STUDY: Dietary interventions for multiple sclerosis

[ActiveMSers]

Dietary interventions for multiple sclerosis.
Farinotti M, Vacchi L, Simi S, Di Pietrantonj C, Brait L, Filippini G.

Neuroepidemiology Unit, Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta,
via Celoria 11, Milano, Italy, 20133.

BACKGROUND: Clinical and experimental data suggest that certain dietary regimens,
particularly those including polyunsaturated fatty acids (PUFAs) and vitamins,
might improve outcomes in people with multiple sclerosis (MS). Diets and dietary
supplements are much used by people with MS in the belief that they might improve
disease outcomes and overcome the effectiveness limits of conventional
treatments.This is an update of the Cochrane review "Dietary intervention for
multiple sclerosis" (first published on The Cochrane Library 2007, Issue 1).

OBJECTIVES: To answer MS patients' questions regarding the efficacy and safety of
dietary regimens for MS. Can changes in dietary habits be an effective
intervention for MS patients? Are the potential side effects of these
interventions known, and have they been measured? Are potential interactions
between dietary interventions and other curative or symptomatic treatments known
and have they been studied?

SEARCH METHODS: We searched the Cochrane Multiple Sclerosis and Rare Diseases of
the Central Nervous System Group Specialised Register (November 2011), CENTRAL
(The Cochrane Library 2011, Issue 4), MEDLINE (PubMed) (1966 to November 2011),
EMBASE (embase.com) (1974 to November 2011) and reference lists of papers found.

SELECTION CRITERIA: All controlled trials (randomised controlled trials (RCTs)
and controlled clinical trials (CCTs)) on a specific dietary intervention, diet
plan or dietary supplementation, except for vitamin D supplementation, compared
to no dietary modification or placebo were eligible.

DATA COLLECTION AND ANALYSIS: Two review authors independently selected articles,
assessed trial quality and extracted data. Data were entered and analysed in
RevMan.Dichotomous data were summarised as relative risks (RR) with 95%
confidence intervals (95% CI) using a random-effects model in the presence of
heterogeneity (I² > 60%). Continuous data were analysed using weighted mean
differences, determined by the difference between the pre- and post-intervention
changes in the treatment and control groups.

MAIN RESULTS: Six RCTs that investigated PUFAs emerged from the search strategy,
accounting for 794 randomised patients.PUFAs did not have a significant effect on
disease progression at 24 months. Omega-6 fatty acids (11 to 23 g/day linoleic
acid) didn't show any benefit in 144 MS patients (RR 1.04, 95% CI 0.66 to 1.63).
Linoleic acid (2.9 to 3.4 g/day) had no benefit in 65 chronic progressive MS
patients (RR 0.78, 95% CI 0.43 to 1.42). Omega-3 fatty acids had no benefit in
292 relapsing remitting MS patients (RR 0.82, 95% CI 0.65 to 1.03, P =
0.08).Slight potential benefits in relapse outcomes were associated with omega-6
fatty acids in some studies, however these findings were limited by the reduced
validity of the endpoints. No judgements about safety or patient-reported
outcomes were possible. In general, trial quality was poor. No studies on vitamin
supplementation and allergen-free diets were analysed as none met the eligibility
criteria, mainly due to lack of clinical outcomes.

AUTHORS' CONCLUSIONS: PUFAs seem to have no major effect on the main clinical
outcome in MS (disease progression), but they may tend to reduce the frequency of
relapses over two years. However, the data that are available are insufficient to
assess a real benefit or harm from PUFA supplementation because of their
uncertain quality. Evidence on the possible benefits and risks of vitamin
supplementation and antioxidant supplements in MS is lacking. More research is
required to assess the effectiveness of dietary interventions in MS.

PMID: 23235605 [PubMed - in process]

[Niko]

Not exactly a positive answer, but I'm glad that they acknowledged the poorness of the study and insufficiency of tests and trials.
More trials need to be done, and with better funding- not just from pharmaceutical companies and little university labs!

I still have hope

[LivWell]

Interesting. I would think any dietary changes that would help inhibit inflammation would produce some benefit. Granted, the disease will run its course, but I see no reason to help it along.

[teena marie]

There is some compelling evidence that low saturated fat inhibits inflammation. George Jelinek, a doctor with MS in australia has some excellent information in his book Overcoming Multiple Sclerosis as well as on the website of the same name. Dr Roy Swank also has some evidence from his study. This is one of the things, along with exercise, vitamin d and meditation, that has helped me.

Teena Marie

[Niko]

When I went to see a holistic nutritionist, whom others I know with MS have seen as well, she told me I was borderline diabetic. I've always eaten very very healthy, with lots fats, few processed foods, etc, but maybe too many sugars?
In any case, I've been doing research and there seems to be a very strong connection for those with MS to also have diabetes (though I don't know which came first).

I wonder why?

[Guitar_grrrl]

These are small studies. There is evidence PUFAs are more detrimental than helpful to anyone's health in general, especially when heated. Heating these oils cause increased oxydation, and who needs all that oxydative stress? Free radical free-for-all!

