation or Enlargement of Multiple Sclerosis Plaques

This is a review article with 44 references. In this article, Dr. Poser proposes that in some patients with multiple sclerosis (MS), trauma may act as a trigger for the appearance of new or recurrent symptoms. He notes that only trauma affecting the head, neck, or upper back, affecting the brain and/or spinal cord, can be considered significant. This premise is based on the two considerations:

• An alteration of the blood-brain barrier (BBB) is a necessary step in the pathogenesis of the MS lesion.
• Trauma to the central nervous system (CNS) can result in a breach of the BBB.

Dr. Poser notes that the fact that an alteration of the BBB is an important step in the formation of the MS lesion has been demonstrated many times by serial magnetic resonance imaging (MRI) studies and from positron emission tomography (PET) studies. The alteration in the permeability of the BBB for the development of MS is most frequently triggered by an inflammatory immunological phenomenon.

Dr. Poser argues that:

• Repeated episodes of asymptomatic breakdowns of the BBB eventually lead to demyelination and symptomatic relapse.
• Without BBB penetration, myelin injury would not occur.
• Multiple sclerosis is explainable as a focal breakdown of the BBB.
• Breakdown of the BBB is an early if not first step in multiple sclerosis plaque generation.

Dr. Poser points out that for many years, trivial head injuries such as concussion were considered to result only in physiological disruption of neural function without anatomical changes. However, both spontaneous and experimental concussive CNS injury can cause diffuse microscopic lesions of blood vessel walls that often escape notice on superficial examination of the brain.

Pertaining to whiplash trauma, Dr. Poser states:

“The effects of minor trauma on the CNS assume great importance because whiplash injury is a frequent result of minor vehicular accidents, in particular, the rarely mentioned minor rear-end collision.”

“Direct impact to the head is not necessary for brain injury; whiplash injuries can cause brain damage.”

“The degree of associated bone and soft tissue injury has no bearing on the extent of the spinal cord injury or neurologic deficit.”

The fact that CNS trauma affects the deep cerebral white matter has been demonstrated by MRI, even in patients who had experienced mild head injuries. Such white matter changes indicate alteration of the BBB. Research on monkeys has shown that a blow to the occipital area altered the BBB in the medulla and in the cervical spinal cord.

Other experiments have shown small cerebral vessels and capillary damage in animals sustaining mechanical brain injury “too slight to produce microscopic intraparenchymal hemorrhage or other neuropathological changes but strong enough to provoke a physiological concussive response.”

Others have shown a “significant increase in BBB permeability in the brains of animals subjected to whiplash injury that had no head trauma.”

Research has “implicated trauma as a pathogenetic factor in the formation of MS lesions in the cervical spinal cord in cases studied postmortem, as a result of the normal stretching of the tethered cord during flexion and extension of the neck, especially in the presence of cervical spondylosis.” Others blame “repeated episodes of trauma to the cervical cord to explain the frequent clinical association between cervical spondylosis and MS. This relationship has now been well documented by MRI in many patients with MS, revealing a close anatomical correspondence between compression of the cervical spinal cord by spondylosis or herniated discs, even in the absence of external trauma, and intraspinal plaques at the same level. Such MRI changes in the spinal cord have not been seen in patients with the same degree of spinal stenosis who do not have MS.” “Magnetic resonance images of the neck in voluntary flexion show how traumatic hyperflexion-extension augments the degree of impingement on the spinal cord, while it cannot fully reflect the much more severe impact during the actual whiplash injury.”

Other multiple sclerosis experts have recognized the potential role played by trauma in the alteration of the BBB in multiple sclerosis, noting:

“Although there are many potential reasons for the BBB break, a simple model of traumatic damage could account for the commoner sites of lesions being in the highly mobile optic nerve and cervical cord, especially when tethered by the dentate ligaments.”

“Any mechanism which physically destroys the components of the BBB will render the CNS open to the cellular and molecular constituents of the blood. This causes inflammatory participants to be rapidly delivered to the site of injury in a gross, nonspecific fashion.”

Dr. Poser notes that trauma-induced alteration of the BBB does not always result in demyelination in patients with multiple sclerosis, but that there is biological plausability to link physical trauma to multiple sclerosis, “based on clinical, neuropathological, radiological, and experimental evidence.”

