
The
Multiple Sclerosis and Diet Saga
The End
and a New Beginning
People
often ask me: Why are you spending $750,000 from the
McDougall Research and Education Foundation to study the
treatment of multiple sclerosis (MS) with your diet? Why not
carry out research on a more common problem, like obesity,
heart disease, or diabetes?
Most
people can’t even pronounce “multiple sclerosis”—so they
just call it MS. It is likely you don’t personally know
anyone with this disease; after all, only 350,000 people in
the United States and one million worldwide have it. You may
have heard of it because a few famous people have made their
disease
public, like: lead anchor on Fox News Channel Neil
Cavuto, former Mouseketeer Annette Funicello, singer Lena
Horne, comedian Richard Pryor, and talk show host Montel
Williams. Only 10,000 new cases are diagnosed in the
United States annually, compared to half a million new major
cancers and 1.25 million fresh heart attacks. So why pick
MS?
For me,
stopping multiple sclerosis with the cost-free,
side-effect-free McDougall Diet is equivalent to throwing
the biggest rock I can find at the biggest picture window in
town. The shatter will be heard around the world. If
diet can effectively treat a disease as mysterious and
deadly as MS, then diet has to be a medical miracle—and
could easily be capable of bringing to an end diseases long
accepted as due to diet, like type-2 diabetes, heart
disease, and common cancers. A simple cure for MS would
startle even the most unconscious medical doctors into
awakening. Plus, I owe this study, and much more, to my
mentor Roy Swank, MD for his friendship, guidance, and
pioneering work.

The first
part of the saga of the treatment of MS with a low-fat diet
ended less than 2 months ago on November 16, 2008 with the
death of Dr. Swank at age 99. The saga begins anew
with the approval of “A
randomized, controlled study of diet and multiple sclerosis”
by the
Oregon
Health & Science University Research Integrity Office on
January 15, 2009. This landmark approval only happened
after years of hard work by many of us. You have made
important financial contributions to the McDougall Research
and Education Foundation (a nonprofit, 501(c) (3)
corporation) over the past 5½ years. Raising sufficient
funds allowed me to make my first contact with the Neurology
Department of the medical school at the University of Oregon
on September 15, 2007. After nearly a year and a half of
working with a few of the top people at the medical school,
especially Vijayshree Yadav, MD, we are ready to begin.
The
Disease
MS is an
autoimmune disease—one in which the body attacks
itself—in this case the immune system attacks the tissues of
the brain and spinal cord (more specifically, the myelin
sheaths surrounding the nerve fibers). Isolated areas become
intensely inflamed with sores. In time, the damaged tissues
heal, but often leave thickened, fibrous scars (scleroses),
which doctors commonly call “plaques.”
The
diagnosis is most often made between the ages of 15 and 50,
with women three times more likely than men to develop MS.
The initial and subsequent attacks can last one to three
months. During an attack the patient experiences visual
disturbances, weakness, clumsiness, spasticity, fatigue,
numbness, tingling, problems with thinking, slurred speech,
pain, depression, difficulty swallowing, bladder and bowel
incontinence, and/or sexual difficulties. Rather than on
any fancy tests, the diagnosis is based upon a patient's
history and the physician’s examination. Apparently random
damage to the nervous system—as if an inexpert marksman shot
bullets at the brain and spine—is the hallmark of MS.
Sophisticated technologies, like magnetic resonance imaging
(MRI) of the brain and associated areas, can help with the
diagnosis and show the size and location of active lesions
and plaques.
Patients are most often
classified as having one of two forms of MS: “relapsing-remitting” characterized by intermittent
attacks; and “primary-progressive” with a steady, but
usually slow, decline. Actually these “doctor-invented”
subtypes are just different stages of the same disease.
Usually (80% of the time) at the beginning of the disease
the attacks seem to come and go, but in time most cases
become progressive. Those patients who appear to start with
a progressive decline (20%) have simply skipped the more
common initial appearance of relapse and remittance.1
These artificial categories can be counterproductive,
leading to false reassurance and unwarranted despair, and do
not predict the prognosis or improve the chances of an
effective treatment for the patient.1,2 Even with
the use of the most modern medications, costing $20,000 a
year, the future prospect is dismal with half of those
people afflicted with MS unable to walk unassisted,
bedridden, wheelchair bound, or dead within 10 years of
diagnosis.2-6 The absolute advantage for slowing
disability with the use of the most popular medications
(interferon beta) is clinically small (8%), and the costs
and side effects are huge.7,8 The lack of
substantial benefits from current drug therapies is one more
important reason I picked MS to study.
