Apo E2/E2 with AD need help on ReCode !!

[Damien06]

Hi everyone,

My name is Damien. I come here to find help for my dad, I am very worry for him and lost. He is 56 years old, and got diagnosed with early stage AD. He is APOE2/E2 and a heart stent + vascular medical family history. We're living in France, we had to find a practitioner in UK who is trained for Bredesen's protocole.

The thing is the treatment the doctor gives doesnt follow completely Recode like : no ketogenic diet but mediterranean/anti-inflammatory diet, luminotherapy, mct oil, some supplements, and Amphotericin B medic next to positive results on mold urine test (not the Recode/Shoemaker tests). We did some tests from Recode, not all of them, or differents : for example, no c4a, tgfb1, msh but heavy metals, mycotoxins, and organic chemical exposure urine tests. No volumetric MRI but want a QEEG.

I need some opinions about it. Is it normal ? Or do you recommend to order the Recode report, or a 2nd medical consultation with another practitioner ?

I struggle since 6 months to help him. Thank you a lot for your responses.

[slacker]

Damien, my heart goes out to you, your dad, and the rest of your family. This a confusing situation to navigate through. I find that Bredesen Protocol certified practitioners have a great variety of approaches to testing and treating, and don't necessarily implement Dr Bredesen's specific recommendations. And I'm sure that Dr B changes how he does things as he works with more patients. It's possible that not all suggested tests are available in all countries, and/or different practitioners don't agree on the best approach.

Have other members of your extended family developed AD at an early age? There are genes different than ApoE that put people at risk for early AD, but typically have a strong family history of AD at a young age. If not, it's possible that your dad has what Dr Bredesen calls "Type 3" AD; people tend to develop symptoms at an earlier age with type 3. Mold mycotoxins are the most common source of type 3/CIRS (Chronic Inflammatory Response Syndrome). Dr Bredesen mentions the mold urine test in his book, but not as the first test to do to evaluate for CIRS. I'm not an expert, but I don't think all the CIRS blood tests need to be done for diagnosis. For example, I started evaluation with a "budget" plan, with resulting abnormal TGF beta 1 and MSH, enough to determine the need to find the underlying cause of CIRS.

I have passing familiarity with two Bredesen practitioners (MDs) in the UK who seem competent. If you want to PM (private message) me, we can exchange UK practitioner names. Just click on my green username to get to the PM option. If you do decide to get a second opinion, see if they will do a case review and explain their approach before you commit to continuing with them. This way you can feel more comfortable about it being a good match, kind of like a test drive. It's might also be possible to connect through telemedicine with a US east coast Bredesen provider. There are also practitioners in the US that are specifically trained with Shoemaker; they will most likely only address CIRS though.

[NF52]

Hi everyone,

My name is Damien. I come here to find help for my dad, I am very worry for him and lost. He is 56 years old, and got diagnosed with early stage AD. He is APOE2/E2 and a heart stent + vascular medical family history. We're living in France, we had to find a practitioner in UK who is trained for Bredesen's protocole.

The thing is the treatment the doctor gives doesnt follow completely Recode like : no ketogenic diet but mediterranean/anti-inflammatory diet, luminotherapy, mct oil, some supplements, and Amphotericin B medic next to positive results on mold urine test (not the Recode/Shoemaker tests). We did some tests from Recode, not all of them, or differents : for example, no c4a, tgfb1, msh but heavy metals, mycotoxins, and organic chemical exposure urine tests. No volumetric MRI but want a QEEG.

I need some opinions about it. Is it normal ? Or do you recommend to order the Recode report, or a 2nd medical consultation with another practitioner ?

I struggle since 6 months to help him. Thank you a lot for your responses.

Bonsoir, Damien06,

I apologize for not being able to reply en Francais and hope this is not too confusing to read or translate.

I am sorry to learn that you are feeling lost and worried about your dad, since I am guessing you are only in your 20's or maybe early 30's--way too young to have to carry such worry. My father also had severe heart disease when I was in my early 30's and he was in his mid-60's. I know that the sudden news of that gave me a sense of the world shifting to a scary place, with little idea of what to do.

Your questions are good ones; the answers may not be easy for us to give you. So instead, I will suggest some more questions that you may want to raise with specialists in France. The reason I have questions is that ApoE 2/2 is a rare combination, and is usually seen as being much less likely to be a cause of Alzheimer's disease.

I wonder if your father has had a thorough evaluation by a specialist in metabolic issues? In the U.S. that would be an endocrinologist. While I have high LDL cholesterol from having ApoE 4/4, it seems your father may have an even higher risk of that. Here is what a researcher on ApoE with about 30 years of experience at the well-respected Gladstone Institutes in California wrote in 2016:

ApoE2 is associated with the genetic lipid disorder type III hyperlipoproteinemia (1–3, 16). ApoE2-enriched β-VLDL in patients resemble the cholesterol-containing lipoproteins in cholesterol-fed animals and are associated with peripheral artery atherosclerosis and unique cholesterol deposits in macrophages in skin folds. β-VLDL accumulate in the plasma because apoE2 is defective in LDLR binding (approximately 2% of normal). ApoE2 homozygosity sets the stage for the development of type III hyperlipoproteinemia. The hyperlipidemia is precipitated by so-called second hits (e.g., diabetes, hypothyroidism, estrogen deficiency, obesity, and other genetic and environmental factors) that stress hepatic clearance pathways or by enhancing VLDL overproduction