••••

The following year, in November of 2001, Abhijit Chaudhuri, PhD, and Peter Behan, DSc, from the Department of Neurology at the University of Glasgow published an article in the European Journal of Neurology titled (5):

Acute cervical hyperextension-hyperflexion injury may precipitate and/or exacerbate symptomatic multiple sclerosis

The authors reported on 39 cases in which definite multiple sclerosis (MS) was precipitated or exacerbated by specific hyperextension-hyperflexion cervical cord trauma. The worsening or onset of the symptoms bore a striking temporal relationship to the focal injury. They state:

“Our data suggests that central nervous system (CNS)-specific acute physical trauma such as cervical cord hyperextension-hyperflexion injury may aggravate latent clinical symptoms in multiple scelerosis.”

“The deterioration of multiple sclerosis bore no direct relationship with the severity of neck injury.”

These authors discuss the possible pathogenic mechanisms of focal CNS-specific trauma aggravating the course of asymptomatic or benign multiple sclerosis. Their discussion includes that axonal pathology from focal trauma can increase nitric oxide in the brain, leading to demyelinating injury.

These authors agree with Dr. Poser in that physical trauma is linked to multiple sclerosis as a consequence of disruption of the blood brain barrier. The critical role of changes in the BBB influencing the clinical course of MS has been evident since 1950. They note evidence for massive breakdown of the BBB of the cord and of the brain follows experimental induction of whiplash injuries in monkeys. There are many studies showing pathologically verified new MS plaques surrounding the specific areas where the BBB had broken down. Therefore, any external factor that can influence the integrity of the BBB of an individual will increase chances to develop MS and have the potential to trigger the disease symptoms. They state:

“Breakdown in the blood-brain barrier (BBB) is an early and obligatory event in the development of acute multiple sclerosis lesions.”

“Research has clearly established that an abnormal BBB plays a critical role in the initiation and progression of demyelination.”

“Our hypothesis is that acute hyperextension-hyperflexion injuries of the neck will at the very least produce a local breakdown of the BBB.”

They reitirate that hyperextension-hyperflexion injuries to the cervical spinal cord have been shown to cause a severe disruption of the BBB both locally and generally. In this study they documented 39 patients who developed symptomatic multiple sclerosis or in whom a stable disease with minimal disability was converted to a rapidly progressive form within some days to weeks after an acute hyperextension-hyperflexion injury to the cervical spinal cord.

Of the 39 cases, 24 were of new onset. These cases had no previous history of neurological symptoms and were previously in excellent health. The onset of symptoms occurred within 12 hours to 12 weeks post-trauma with a peak between 2 and 3 weeks.

In the other 15 cases with pre-injury mild MS, their condition rapidly accelerated to a progressive form following their injury. The worsening of their MS occurred between 1 and 12 weeks post-trauma with a peak at 1-2 weeks.

In both groups, there was no correlation between the severity of injury and the subsequent deterioration of MS symptoms. There were no cervical vertebral fractures, dislocations or spinal cord compressions.

These authors cite 9 studies (1946, 1950, 1957, 1964, 1966, 1975, 1975, 1988, 1991, 1992) that support that specific CNS trauma may precipitate or aggravate MS. The proposed mechanism in these studies includes:

• specific focal trauma
• co-existence of cervical spondylitic myelopathy
• mechanical stresses communicated to the cord via the denticulate ligaments during flexion of the spine
• repetitive stresses that cause breakdown of the BBB

Important comments made by these authors in this study include:

“The role of physical trauma on MS has been debated for a number of years.”

“It is important to stress that the trauma was of a uniform type in all cases, i.e. an acute hyperextension-hyperflexion focal injury to the cervical spinal cord.” The majority of cases occurred in motor car accidents.

“The severity of the soft tissue injury was mild to moderate in the vast majority of the cases.”

“The cervical region is the commonest site of spinal cord involvement in MS and spinal cord atrophy provides the best correlate of the degree of disability. Thus, it would only seem logical that rapid progression of disability was a direct consequence of the cervical cord disease in our cases.”

CNS-specific focal trauma has a role in “precipitating the symptoms of undeclared MS and adversely affecting the course of benign MS.”

Cervical cord hyperextension-hyperflexion injury is likely to unmask or worsen the natural course of MS in a subgroup of affected patients.

••••

The largest study I am aware of in assessing the relationship between physical trauma and multiple sclerosis was published in the Journal of Neurotrauma in 2012, and titled (6):

Increased Risk of Multiple Sclerosis After Traumatic Brain Injury:
A Nationwide Population-based Study

The aim of this study was to investigate the risk for MS following a traumatic brain injury (TBI) using a large-scale cohort study using data from the National Health Insurance Research Database. A total of 72,765 patients with TBI were identified for the study cohort, and 218,295 randomly selected subjects were matched and used as controls. Each group was followed for a period of 6 years.

