Welcome! This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of CCSVI and cerebral hypoperfusion. This blog is informative only--all medical decisions should be discussed with your own physicians.

The posts are searchable---simply type in your topic of interest in the search box at the top left.

Almost all of MS research is initiated and funded by pharmaceutical companies. This maintains the EAE mouse model and the immune paradigm of MS, and continues the 20 billion dollar a year MS treatment industry. But as we learn more about slowed blood flow, gray matter atrophy, and environmental links to MS progression and disability--all things the current drugs do not address--we're discovering more about how to help those with MS.

To learn how this journey began, read my first post from August, 2009. Be well! Joan

Thursday, November 21, 2013

"Good" Cholesterol and the Brain

New research, presented at the annual meeting of the Society of Neuroscience, finds a link to the level of a cholesterol transport protein and MS disease severity.  This research provides us another link to blood and the cardiovascular system, which I'll get into at the end of this note. 

First, let's review the announcement.
http://www.medscape.com/viewarticle/814798

ApoA1 is the main structural protein found in HDL, or what we call "good" cholesterol, and it is found to be low in pwMS.
Blood levels of the reverse cholesterol transport protein apolipoprotein A1 (ApoA1) are low in patients with multiple sclerosis (MS) and correlate with disease severity, new research shows.
ApoA1 is the most abundant component of high-density lipoprotein cholesterol and is known to protect against inflammation.
Dr. Gardner and colleagues investigated ApoA1 levels in 53 patients with relapsing-remitting MS, 50 with secondary progressive MS, 53 with primary progressive MS, and 57 healthy controls. "Remarkably, all MS patients had less ApoA1 than controls," they report in a meeting abstract.
ApoA1 was reduced by approximately 25% in patients with relapsing-remitting MS, 50% in those with secondary progressive MS, and 75% in patients with primary progressive MS, the most severe form of the disease.
I'm always alarmed when neurologists claim a finding like this is "surprising"--especially since lower levels of ApoA1 have been found in other diseases of neurodegeneration.
In Alzheimer's, the connection of more severe AD with low levels of ApoA1 has been established.  Higher levels of ApoA1 are related to sharper mental abilities and memory. 
Low levels of ApoA1 are correlated with more severe Alzheimer's Disease, and high levels of ApoA1 with a lower risk of AD --see Merched et al., 2000Saczynski et al., 2007Bates et al., 2009 
Other studies have hinted at a cognitive effect. High HDL levels associate with sharper mental abilities in the elderly (see ARF related news story on Barzilai et al., 2006), while low HDL levels are a risk factor for memory decline in middle-aged adults (see Singh-Manoux et al., 2008). What might be behind these apparent benefits? ApoA1 is known to have anti-inflammatory effects, and indeed, in a mouse model of brain inflammation, an ApoA1 mimetic improved cognitive deficits (see Buga et al., 2006). http://www.alzforum.org/new/detail.asp?id=2574
In Parkinson's, the connection of ApoA1 as a biomarker for disease risk has been established.  Lower levels of ApoA1 correlated with earlier onset of Parkinson's Disease while higher levels of ApoA1 were shown to be protective.
One of the best candidate protein biomarkers to emerge from discovery screening was apolipoprotein A1 (ApoA1; p = 0.001). Low levels of ApoA1 correlated with earlier PD onset, with a 26% decrease in risk of developing PD associated with each tertile increase in ApoA1 (Cox proportional hazards, p < 0.001, hazard ratio = 0.742). The association between plasma ApoA1 levels and age at PD onset was replicated in an independent cohort of PD patients (p < 0.001). Finally, in the PARS cohort of high-risk, asymptomatic subjects, lower plasma levels of ApoA1 were associated with greater putaminal DAT deficit (p = 0.037).
Lower ApoA1 levels correlate with dopaminergic system vulnerability in symptomatic PD patients and in asymptomatic individuals with physiological reductions in dopamine transporter density consistent with prodromal PD. Plasma ApoA1 may be a new biomarker for PD risk.

What does this all mean?  
It means ApoA1 levels are not just important for pwMS, they are important to monitor in all neurodegenerative disease.  It means the heart and brain are connected by our blood flow.  It means you can protect your brain by raising your HDL numbers.
I believe it's important to look at all diseases of neurodegeneration and consider blood flow and serum markers.
This also means that we have to look at the connection between our lives, our hearts and our brain health.  How can we increase our HDL, or good cholesterol--and thereby protect our brains from inflammation and further damage?  While labs work on ways to make drugs to raise our good cholesterol, we can consider how to do this ourselves.

How to raise HDL--or good cholesterol and help your brain.
LIFESTYLE is the most important means to increase HDL.
1. Don't smoke.  Quitting smoking will increase good cholesterol by 10%
2. Lose weight.  Extra weight depletes HDL.
3. Exercise.  Within 2 months of regular exercise, you can increase your HDL by 5%
4. Choose healthier fats for your diet. Avoid transfats, choose omega 3s and monosaturated fats found in nuts, olive oil, and fish

5. Add fiber to your diet--lots of fresh fruits and vegetables, legumes and oats

6. Limit alcohol consumption.
http://www.mayoclinic.com/health/hdl-cholesterol/CL00030/NSECTIONGROUP=2

7. Check your vitamin D, magnesium, calcium and zinc levels--make sure they are in balance.
http://www.ncbi.nlm.nih.gov/pubmed/7608827

Hope this information helps your heart and helps your brain.
Because they are connected,
Joan


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