.
http://clinchem.aaccjnls.org/content/cl ... 4.full.pdf

The National Organization for Rare Disorders, an non-profit that advocates for people with rare disorders, has this information Hyperlipoproteinemia Type III
and explains that not everyone with ApoE 2/2 develops hyperlipoproteinemia

Hyperlipoproteinemia type III, also known as dysbetalipoproteinemia or broad beta disease, is a rare genetic disorder characterized by improper breakdown (metabolism) of certain fatty materials known as lipids, specifically cholesterol and triglycerides. This results in the abnormal accumulation of lipids in the body (hyperlipidemia). Affected individuals may develop multiple yellowish, lipid-filled bumps (papules) or plaques on the skin (xanthomas). Affected individuals may also develop the buildup of fatty materials in the blood vessels (artherosclerosis) potentially obstructing blood flow and resulting in coronary heart disease or peripheral vascular disease. Most cases of hyperlipoproteinemia type III are inherited as an autosomal recessive trait....
There is no specific diagnostic test for hyperlipoproteinemia type III. A diagnosis is made based upon a thorough clinical evaluation, a detailed patient history, and identification of characteristic findings such as xanthoma striata palmaris. Tests may be performed that demonstrate elevated levels of cholesterol and triglycerides (hyperlipidemia), which occurs after fasting; reveal the presence of very low density lipoproteins (VLDLs), a type of lipoprotein that is elevated in individuals with hyperlipoproteinemia type III; and demonstrate an increased ratio between VLDLs to plasma triglycerides. A test known as electrophoresis may be used to demonstrate abnormal lipoproteins. Electrophoresis is a laboratory test that measures protein levels in the blood or urine by using an electric current to separate proteins by molecular size.

Genotyping is a test that determines what form (allele) of gene is present. A simple blood test can determine whether an individual has two apo e2 genes. When these genes are found a person with characteristic symptoms, it is diagnostic of hyperlipoproteinemia type III.

[Emphasis added.]

It also appears that the Bredesen-protocol ketogenic diet may not be appropriate for your father, if he is in fact diagnosed with hyperlipoproteinemia Type III, because of the already high levels of lipids. Here's another excerpt from the same source:

Treatment
Most individuals with hyperlipoproteinemia type III respond to dietary therapy that consists of a diet that is low in cholesterol and saturated fat. The reduction of the intake of dietary cholesterol and other fats generally prevents xanthomas and high lipid levels in the blood (hyperlipidemia). Exercise in addition to dietary therapy may help lower lipid levels.

In individuals in whom dietary modification does not lower lipid levels, certain drugs may be used. These drugs include niacin, gemfibrozil, clofibrate, and/or lovastatin. Other drugs, such as cholestyramine and colestipol are not effective for the treatment of Broad Beta Disease; they may actually raise blood levels of beta-lipoproteins.

[Emphasis added.]

I know that this does not talk about his early stage AD diagnosis, but since diabetes and other metabolic disorder are linked with the risk for AD, it seems important in his case to try to find if he needs a very specific diet--not the Bredesen protocol or the Mediterranean diet, but something targeted for his rare profile.

I hope you will be able to find a specialist to answer those questions, and hope even more that he gives you good news that your father does not have hyperlipoproteinemia. At that point, I think you will be better able to come up with a plan that helps him , using some biomarkers (blood tests, for example) and especially using how he feels and is able to enjoy life.

Please let us know what you learn. We hope for both of you to have happier days ahead.

[SamNZ]

Hi everyone,

My name is Damien. I come here to find help for my dad, I am very worry for him and lost. He is 56 years old, and got diagnosed with early stage AD. He is APOE2/E2 and a heart stent + vascular medical family history. We're living in France, we had to find a practitioner in UK who is trained for Bredesen's protocole.

The thing is the treatment the doctor gives doesnt follow completely Recode like : no ketogenic diet but mediterranean/anti-inflammatory diet, luminotherapy, mct oil, some supplements, and Amphotericin B medic next to positive results on mold urine test (not the Recode/Shoemaker tests). We did some tests from Recode, not all of them, or differents : for example, no c4a, tgfb1, msh but heavy metals, mycotoxins, and organic chemical exposure urine tests. No volumetric MRI but want a QEEG.

I need some opinions about it. Is it normal ? Or do you recommend to order the Recode report, or a 2nd medical consultation with another practitioner ?

I struggle since 6 months to help him. Thank you a lot for your responses.

Hi Damien, welcome to our site. I am so sorry for you going through this at the moment but love the hope and perseverance you are showing to help your dad navigate through his health issues.
From everything I have read so far ( and I am on a steep learning curve), it does seem that with the very early onset of the AD symptoms and the gene profile heavy metal toxicity or similar would be well worth spending some more time investigating. Any Functional Medicine doctor should be able to help you with that side of things but obviously if you can get a Bredesen Trained one in as part of the package that would be ideal. It can take quite a long time to remove the toxins from the system and you and your father may benefit from some additional support during this time.
There is lots more information on this, I have had a look and found this thread you may be interested in what is the prevelance of atrophic Alzheimers, there is a link in the article that is sends you to which is also quite interesting. Remember that you are helping him already, and it has taken your dad 56 years for his biology to become upset and bring him to this point, we cannot reverse everything overnight.
There are some amazing successes in reversing the disease, (one lady in NZ has just walked again for the first time in several years!) Keep learning, keep asking the questions and feel free to approach us in this community whenever you want. We are all here to try to be a cog in reversing this big disorder and look forward to hearing more about how you are getting on. SamNZ

[cflegal]

The diet you describe should be ketogenic like the "Bredesen diet." The doctor may have had other considerations in diet recommendations.