Patients with TBI had a 97% increased risk of developing MS as compared to the control group. They concluded:

“Our study concludes that patients with TBI are at higher risk for subsequent MS over a 6-year follow-up period.”

••••

Adjunct Management Suggestions

I use a number of adjunct approaches in patients with multiple sclerosis. They include:

• Paleo diet
• Vitamin D
• Omega-3s
• Resveratrol
• Curcumin
• Sodium restriction

Paleo Diet

Physician Terry Wahls, MD, had an active, productive life, until she was stricken with mutiple sclerosis. Being cared for at the prestegious Cleveland Clinic, her signs and symptoms steaidly worsened. Dr. Wahls claims her low point occurred when her hospital staff privlidges were revoked. Realizing that what she was doing was not working, she decided to take charge of her own health and do her own due deligence. She accessed the appropriate literature using the PubMed search engine of the National Library of Medicine. Dr. Wahls radically changed her eating habits, and went “Paleo.” Subsequently, her signs and symptoms began to steadily improve, and her vitality was restored.

Dr. Wahls now lectures on her recovery approach, and she has become viral on the internet. We have all of our multiple sclerosis patients watch the Terry Wahls YOUTUBE video that is 17m 47s in length, titled Minding Your Mitochondria (7).

Vitamin D

It has been known for decades that low levels of the active form of vitamin D are associated with increased incidence of multiple sclerosis. Using the words “vitamin D” AND “multiple sclerosis” in the PubMed search engine of the National Library of Medicine finds 645 articles ( as of 7/11/13), the oldest being dated in 1986.

For our multiple sclerosis patients, we target 50-70 ng/mL of 25(OH) vitamin D. We use the dosing recommendations of Pizzorno (8):

The loading dose of supplemental vitamin D3 should be about 20,000 IU/day for 3 – 6 months with a maintenance dose of 5,000 IU/day. Those taking this amount of supplemental vitamin D3 should periodically have their serum 25(OH)D3 levels measured. Prolonged intake of 10,000 IU of supplemental vitamin D3 “is likely to pose no risk of adverse effects in almost all individuals.”

Omega-3s

There is potential for omega-3 fatty acids to improve the signs and symptoms of multiple sclerosis. This is probably linked to an atenuated response of some aspects of the autoimmunity cascade. Using the words “omega-3 and multiple sclerosis” in the PubMed search engine of the National Library of Medicine finds 56 articles (as of 7/11/13). Reading the abstracts shows varying cliniical outcomes.

Of interest is the case of Randal McCloy. On January 2, 2006, in Upshur County, West Virginia, there was an explosion in the Sago Coal Mine. The blast trapped 13 miners for nearly two days; only one miner survived. The lone survivor was Randal McCloy, age 26. He was found practically dead, unconscious and suffering from carbon monoxide posioning. The carbon monoxide had stripped the protective myelin sheath from most of his brain’s neurons (multiple sclerosis pathology also involves demyleniation). His prognosis for survival was extremely grim, let alone prospects for recovery. McCloy’s neurosurgeon started to enternally feed him a daily dose of 15,000 milligrams (mg) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) fish oil. Soon, his brain electrical activity returned and he emerged from his coma, gradually regaining his ability to walk, talk, and see. Apparently the omega-3s helped rebuild the damaged gray and white matter of his brain. McCloy is the longest exposure to carbon monoxide poisoning to have survived. McCloy is now married, has children, and is largely functioning normally (9).

In accordance with physician/geneticists Artemis Simopoulos, MD, we target an omega-6/omega-3 ratio of 2/1 (10). For most, this will require supplementation with about 3000 mg of EPA + DHA daily.

Resveratrol

There is evidence that multiple sclerosis is an autoimmune disease, driven by thymus helper 17 cells (Th17). There is evidence that this autoimmune response in multiple sclerosis patients can be improved with supplementation of the “potent anti-inflammatory compound” resveratrol (11). Consequently, we recommend that all of our multiple sclerosis patients supplement with 100 mg of resveratrol per day.

Curcumin

There is also evidence that the multiple sclerosis autoimmune thymus helper 17 cells (Th17) response in multiple sclerosis patients can be improved with supplementation of the “outstanding anti-inflammation and neuroprotective” compound curcumin (12). Consequently, we recommend that all of our multiple sclerosis patients supplement with 200 mg of curcumin per day.

