It is not really a mutant gene, just one of the variant genes found in the human population. Unfortunately the APOE4 variant is rather bad to have and a major risk factor for Alzheimers.

Are you homo or heterozygous for E4?

heterozygous

That is good. Your risk is higher, but nowhere near as high as for homozygous E4 carriers. Assuming you are youngish it is a problem a long way off and with luck there will be progress in curing or preventing Alzheimer's before you really have to worry.

I hadn’t heard that body fat composition affected Alzheimer’s risk. Out of curiosity, do you have a reference?

Body fat is a risk for multiple disease. The general idea is that whenever viruses enter the adipose tissue they are hard to reach by the immune system. We dont really understand yet what causes Alzheimer but now there is suspicion of a viral link.

There is another hypothesis making the rounds that obesity is linked to chronic metabolic stress and eventual damage (so far uncontroversial), which is linked to many separate diseases.

internet articles point fingers at long term insulin resistance, e.g. https://www.psychologytoday.com/us/blog/diagnosis-diet/20160...

the receptors responsible for escorting insulin across the blood-brain barrier can become resistant to insulin, restricting the amount of insulin allowed into the brain. While most brain cells don’t require insulin in order to absorb glucose, they do require insulin in order to process glucose. [..] Despite swimming in a sea of glucose, brain cells in people with insulin resistance literally begin starving to death. [..] Which brain cells go first? The hippocampus is the brain's memory center. Hippocampal cells require so much energy to do their important work that they often need extra boosts of glucose. While insulin is not required to let a normal amount of glucose into the hippocampus, these special glucose surges do require insulin, making the hippocampus particularly sensitive to insulin deficits. This explains why declining memory is one of the earliest signs of Alzheimer’s, despite the fact that Alzheimer’s Disease eventually destroys the whole brain.

researchers have discovered that Alzheimer’s Disease is preceded by DECADES of gradually worsening glucose hypometabolism.

2012 study showed that a low-carbohydrate high-fat diet improved memory in people with “Mild Cognitive Impairment” (Pre-Alzheimer’s Disease) in only six weeks.

https://coconutketones.com/ - Dr Mary Newport's work on coconut oil and low carb diet with her husband with early onset alzheimers and dementia, intended to provide an alternative ketone source of fuel for the brain instead of glucose.

Grain and sugar elimination: that’s huge, because it’s anti-inflammatory. A big driver of cognitive decline and dementia is inflammation. By going grain-free sugar-free we drop inflammation dramatically. If you were to track inflammatory measures like C-reactive protein or interleukin-6 or tumor necrosis factor (TNFα) or other measures, you would see them drop precipitously, as inflammation recedes, and risk for Alzheimer’s with it. - https://www.wheatbellyblog.com/2017/11/preventing-cognitive-...

Alzheimer's is starting to be referred to as Type 3 diabetes that the correlation between metabolic syndrome and the disease is incredibly high.

I wonder how much this has to do with the relative uptake of carbohydrate sources and in particular refined sugars (namely fructose) in the typical diet. It seems the more that we learn, the less good refined vegetable oils and the level of fructose intake in people's diets is. I'm not convinced the amount of refined grains people eat is particularly good either.

However is seems that sugar (fructose specifically) and refined oils (linoleic acid specifically) are particularly bad in the increased quantities since the early 1900's.

Which service did you use for gene sequencing?

23andme

Related question, is there any service or open source tool people use to get more thorough insights on the raw data you can download from 23 and me?

I'm not sure there is such a service. You can download the raw data on 23andme, it's just a bunch of SNPs though. I'm not sure there's much known about them other than what's already flagged by their service.

There's a actually a lot more info than what they show you. They won't show you something depending on many factors including FDA approval, etc. So there's a potential whole lot of information that you are missing out if you don't run your data through other services and tools.

I did a google search and found a bunch of resources, but I though some ppl here may have actual experiences to share.

low fat as in to not be overweight, or consume a diet that is low in fat? I don't want any of them 'zheimers

tangent: low-fat diets don't actually help with weight loss

Well, partially true. Fat is very energy rich so low fat diets will typically have less calories and calories are basically the only thing you need to worry about when trying to lose weight.

On the flip side protein in particular is very sating, and protein + fat (in the absence of carbs) has a much lower insulin response. So a higher fat diet with protein sources will have an increased satiety.

Calories do count, but hormonal response is a primary factor.

Edit: it's worth noting that a certain amount of fat is absolutely needed and is sating in and of itself.

Personally, I don't think the amount of fat you get (in terms of calories) should be lower than the amount of protein you consume, and should come from better sources excluding refined vegetable oils (which are everywhere). My opinion on this is somewhat based on the relative amounts of fat to protein in sources where you get protein naturally. I also feel that not getting enough fat is a big factor in gallbladder dysfunction and stones.

A lot of my opinions are just from common sense, observation and a lot of reading on relatively recent diet and nutrition shifts, and feel levels/extremes can vary based on general health, metabolic syndrome indicators and outright diabetic progression.