new e3/e4

Newcomer introductions, personal anecdotes, caregiver issues, lab results, and n=1 experimentation.
MAC
Senior Contributor
Senior Contributor
Posts: 329
Joined: Mon Aug 29, 2016 2:24 pm

new e3/e4

Postby MAC » Mon Aug 29, 2016 2:40 pm

Hello everyone.

Recently obtained 23andme results of e3/e4.

My mom has AD (1st symptoms I'd say around 70, she's now 75), and my dad has Parkinsons (Diagnosed also around 70, he's 76) and prostate cancer (diagnosed when about 65).

My aunt (father's side) passed with AD, regular LOAD.

My other aunts/uncles no AD that I can recall (5 in total), although one had a stroke (fathers side).

I think I have pretty good memory (relative to peer group), but do notice some long term memory more challenging than say 10-20 years ago.

I am 51, eat healthy, exercise moderately, otherwise normal health.

Just introducing myself, asking for general thoughts on approximate risk factor for AD given background?

User avatar
KatieS
Senior Contributor
Senior Contributor
Posts: 1217
Joined: Wed Mar 05, 2014 1:45 pm

Re: new e3/e4

Postby KatieS » Mon Aug 29, 2016 4:34 pm

Welcome MAC to our learning and support forum. Given your family history, you are likely to feel stressed. To gain a great overview on Apoe4 and to reinforce your good basic preventative strategies, please read thru Stavia's Intro section. For me, being able to act on some of these preventative strategies decreased the initial stress of carrying this "fragility" gene.

As a 3/4, your lifetime AD risks vary to low if you're a male (more likely to have cardiovascular disease first) up to ~30% as a female. At your age, hormones begin to lower, so it's ideal to have this knowledge so you can respond to these changes.

Generally, long-term memory is the last to be affected by AD. You might consider joining the free study at the Brain Registry as they send out memory tests every six months. Alternatively, you could pay for MemTrax or have formal testing done for reassurance.

MAC
Senior Contributor
Senior Contributor
Posts: 329
Joined: Mon Aug 29, 2016 2:24 pm

Re: new e3/e4

Postby MAC » Mon Aug 29, 2016 4:43 pm

Thank you KatieS.

I am male. The immediate (1st degree) family history does not convey an elevated risk factor, as I have read?

Is PD at all related to AD risk factors? I've read almost completely unrelated?

I have read Stavia's intro section and general epigenetic factors (environmental accounts for abut 30% risk, whereas genetics 70%, based on identical twin AD studies).

I am an engineer, work with numbers and data a lot, but trying to expand the brain stimulation opportunities...more social connections, etc.
MAC
E3/E4-55/MALE

Lucy5
Support Team
Support Team
Posts: 480
Joined: Sat Oct 03, 2015 10:52 am
Location: Colorado

Re: new e3/e4

Postby Lucy5 » Mon Aug 29, 2016 5:17 pm

Welcome Mac, so glad you found your way to our site! I'm so sorry to hear about your folks; dealing with both AD and Parkinson's is tough. My grandfather developed Parkinson's in his late 60's, and I know first hand some of the challenges it presents.

With regard to your question of risk of LOAD based on your background, I know many of us here have spent some time trying to tease out our own personal risk (I know I have!), and I believe I can tell you with confidence: it's complicated. We humans are just so complex with thousands of genes - a few of which are known/suspected to modify the affect of APOE-e4 in various ways, with the search for additional genetic influences continuing. You can certainly find studies online that will include estimated risk ranges for e4 carriers, but those ranges can't possibly factor in all the complexities of you as an individual.

As you browse through our forums, you'll find that many of us here (along with a growing number of researchers in the field) strongly believe that certain lifestyle strategies can positively impact our risk of developing this disease. If you haven't already, please browse through our Newcomers Forum Primer. It was written by our physician member, Stavia, and is an excellent, comprehensive source of information about this gene variant.

Also, please feel free to ask questions anytime. We welcome debate as we are all in this together!