Sodium Restriction

Earlier this year (4/25/13), researchers from the Yale School of Medicine, Departments of Neurology and Immunobiology, published an interesting and important study in the journal Nature, titled (13):

Sodium chloride drives autoimmune disease
by the induction of pathogenic TH17 cells

These authors state that thymus helper 17 cells (Th17) play a key role in autoimmune diseases, specifically emphasizing multiple sclerosis. The authors use a number of sophisticated and detailed experiments on human and murine cell cultures and on mice to establish their findings and conclusions, stating:

“There has been a marked increase in the incidence of autoimmune diseases in the past half-century.”

“Diet has long been postulated as a potential environmental risk factor for this increasing incidence of autoimmune diseases in developed countries over recent decades. One such dietary factor, which rapidly changed along with the Western diet and increased consumption of processed foods or ‘fast foods’, is salt (NaCl).”

“The salt content in processed foods can be more than 100 times higher in comparison to similar home-made meals.”

“Increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic TH17 cells.”

These authors describe how increased NaCl concentrations specifically promote the generation of a highly pathogenic TH17 cell type. Even modest increases in NaCl concentration stimulate an almost logarithmic in vitro induction of Th17. Salt restriction protocol should be used in all cases of multiple sclerosis. Excess salt in the diet is a potential risk factor for all autoimmune diseases.

Logistically, high dietary salt levels are very problematic. Salt (NaCl) is added to nearly all processed, fast, convenience, and tasty foods because it adds to their addiction factor. This is very well documented in the books The End of Overeating by former FDA Commissioner David Kessler, MD (14), and Salt, Sugar, Fat by Pulitizer Prize winner Michael Moss (15). In population based studies, 7% of salt consumption is naturally found in food, 10% of salt consumption is from the salt shaker; and about 83% of consumed salt is pre-added to processed foods by the food packaging manufacturer.

We put all of our autoimmune patients, including those with multiple sclerosis, on very low sodium diets. This necessitates strict avoidance of pre-packaged/processed foods. I remind the reader to view the Terry Wahls, MD YOU TUBE (Paleo Diet).

••••

An Interesting Chiropractic Connection

Adding recently to the biological plausability of physical trauma contributing to the development/exacerbation of multiple sclerosis is the primary research of Raymond V. Damadian and David Chu. Their article was published in the journal Physiological Chemistry and Physics and Medical NMR in September of 2011, and is titled (16):

The Possible Role of Cranio-Cervical Trauma and Abnormal CSF Hydrodynamics in the Genesis of Multiple Sclerosis

In their study, 8 multiple sclerosis patients and 7 normal volunteers were MRI scanned to visualize cerebral spinal fluid (CSF) flow patterns within the cranial vault and spinal canal. Seven of 8 MS patients in this study had a history of serious prior cervical trauma which resulted in significant cervical pathology. The MRI revealed “significant obstructions to CSF flow were present in all MS patients. The obstructions are believed to be responsible for ‘leakages’ of CSF from the ventricles into the surrounding brain parenchyma. These ‘leakages’ can be the source of the MS lesions in the brain that give rise to MS symptomatology.” All MS patients exhibited CSF flow interruptions or obstructions somewhere in the cervical spinal canal, corresponding to the location and extent of their cervical spine pathology. Normal examinees did not display these flow obstructions.

These authors suggest that trauma induced blockages to CSF flow increases CSF pressure, driving out protiens that becomed antigenic, initiating the multiple sclerosis autoimmune response. They state:

“All seven patients had distinct cervical anatomic pathology on their current MR images that corresponded with their trauma histories, thereby establishing that the historical trauma events contributed directly to their permanent pathologies of the cervical spine and that their cervical trauma histories were not inmaterial.”

“The abnormal CSF flow dynamics found in the MS patients of this study corresponded to the MR cervical pathology that was visualized.”

“The findings raise the possibility that interventions might be considered to restore normal intracranial CSF flow dynamics and intracranial pressure.”

“Victims of Motor Vehicle Whiplash injuries with persisting symptoms, e.g., headache, neck pain, should be scanned by MRI to assure that their CSF hydrodynamics and cervical anatomy (C1-C7) are normal. Should their CSF hydrodynamics prove abnormal, they should be monitored by UPRIGHT(R) MRI to assure they are restoring to normal over time, or ultimately decompressed by expansion stenting or cervical realignment if they are not.”

“In conclusion, the results of our investigation suggest that Multiple Sclerosis may be biomechanical in origin wherein traumatic injuries to the cervical spine result in cervical pathologies that impede the normal circulation of CSF to and from the brain.” “The obstruction to CSF outflow would result in an increase in ventricular CSF pressure (ICP) which in turn could result in ‘leakage’ of cerebrospinal fluid and its content antigenic proteins (e.g., tau proteins) into surrounding brain parenchyma. The attachment of antigenic proteins to surrounding brain nerve fibers would stimulate the antigen-antibody reactions that produce the axon demyelinations characteristic of multiple sclerosis.”

