What Doctors Don't Tell YouMultiple sclerosis (MS) often follows a highly individual and unpredictable course, sometimes leading to chronic and occasionally devastating disability. MS is one of the most common diseases of the central nervous system and it can affect any part o
MS occurs because of damage to the myelin sheath the thin protective layer of fatty membrane that surrounds the nerve tracts in the brain and, more importantly, the spinal cord.
Myelin sheath acts like the insulation around electrical wires, allowing the current or in the case of the human body, the electrical signals to travel through without loss of power or strength. Any damage to this protective layer can cause the electrical signals to “leak” and so lose power and become distorted.
Development and maintenance of a healthy myelin sheath depends on several things, including the presence of dietary essential fatty acids (Neuroepi demiology, 1992; 11: 214-25; Nature, 1967; 215: 821-3). This may be one reason why babies who are breastfed are less likely to develop MS in later life (BMJ, 1994; 308: 1411-2) breastmilk is a rich source of EFAs.
In MS this damage is caused by inflammation, which makes the sheath lose some of its covering a process known as demyelination. Hard scar tissue then forms over these damaged patches or lesions and MS (literally “many scars”) is the result.
These patches of demyelination (known as plaques) can occur anywhere. Scarring means that wrong signals go to the muscles via the brain, and so the muscles don’t work properly or at all. It can affect any part of the body, but the most usual areas are the eyes, brain, brain stem and spinal cord.
The most commonly reported symptoms of MS are double or blurred vision in one or both eyes, pins and needles in the extremities, slurred speech, difficulty in walking, dragging either foot, loss of coordination and balance, and loss of sensation anywhere in the body.
Thanks to magnetic resonance imaging (MRI) scanning, doctors can now confirm a diagnosis of MS with 95-99 per cent certainty (Radiology, 1991; 178: 447-51). But this doesn’t take into account a patient’s reactions to MRI, which involves putting the patient into a small enclosed cylindrical magnet and subjecting him or her to a magnetic field 50,000 times stronger than that of the earth. Reactions can range from mild stress to acute claustrophobia, panic attacks, memory loss and nausea (JAMA, Aug 1, 1993; Lancet, Sept 21, 1991). There is also concern about the possible cancer causing effect of MRI (People’s Doctor, 1984; 10: 11) and the potential dangers of the magnetically active contrast agents injected into the patient to enhance the picture on the scanner.
In addition, while MRI is used to visualize the progress of the disease, assessing the progress of the disease can be fraught with uncertainties. For instance, there is often no correlation between the extent of the damage seen through MRI and the extent of the disability in MS patients (Ann Neurol, 1989; 25: 43-9; BMJ, 1990; 301: 44). MRI can tell a person how many lesions they have, but not the extent to which this may or may not affect their prognosis, supporting the view that good clinical judgement is the best way to diagnose MS.
Many theories lifestyle, dietary, physical trauma particularly to the head, viral, bacterial, geographical origins and genetic predisposition have been put forward as possible causes of MS. It is widely accepted now that multiple sclerosis has something to do with a response by the immune system (Clin Microb Rev, 1993; 6: 382-427). Because of this, much of medicine’s time and energy has been spent looking for a “bug” which causes it. But while it’s true that viruses such as shingles and herpes are often present in certain types of MS sufferers (Ann Int Med, 1984; 101: 514-26), it could be that they are fulfilling the role of opportunists in a weakened immune system.
One of the most compelling theories about MS is that of a kind of slow poisoning. The human body contains a sophisticated filtering system within the walls of blood vessels called the endothelium which keeps away separate harmful substances that can damage nerves. In the brain this filtering system is known as the blood brain barrier. In persons suffering from MS something happens to allow harmful neurotoxins to penetrate the blood brain barrier. Penetration of the blood brain barrier is often the earliest detectable abnormality in MS.
A number of things can cause the barrier to be breached, including stress, fever, emotional upset, heat, injury and eating too much fat. These things allow poisonous chemicals in the blood to leak into the blood stream where they can cause severe damage.
MS sufferers may be victims of a kind of toxic overload from man made poisons. A convincing example of this would be the “outbreak” of MS in Key West, Florida between 1983-85. During that time 30 to 40 people developed MS. This was eventually traced to the dumping of toxic debris containing high levels of mercury and lead nearby (Am J Forensic Med & Pathology, 1986; 7(1): 3-8).
Mercury is one of the most potent neurotoxins known to man. Over the years there have been other convincing pieces of research into the mercury MS connection (Br Dental J, 1993; 175(10): 355-62). Most recently, a Swedish study showed that the normal mercury level in the spinal fluid contained 0.4 micrograms per litre; in MS victims studies that level rose to an average of 3.0 micrograms per litre more than seven times the normal level.