The
Cause
Worldwide,
multiple sclerosis is common in Canada, the United States
and northern Europe; and rare in Africa, Japan, and other
Asian countries. This difference most likely reflects the
populations’ different diets (animal- vs. starch-based).
Scientists have found a very strong positive correlation
when consumption of cow's milk is compared with the
incidence of MS worldwide.9,10 One theory
proposes that cow’s milk consumed in infancy lays the
foundation for injuries to the nervous system that appear
later in life.11 Cow’s milk contains one fifth as
much of an essential fat, called linoleic acid, as does
human mother's milk. Children raised on a linoleic
acid-deficient, high-animal fat diet—as are most kids in our
modern affluent society—are quite possibly starting life out
with a damaged nervous system, susceptible to insults and
injuries in later life. The possible sources of injury that
can precipitate the attacks of multiple sclerosis in
mid-life are suspected to be viruses, allergic reactions,
and/or disturbances of the flow of blood to the brain caused
by a high-fat diet.
The most
commonly held theory these days proposes an autoimmune basis
for this disease. MS has much in common with autoimmune
type-1 diabetes mellitus, including nearly-identical ethnic
and geographic distribution, and genetic factors.12,13
The damage to the nervous system may occur through a process
known as molecular mimicry. In susceptible people,
cow’s milk protein may enter the bloodstream from the
intestine. The body recognizes this as a foreign protein,
like a virus or bacteria, and makes antibodies against it.
Unfortunately, these antibodies are not specific only to the
cow’s milk protein; they find similar proteins in the
nervous system (the myelin). The antibodies attach to these
nerve tissues and destroy them. In the case of diabetes, the
antibodies looking for cow's milk protein attack the
insulin-producing cells of the pancreas.
Roy
Swank, MD—My Mentor

There are
many people whose shoulders I stand on and the founder of
the Swank Diet for MS was one of my most important
teachers. In 1977, I was on my neurology rotation for my
Internal Medicine Residency at the University of Hawaii. I
was given an assignment to present a conference to fellow
doctors on any subject of my choosing. My trip to the
library that afternoon led me to the discovery of Dr.
Swank’s work.
Swank
devised his low-fat diet and began treating MS patients at
Montreal Neurological Institute in 1948. He recommended not
more than 40 to 50 grams of total fat (compared to 150 to
175 grams in the American/Canadian diet) and 0 to 15 grams
of saturated fat (compared to 140 to 165 grams). There was
no limit on the amount of carbohydrate from starches,
vegetables, and fruits. Polyunsaturated fats were increased
a little (from 15 to 25 to 20 to 35 grams). Dr. Swank
believed MS patients were unique in that they had a
heightened sensitivity to saturated fats.
His
research soon showed that with adherence to the diet
relapses decreased by about 70 percent in the first year of
treatment (from 1 relapse per year to 0.2 per year). Then
after the first year there were continued improvements
(about 5% fewer relapses per year for the next 2 years).
For the first 16 years of treatment with a low-fat diet the
rate of exacerbation (new attacks and/or decline) was
decreased by 95%. (Compare this to the dismal results of
drug therapy, mentioned above, where half of patients are in
serious trouble within 10 years.)
For
outstanding results, patients have to follow the Swank Diet
strictly because even small amounts of fat make a huge
difference. In the study he published in the medical
journal, the Lancet, in 1990, Dr. Swank found that a
difference of eight grams of saturated fat intake daily
resulted in a threefold increased chance of dying from
multiple sclerosis.14 (That means daily
consumption of as little as one ounce of pork sausage at 10
grams, one medium cooked hamburger at 14 grams, an
additional three ounces of porterhouse steak, or two ounces
of cheddar cheese at 12 grams, significantly increases the
risk of dying.)
Early
cases are expected to do especially well on the diet.14-17
As the years with the disease accumulate then the response
to diet is expected to be less dramatic, but there are
exceptions with some advanced cases responding very well.
If a person begins the program with limited disability and
follows the Swank Diet carefully he or she has less than a
5% chance of dying from MS over the next 34 years—those who
do not follow the diet have an 80% chance of dying.14
If patients go off of the diet for a month or so they will
get into trouble. Dr. Swank states, “Our figures show that
at least 95% of people with MS that follow a low-fat diet
show no progression of disease.” However, with normal aging
there is deterioration of the nervous system even when the
MS disease is not active.