This is an important article for chiropractors. These authors suggest that cervical spine trauma and malalignment obstructs the flow of cerebral spinal fluid. This obstruction of CSF flow increases intracranial pressure, causing cerebral spinal fluid to leak out, along with antigenic proteins. The immune system’s response to these antigenic proteins cause the demyelination of multiple sclerosis.

These authors suggest that the improvement of spinal malalignment could improve cerebral spinal fluid flow, stopping the aforementioned cascade to MS. In fact, in one of the MS patients, the MRI found a malalignment of the atlas. This malalignment “was successfully treated” by a chiropractor using a specific upper cervical technique. “The patient’s symptoms, severe vertigo accompanied by vomiting when recumbent and stumbling from unequal leg length, ceased upon treatment.” Objective improvements in obstructed CSF fluid was also noted immediately following the chiropractic upper cervical adjustment.

••••

All chiropractors have patients with multiple sclerosis. We usually treat these patients for musculoskeletal symptoms, primarily pain and stiffness. The adjuncts mentioned in this review have the potential to further enhance the clinical improvements of signs and symptons. Especially intriguing is the pathophysiology related to trauma, especially upper cervical spine trauma, and the response these patients have to specific upper cervical chiropractic approaches to realingment.

REFERENCES

• Warren SA, Olivo SA; Contreras JF, Turpin KV, Carroll LJ, Warren KG; Traumatic injury and multiple sclerosis: a systematic review and meta-analysis; Canadian Journal of Neruological Science; March 2013; Vol. 40; No. 2; pp. 168-76.
• Poser CM; The role of trauma in the pathogenesis of multiple sclerosis: a review; Clinical Neurology and Neurosurgery; May 1994; Vol. 96; No. 2; pp. 103-110.
• Christie B; Multiple sclerosis linked with trauma in court case; British Medical Journal, Vol. 313, November 16, 1996.
• Poser CM; Trauma to the Central Nervous System May Result in Formation or Enlargement of Multiple Sclerosis Plaques; Controversies in Neurology; Archives of Neurology; July 2000; Vol. 57; No. 7; pp. 1074-77.
• Chaudhuri A, Behan PO; Acute cervical hyperextension-hyperflexion injury may precipitate and/or exacerbate symptomatic multiple sclerosis; European Journal of Neurology; November 2001; Vol. 8; No. 6; pp. 59-64.
• Kang JH, Lin HC; Increased risk of multiple sclerosis after traumatic brain injury: a nationwide population-based study; Journal of Neurotrauma; January 1, 2012; Vol. 29; No. 1; pp. 90-95.
• Minding Your Mitochondria: Dr. Terry Wahls at TEDxIowaCity – YouTube
• Pizzorno J; What We Have Learned About Vitamin D Dosing?; Integrative Medicine; 9, No. 1, Feb/Mar 2010.
• Roberts L, Bailes J, Dedhia H, et al.; Surviving a mine explosion; J Am Coll Surg, 207 (2) (2008), pp. 276–283
• Simopoulos AP; Evolutionary Aspects of Diet: The Omega-6/Omega-3 Ratio and the Brain; Molecular Neurobiology; October 2011; Vol. 44; No. 2; pp. 203-15.
• Petro TM; Regulatory role of resveratrol on Th17 in autoimmune disease; Int Immunopharmacol; March 2011;Vol. 11; No. 3; pp. 310-18.
• Xie L, Li XK, Takahara S; Curcumin has bright prospects for the treatment of multiple sclerosis; Int Immunopharmacol; March 2011; Vol. 11; No. 3); pp. 323-330.
• Kleinewietfeldt M, Manzel A, Titze J, Kvakan H, Yosef N, Linker R, Muller D, Hafler D; Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells; Nature —International Weekly Journal of Science; April 25, 2013; 496; No. 7446; pp. 518-522.
• Kessler D; The End of Overeating, Taking Control of the Insatiable American Appetite, 2009.
• Moss M; Salt, Sugar, Fat: How the Food Giants Hooked Us, Random House, 2013.
• Damadian RV, Chu D; The Possible Role of Cranio-Cervical Trauma and Abnormal CSF Hydrodynamics in the Genesis of Multiple Sclerosis; Physiological Chemistry and Physics and Medical NMR; September 20, 2011; 41: 1–17.

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