Starfish77
Senior Contributor
Senior Contributor
Posts: 397
Joined: Mon Nov 25, 2013 4:36 pm
Location: San Francisco,CA

Re: new e3/e4

Postby Starfish77 » Mon Aug 29, 2016 8:37 pm

Welcome Mac, I'm glad you found us. We all are constantly learning from each other. I'm working hard to increase my green vegetables
and add olive oil. I'm trying to do 100 days without dairy to see if it makes a difference with my joints. Being in a group makes me more likely to stick to a program. You are wise to be adding more social connections because it is always included as a positive step for keeping
our brains active.
Starfish e4/e4 79

Nancy
Contributor
Contributor
Posts: 460
Joined: Wed Jun 08, 2016 1:30 pm

Re: new e3/e4

Postby Nancy » Mon Aug 29, 2016 10:08 pm

Yes, welcome! Your chances have just improved...by reading the primer as you have (knowledge) and clearly doing some of your own research. Thankfully, lifestyle changes are proving to be quite effective at preventing AD, and there are some promising medicines that are being developed, as well.
3,4

User avatar
Stavia
Mod
Mod
Posts: 5265
Joined: Tue Apr 29, 2014 6:47 pm
Location: Middle Earth

Re: new e3/e4

Postby Stavia » Mon Aug 29, 2016 11:33 pm

hi MAC and welcome.
Great questions, unfortunately not good answers available...
1. Too many unknown input variables to be able to confidently predict output. There is no way with current science you can quantify your risk of AD or PD IMO
2. Then I kinda thought that there were common risk factors in AD and PD - I confidently looked for a supporting link and found confusion....
http://care.diabetesjournals.org/content/34/12/2614
sorry, more grey :(

what are your thoughts on these areas?

User avatar
TheresaB
Mod
Mod
Posts: 1034
Joined: Wed Feb 03, 2016 9:46 am
Location: Front Range, CO

Re: new e3/e4

Postby TheresaB » Tue Aug 30, 2016 10:45 am

Mac wrote,
Just introducing myself, asking for general thoughts on approximate risk factor for AD given background?


I can't address your risk but you did mention family history of Alzheimer's and Parkinson's, to which you may or may not know there does seem to be a connection.

Alzheimer’s, Parkinson’s, Multiple Sclerosis are all degenerative neurological conditions. Although they manifest differently, the connection between these seem to have something to do with the mitochondria. I recommend following Stavia's write up on strategies for newcomers which stresses insulin control first, but given your family history of Parkinson's and AD, you might want to be mindful of your mitochondria while doing this.

Terry Wahls is a medical doctor who was diagnosed with multiple sclerosis. Despite seeking the best in medical care, her condition degenerated to her needing a tilt recline wheel chair because she couldn’t even sit up. But through her own research, she largely addressed her situation through diet, specifically eating to feed her mitochondria. She reversed her multiple sclerosis. She gave a TedTalk which addresses her journey, http://terrywahls.com/minding-your-mito ... xiowacity/

If you’ve perused the subjects on this forum, you may have seen Dr Dale Bredesen mentioned. He’s researched neurodegeneration for decades, focusing on cognition issues. He feels there should be no Alzheimer’s and has reversed cognitive decline through a protocol he’s developed. In his paper “Reversal of Cognitive decline: A Novel Therapeutic Program” http://www.aging-us.com/article/NjJf3fWGKw4e99CyC/text published in September 2014 he discusses the protocol he developed. The paper has a table which cites about 25 things he looks at/addresses to reverse cognitive decline and one of those 25 things is “optimize mitochondrial function.”

Dr Bredesen’s paper cites supplements to optimize mitochondrial function, but how my husband (3/4) and I (4/4) address this strategy is by applying Dr Wahls’ protocol concept of eating vegetables as follows: 1/3 greens, 1/3 colors, 1/3 sulphur. She likes 9 total cups of vegetables a day total, we aren’t quite able to make that, but we do have a very large salad incorporating the 1/3, 1/3, 1/3 strategy every night and we avoid processed foods.

But earlier I qualified that the vegetables should be “good.” We follow Dr Wahls’ protocol but within the dietary restrictions of our doctor, Dr Gundry, who is another doctor who if you read through forum subjects is often referenced. Dr Gundry has been testing for ApoE4 for 15 years, and has minimized the negative effects of this gene in thousands of patients. ApoE4 is an ancient gene, and Dr Gundry takes an evolutionary tact to his dietary recommendations. He says there are certain foods that are now widely eaten that have only been introduced to human diet in “recent” (think evolutionary) years. The body reacts negatively, although often imperceptibly, to these foods. We follow his guidance in our diet specifically avoiding certain foods in the plant family, which contain lectins, e.g.s beans, grains, nightshades.