According
to Dr. Swank, about one in 500 people will have a downhill
course even when they follow the diet strictly. About 50%
of his patients followed the Swank Diet really well, whereas
25% were a little over on fat intake and another 25% were a
lot over. Dr. Swank said to me, “I tell people that they
have to have persistence and a real desire to get well or be
well or there is no point on going on this (the diet). If
they are not devoted to taking care of their health then
they are going to have trouble; and finally, I tell them to
be optimistic, it’s very helpful.”
You can
listen to a free
podcast of a radio interview I did with Roy Swank in
1995.
The
Swank vs. The McDougall Diet
The Swank
Diet focuses on drastically reducing saturated fats, which
are abundant in red meats and high-fat dairy products.
Included in his diet are low-fat dairy foods (skim milk,
fat-free cheese, fat-free ice cream, etc.), egg whites,
skinned white-meat chicken, white fish and shellfish. Meats
with significant amounts of saturated fats are allowed only
in very small amounts.
Dr. Swank
also included additional vegetable and fish oils in his
diet. He explained to me that he did this mostly because he
believed that this addition would make the diet easier to
follow. He found that when people ate more polyunsaturated
oil they then ate less saturated fat. He also felt the
patients’ skin was better with a little oil added, and that
they felt more energetic. As far as the fundamental course
of the disease was concerned, he did not believe adding the
vegetable or fish oil made any real difference—as he
explains, “It just makes it easier to follow the diet.”
Dr. Swank
approved of The McDougall Diet for the treatment of MS, and
said so many times. The McDougall diet is very low in
saturated fats. As an internist concerned about all aspects
of a patient’s health I prescribe a stricter and, I believe,
a much more effective (and tastier) diet. Even low-fat dairy
and meat products are a health hazard causing infectious
diseases, allergic reactions, as well as delivering high
loads of animal protein (causing osteoporosis, kidney
stones, liver, and kidney damage) and environmental
chemicals. These animal foods are completely deficient in
dietary fiber and low in carbohydrate. Although lower in fat
and cholesterol, low-fat meats and dairy products can still
contain substantial amounts of both harmful ingredients.
The dairy
proteins are of particular concern to me because they are
the leading cause of autoimmune diseases. As I mentioned
above, MS is an autoimmune disease and has substantial
similarities to another autoimmune disease, type-1 diabetes,
which an abundance of scientific research says is caused by
dairy protein.18
I do not
add “free” vegetable or fish oils because they are, at best,
medicines, and at worst, toxins. At the very least they can
produce weight gain—“the fat you eat is the fat you wear.”
These polyunsaturated oils “thin the blood,” contributing to
the risk of bleeding, say, following an auto accident.
These fats also suppress our immune system— we need our
immune system functioning at full capacity to fight off
infections and cancer.19
Why Is
Diet-therapy for MS Virtually Unknown?
Dr. Swank
told me, “One problem is culture: we are a meat and potatoes
society. Most importantly there is an economic problem,
there is really not much money in a diet. Nutrition has not
been taught in medical school for many years now.”
More than
20 years ago, during one of my many visits with Dr. Swank at
his Oregon medical school office, I asked him, “Why is it
that when MS patients ask their doctors about changing their
diet, they are told this is quackery? And why does the MS
Society offer a similar message? You have published in the
world’s most respected scientific journals that a simple,
cost-free diet can stop this disease. Yet, they summarily
dismiss you and your work.”
He leaned
back in his chair, took a moment for thought, and then
explained, “You know, most people in this country expect to
be cured by a pill, and to have a cure that is almost
instantaneous. With the low-fat diet, the people actually
have to work to get better, and have to cure themselves. And
as far as the MS Society is concerned, John, they don't
mention it because they didn't discover it. It wasn't their
research dollars that found this treatment. So they're not
going to tell anybody. I discovered it in my small office
here, in the basement of the University of Oregon Medical
School.”
So it is
not just money that keeps people from highly effective
dietary cures; egos are also involved—the well-known
business doctrine, "Not Invented Here,” is working to keep
you and your family sick. Self-centered people think, “If I
didn’t invent it then there is no real reason for me to
promote it, especially when there is no fame or fortune in
it for me.”