I went Paleo 1 1/2 years ago, and I haven't looked back. Yes, I still have MS, but I'm no longer carrying excess weight, my digestion has never been better, my IBS is gone, my blood sugar and total cholesterol have dropped (my HDL has risen ), and my energy has actually improved a little.

I would like to see more and larger studies on autoimmune processes with low carb, real food diets. No additives allowed! Real, grass-fed meats (they're higher in Omega-3 than grain fed meats), fresh fish, veggies, fruit, and nuts.

I maintain I'm healthier without all that weird stuff added into my foods.

[Niko]

Awesome, Guitargrrrl!! I'm really happy to hear that. I've heard similar positive reviews from other MSers who are following the Paleo diet (and Dr Terry Wahls).

I've also been making connections with CANDIDA and those with MS (as well as other illnesses). Strong connections are particularly demonstrated in Ayurvedic health and Chinese Medicine texts. Here's a text that I found really uplifting yesterday: http://www.wds-global.com/news/2009_09_Cornell_ME.aspx
(or type Susie Cornell Candida).

I too discovered that I had Candida and hypoglycemia (the two are often connected) and it was probably the one of the main reasons why I ended up with so many digestive problems (like IBS) and MS. This past winter, I stuck to a diet plan that was aimed at eliminating my candida overgrowth and then strengthening my digestive system. I swear, I had virtually NO symptoms for three months.... until exams rolled around and I started eating things I shouldn't have, combined with stress and overworking and little exercise. But even then my MS symptoms were not as bad as when I was initially diagnosed. Now I'm doing pretty well still, and will probably edge back to the same diet, now that I've gone through trial and errors.

Food for thought

[Cvfactor]

There is more and more evidence that the mitochondria are damaged in MS which leads to neurodegeneration. If these diets promote the health of mitochondria it may be of benefit:

http://www.ncbi.nlm.nih.gov/m/pubmed/19664372/

[ActiveMSers]

Thanks CV. Here's a link to all published papers/studies involving mitochondrial and MS. There are over 400 (not all apply, though). It will be interesting to see how the research will all shake out.

http://www.ncbi.nlm.nih.gov/m/pubmed...e+sclerosis%22

[ActiveMSers]

This study just published yesterday. Not exactly sure what it all means--it's darn technical. - Dave

No excess of mitochondrial DNA deletions within muscle in progressive multiple sclerosis
Graham R Campbell1
Amy K Reeve2
Iryna Ziabreva2
Richard Reynolds3
Doug M Turnbull2
Don J Mahad1

1Centre for Neuroregeneration, University of Edinburgh, Chancellor’s Building, UK

2Wellcome Trust Centre for Mitochondrial Research, Newcastle University, UK

3Wolfson Neuroscience Laboratories, Imperial College Faculty of Medicine, UK

Don Mahad, Centre for Neuroregeneration, University of Edinburgh, Chancellor’s Building, Edinburgh, EH16 4SB, UK.

Background: Mitochondrial dysfunction is an established feature of multiple sclerosis (MS). We recently described high levels of mitochondrial DNA (mtDNA) deletions within respiratory enzyme-deficient (lacking mitochondrial respiratory chain complex IV with intact complex II) neurons and choroid plexus epithelial cells in progressive MS.

Objectives: The objective of this paper is to determine whether respiratory enzyme deficiency and mtDNA deletions in MS were in excess of age-related changes within muscle, which, like neurons, are post-mitotic cells that frequently harbour mtDNA deletions with ageing and in disease.

Methods: In progressive MS cases (n=17), known to harbour an excess of mtDNA deletions in the central nervous system (CNS), and controls (n=15), we studied muscle (paraspinal) and explored mitochondria in single fibres. Histochemistry, immunohistochemistry, laser microdissection, real-time polymerase chain reaction (PCR), long-range PCR and sequencing were used to resolve the single muscle fibres.

Results: The percentage of respiratory enzyme-deficient muscle fibres, mtDNA deletion level and percentage of muscle fibres harbouring high levels of mtDNA deletions were not significantly different in MS compared with controls.

Conclusion: Our findings do not provide support to the existence of a diffuse mitochondrial abnormality involving multiple systems in MS. Understanding the cause(s) of the CNS mitochondrial dysfunction in progressive MS remains a research priority.

[Cvfactor]

From what I can gather, it looks like they were trying to see if there were changes in muscle mitochondria in MSers vs. healthy controls which there werent. I'm not sure what they were trying to prove here.

But it does look like there is a lot of research going on about mitocondira dysfunction in axons of MSers. The theory is that after demylination the axons consume more energy than normal peoples axons and they eventually start dying.

I just started reading about Dr. Terry Whals who had SPMS and changed her diet and now seems to be in remission. She wrote a book called "minding your midochondira". I've heard of her in the past but I just thought she was another person on the fringe but maybe she is on the right trail.