But that's what we do, many people find it hard, especially when new to this, to give up some of their favorite vegetables, such as tomatoes, peppers, cucumbers in addition to giving up other favorite foods when trying to control their insulin. There's nothing wrong with taking baby steps, as long as you keep moving forward, I just thought I'd give you some food for thought, or perhaps your mitochondria.
-Theresa
ApoE 4/4

MAC
Senior Contributor
Senior Contributor
Posts: 329
Joined: Mon Aug 29, 2016 2:24 pm

Re: new e3/e4

Postby MAC » Wed Aug 31, 2016 10:10 am

Thank you TheresaB.

As an engineer, I tend to look for proven scientific results.

There are so many epigenetic answers out there, one could not possibly do them all.

My parents who as I have mentioned have AD (mom) and PD (dad) have a leading neurologist doctor, and I have not hear same ANYTHING about proven treatments.

At the moment, trying to live as healthy a lifestyle is all I can motivate myself to undertake.

What is the current state of the art pre early detection LOAD onset and correlation to actual LOAD?

I have read there are many large studies underway, undertaking to try and extend the early detection science by following young cohorts.

I have read that the reason that 99.9% of the AD drugs have failed is that they are too late in the game...the neurodegenerative loss is too far advanced to be reversed (and maybe impossible to reverse), so earlier detection and understanding MIGHT lead to more effective pre LOAD treatments?
MAC
E3/E4-55/MALE

User avatar
Julie G
Mod
Mod
Posts: 8534
Joined: Sat Oct 26, 2013 6:36 pm

Re: new e3/e4

Postby Julie G » Wed Aug 31, 2016 1:43 pm

MAC, when I first saw your post, I was hoping you were my son- also a 3/4 with a similar name (different spelling.) He’s only 23, but needs to begin caring about his health. Alas, no (a Mama can hope ;)) but a warm welcome to YOU.

It sounds as though you are uninterested in epigenetics because they are unproven and you’d rather go straight to Pharma when needed. Am I assessing that correctly? Unfortunately, Pharma has had very little success in treating Alzheimer’s. There are currently 2 classes of FDA approved drugs: Cholinesterase inhibitors & NMDA (N-methyl-D-aspartate) receptor antagonists. Both reduce symptoms a little for a short time, but do nothing to stop the progression of the disease. That doesn’t mean that effective Pharma won’t be found. It just isn’t available yet. Several clinical trials (FINGER, ADEX, MAPT, MIND, and the case studies of Dr. Bredesen) have reversed cognitive decline via various combinations of epigenetic strategies, hence it tends to be a focus of what we discuss here. I think you’ve generally got the right goal in mind to simply optimize your overall health.
What is the current state of the art pre early detection LOAD onset and correlation to actual LOAD?

Surprisingly, there’s not a clearcut answer to that in terms of traditional imaging and other tests. Until fairly recently AD was definitively DXed upon autopsy. Now, PET scans can detect amyloid in the brain, however those with high levels aren’t always symptomatic and there’s a subset of folks with proven AD who don’t have amyloid. A PET-FDG scan can identify a signature loss of glucose utilization. FWIW, E4 carriers (in a dose dependent fashion) exhibit a reduced cerebral glucose utilization in the same regions as AD patients starting in our 20s-30s, but not all E4 carriers go on to develop AD and PET scans are very pricey. A lumber puncture can reveal abeta and tau in the CSF, but because it’s so invasive I’m unaware of any pre-symptomatic correlational studies. Probably the best way that you can monitor your progression is via a simple MRI with Neuroreader to track hippocampal volumetrics. Many of us here just track glycemic and inflammation markers that also correlate with hippocampal volume because it’s easy, inexpensive, and accessible. You could also track your status with neuropsych testing. One drawback is that you can train for the test with repeat online assessments like SAGE and MoCa. Formal neuropsych testing every year may be helpful, but isn't great at capturing the very early SCI (subjective cognitive impairment) stage of the disease.

I also have AD on my Mom’s side and PD on my Dad’s. Given your family history, I think you’re right to be concerned. I wish we had proven, easy, answers for you. The science just isn’t there yet.


Return to “Our Stories”

Who is online

Users browsing this forum: Google [Bot] and 33 guests