Learn more
by reading
articles and
Star
McDougallers found on my web site.
Would
you like to help MS patients?
We can
change medical practice. Donations are almost painless when
made by PayPal to The
McDougall
Research & Education Foundation A Tax Deductible
Corporation
References:
1)
Confavreux C, Vukusic S. Natural history of multiple
sclerosis: a unifying concept. Brain. 2006 Mar;129(Pt
3):606-16.
2)
Andersson PB, Waubant E, Gee L, Goodkin DE. Multiple
sclerosis that is progressive from the time of onset:
clinical characteristics and progression of disability.
Arch Neurol. 1999 Sep;56(9):1138-42.
3) Myhr
KM, Riise T, Vedeler C, Nortvedt MW, Grønning R, Midgard R,
Nyland HI. Disability and prognosis in multiple sclerosis:
demographic and clinical variables important for the ability
to walk and awarding of disability pension. Mult Scler.
2001 Feb;7(1):59-65.
4)
Kremenchutzky M, Cottrell D, Rice G, Hader W, Baskerville J,
Koopman W, Ebers GC. The natural history of multiple
sclerosis: a geographically based study. 7.
Progressive-relapsing and relapsing-progressive multiple
sclerosis: a re-evaluation. Brain. 1999 Oct;122 ( Pt
10):1941-50.
5)
Bergamaschi R, Montomoli C, Candeloro E, Fratti C, Citterio
A, Cosi V. Disability and mortality in a cohort of multiple
sclerosis patients: a reappraisal. Neuroepidemiology.
2005;25(1):15-8.
6)
Cottrell DA, Kremenchutzky M, Rice GP, Koopman WJ, Hader W,
Baskerville J, Ebers GC. The natural history of multiple
sclerosis: a geographically based study. 5. The clinical
features and natural history of primary progressive multiple
sclerosis. Brain. 1999 Apr;122 ( Pt 4):625-39.
7) Pittock
SJ. Interferon beta in multiple sclerosis: how much BENEFIT?
Lancet. 2007 Aug 4;370(9585):363-4.
8) Kappos
L, Freedman MS, Polman CH, Edan G, Hartung HP, Miller DH,
Montalbán X, Barkhof F, Radü EW, Bauer L, Dahms S, Lanius V,
Pohl C, Sandbrink R; BENEFIT Study Group.Effect of early
versus delayed interferon beta-1b treatment on disability
after a first clinical event suggestive of multiple
sclerosis: a 3-year follow-up analysis of the BENEFIT study.
Lancet. 2007 Aug 4;370(9585):389-97.
9) Butcher
J. The distribution of multiple sclerosis in relation to the
dairy industry and milk consumption. N Z Med J. 1976
Jun 23;83(566):427-30.
10)
Malosse D. Correlation between milk and dairy product
consumption and multiple sclerosis prevalence: a worldwide
study. Neuroepidemiology. 1992;11(4-6):304-12.
11)
Agranoff BW. Diet and the geographical distribution of
multiple sclerosis. Lancet. 1974 Nov
2;2(7888):1061-6.
12) Winer
S. T cells of multiple sclerosis patients target a common
environmental peptide that causes encephalitis in mice. J
Immunol. 2001 Apr 1;166(7):4751-6.
13) Lauer
K. Diet and multiple sclerosis. Neurology. 1997
Aug;49(2 Suppl 2):S55-61.
14) Swank
R. Effect of low saturated fat diet in early and late cases
of multiple sclerosis. Lancet. 1990 Jul
7;336(8706):37-9.
15) Swank
R. Multiple sclerosis: fat-oil relationship. Nutrition.
1991 Sep-Oct;7(5):368-76.
16) Swank
R. Multiple sclerosis: the lipid relationship. Am J Clin
Nutr. 1988 Dec;48(6):1387-93.
17) Swank
R. Multiple sclerosis: twenty years on low fat diet. Arch
Neurol. 1970, Nov;23(5):460-74.
18)
Guggenmos J, Schubart AS, Ogg S, Andersson M, Olsson T,
Mather IH, Linington C. Antibody cross-reactivity between
myelin oligodendrocyte glycoprotein and the milk protein
butyrophilin in multiple sclerosis. J Immunol. 2004
Jan 1; 172(1): 661-8.
19) The
August 2007 McDougall Newsletter article:
When Friends Ask: Why Do You Avoid Adding Vegetable Oils?
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