It concluded that dental fillings were the most likely source of this form of poisoning and confirmed that sufferers often responded well when amalgam fillings were replaced (Swed J Biol Med, January 1989). This has been reflected in other journals as well (Psych Reports, 1992; 70(3, pt 2): 1139-51).
Mercury from the dental amalgams in our mouths is one of the most common sources of direct poisoning. In his book, Dr Hal Huggins, a dentist and vociferous critic of mercury fillings (Avery, 1993) quotes a summary by Douglas Swartzendruber, PhD, of all the scientific literature relating MS not only to mercury in general, but specifically from dental fillings.
Dr Patrick Kingsley, the UK’s leading expert on MS, said that of his nearly 4,000 patients seen with the problem, only five didn’t suffer from mercury poison.
The second most common problem, is Dr Kingsley’s view, is food intolerance. Although gluten is most often implicated, he finds that allergies are individual and there is rarely a single culprit that he can point to. A systemic candida infection also is often behind MS.
Next down the line of causes, he finds, are nutritional deficiencies, chiefly B12 and magnesium, but also B6, folic acid amd zinc. Pesticides, moulds and many other environmental toxins play their part.
Kingsley sums the problem up this way. “Multiple sclerosis is a name we’ve given to a collection of symptoms symptoms which could be caused by anything. The problem is that medicine likes to assume that everybody with the same symptoms is suffering from the same disease, which is caused by the same cause and therefore will respond to the same treatment. So for instance, if something like MS responds well to diet, medicine will immediately assume that there is one diet which will cure all.”
According to Dr Kingsley, lack of good clinical skills is at the heart of the impatience of many practitioners with MS sufferers: “Sometimes with MS patients you just have to patiently keep on trying different methods. Through careful observation Kingsley has found that simply changing a patient’s diet can make him or her symptom free in 30-40 per cent of cases, and that B12 deficiency is at the root of many of the cases he sees (see box page 3).
“In my practice I tend to divide my patients loosely into two distinct groups: those which are experiencing motor function loss and those with sensory loss. Those with motor function loss are closely aligned to parkinsonian types and will respond well to diet and supplements of magnesium. Those with sensory disturbance often have had shingles, herpes or chickenpox virus and can be helped greatly by large intravenous doses of B12 sometimes as high as 15,000 mcg weekly.”
MS is currently treated with a wide range of drugs including anti inflammatory, immunosuppressants, immunomodulators, anti spastic and anti infective drugs. While some may help the management of patients with acute symptoms, none has proven to be of any benefit in the long term (BMJ, 1992; 304: 1260-1).
In fact, many cause debilitating side effects which do nothing to help an MS sufferer’s life. For instance anti spastic drugs such as Lioresal (baclofen) can lead to drowsiness, muscular weakness and dry mouth, lowered blood pressure, confusion, insomnia, tremors, slurred speech (ironically many of the symptoms MS sufferers are trying to alleviate) and physical and psychological dependence (Acta Neurol Scand, 1987; 73(3):190-4).
Steroids may curb excessive autoimmune activity, but in the long run will render patients susceptible to viruses which can severely aggravate existing symptoms (Townsend Letter For Doctors & Patients, Feb/Mar, 1996, 32-3; see also WDDTY, 1996, 7(2): 1-3, 11-12).
MS can also be caused by medicines used to treat other conditions, most notably human insulin. Since it was introduced 10 years ago, human insulin has become associated with a catalogue of side effects, most commonly the loss of warning signs of an impending hypo and increased severity of attacks, but also MS like problems including memory loss, pain in the limbs, loss of motor function and epileptic like fits.
Human insulin is not “human” at all but genetically engineered to resemble true human insulin. In the BMJ (August 8, 1992) doctors Gareth Williams and Alan Parker endeavoured to explain why it is associated with neurological complications. “Human and porcine insulins differ in only one out of 51 amino acid residues; although apparently trivial, this change evidently affects the physiochemical and pharmokinetic properties of the molecule, as porcine insulin is more lipophilic than human insulin.” The more lipophilic fat soluble porcine insulin is more easily utilized by the brain and thus able to modulate the effects of low glucose concentrations on hypothalmic or other neurones.
Other drugs might also play a part in bringing on MS. There has been a report of a patient with experimental allergic encephal omyelitis being treated with sulfasalazine and developing multiple sclerosis (Lancet, 1990; 335: 409-10). Finally, while there is a growing body of opinion that childhood vaccinations may cause damage to the myelin sheath and thus precipitate the development of MS later in life little if any research has been done on the subject.
There is, as yet, no research to back up Dr. Kingsley’s findings, and yet his clinical experience may well provide the most hopeful pathway for MS sufferers. As many as 60 per cent of his patients have recovered a remarkable rate when compared to conventional treatments and eventually somebody is going to have to ask why.
Daniel Redwood DC
Tom Ferguson MD
