Sirenofthespring wrote: āFri May 20, 2022 8:28 pm
Given that my mom took such good care of her health, except for the extenuating circumstances of being a caregiver during Covid, what can I do? Could her ovaries being removed have played a role?
You seem well educated on this already, so I probably donāt have to tell you that many factors play into dementia. A person can (apparently) eat well, take good care of their health, and still get dementia.
I added the parenetical āapparentlyā as a modifier to āeatā because what is thought to be healthy eating may not be healthy for everyone. I know a gal whose blood sugar elevates after eating broccoli. Broccoli! The pinnacle of healthy food! I don't know how that happens, but it happens for her. I know I have personally found, through labs with my doctor, that while I donāt have food allergies, I have food sensitivities that I had previously no clue about because I sensed no issues. Such āhealthyā foods as grains (gluten), nightshades (tomatoes, cucumbers, peppers, etc), dairy, and eggs were elevating the inflammation markers in my body. So itās possible your momās āhealthyā diet
may have unknowingly contributed.
Having her ovaries removed at such a young age likely also contributed, especially if there was no hormone replacement therapy. From Dr Bredesenās first book,
The End of Alzheimerās,
āStudies from the Mayo Clinic have shown that women who have their ovaries removed by age 40 (sometimes because they have a genetic risk of ovarian cancer) without hormone replacement therapy have double the risk of Alzheimerās."
There's also this:
Hysterectomy, oophorectomy, estrogen, and the risk of dementia. Neurodegenerative Diseases āIn the Danish study, women who underwent hysterectomy with bilateral ovarian conservation had a 38% increase in risk of dementia with onset at ages 40ā49 years. Hysterectomy with unilateral oophorectomy increased the risk by 110%, and hysterectomy with bilateral oophorectomy increased the risk by 133% [2].ā
Her being a caregiver for your father and not sleeping well certainly didn't help. Chronic stress negatively affects every cell in the body and our brain cells are particularly sensitive. Stress can also come from factors that we donāt even think about as stressful! You might want to read more on our wiki page on stress
Stress
The poor sleep as a caregiver as well as working shifts for 7 years in her 40s disrupts the body's circadian rhythm. From this recently published article,
Circadian clocks, cognition, and Alzheimerās disease: synaptic mechanisms, signaling effectors, and chronotherapeutics "Several recent papers have raised the prospect that the disruption of circadian timing in AD could produce a self-reinforcing feedback loop, where disruption of timing accelerates AD progression and that in turn leads to a further disruption of the circadian timing system. Thus, the disruption of the circadian timing system could be a key contributing factor to both AD neuropathogenesis, and the early and mid-stage cognitive impairments that are a central feature of AD."
There are other factors that could have contributed:
Other genes - APOE is significant, but not the end all/be all. Weāre still learning about additional genes the work for/against APOE as well as independently contribute.
Head injury(ies) from an athletic event or accident seems to predispose to dementia later on. Per this article,
The frightening reality of women's concussions - a personal story āAccording to studies in the Orthopedic Journal of Sports Medicine, women are twice as likely as men, in like-for-like sports, to experience a concussion, symptoms are more severe for women and symptoms are likely to last longer for women in comparison to men.ā
and maybe you've heard of the members of the British football/soccer team that won the World Cup from the 1965-66 season, (all healthy strapping lads) neurodegenerative diseases were a factor in 42 per cent of the deaths among that group so far, presumably from "heading" the ball.
Or perhaps Adverse Childhood Experiences (ACES)
Adverse Childhood experiences (ACES) -- Association Between Adverse Childhood Experiences and Dementia in Older Japanese Adults āParticipants who experienced 3 or more adverse childhood experiences had a greater risk of developing dementia compared with those who grew up without adverse childhood experiences, after adjustment for age, sex, childhood economic hardship, nutritional environment, and education (hazard ratio, 2.18; 95% CI, 1.42-3.35). ā
Other possibilities:
-Mold exposure
-Other environmental exposures ā pollution, toxins, chemicals, pesticides, herbicides, noise, light
-Too much exercise? Even despite the importance of exercise for brain health, it could be argued that too much exercise produces oxidative stress which has a negative effect.
The list goes on, there are so many factors that we know can contribute to dementia, and the result of dementia seems to typically come from a mixture of many factors, not just one or two. Unfortunately, when our loved ones pass, all we're left with are unanswered questions.
I am not a 2/4, so I have only casual knowledge and frankly, there doesnāt seem to be much research on that status. I do know it doesnāt seem to present a simple mathematical solution of the 2 and 4 canceling each other out thus making a person the equivalent of a 3/3.
I do know holding a Īµ4 is associated with CAA and also for Īµ2, although less so:
From
Vascular pathology in the aged human brain āCAA, especially capillary CAA, is associated with the apoE Īµ4 allele [37, 100, 103, 126, 130, 132]. This finding points to an important role of apoE for the development of CAA because apoE4 is less effective in the receptor-mediated clearance of AĪ² [Amyloid Beta] when compared to apoE3 [19]. This property of apoE4 presumably results in capillary AĪ² deposition in apoE Īµ4 carriers as soon as alterations in the perivascular drainage occur. In addition, the apoE Īµ4-genotype promotes AĪ² aggregation in vascular smooth muscle cell cultures [85]. Finally, CAA-related hemorrhage is reported to be associated with the apoE Īµ2 and Īµ4 allele [37, 88, 95, 97].
(The footnotes can be found in the link).
and
APOE and cerebral amyloid angiopathy in community-dwelling older persons After further adjustment for Alzheimerās pathology, both Īµ2 (odds ratio 1.707, 95% confidence interval 1.236ā2.358, p=0.001) and Īµ4 (odds ratio 2.284, 95% confidence interval 1.730ā3.014, p<0.001) were independently associated with amyloid angiopathy. ā¦ We conclude that both APOE Īµ2 and Īµ4 alleles are associated with more severe cerebral amyloid angiopathy, and the direct effect of Īµ2 is masked by the alleleās negative association with comorbid Alzheimerās pathology. ā¦
But there's also this:
Genetics of cerebral amyloid angiopathy: systematic review and meta-analysis Conclusions: There is convincing evidence for a dose dependent association between APOE Īµ4 and sporadic CAA. Further work is needed to better understand the mechanism of this association and to further investigate other genetic associations with CAA. But from results: There was no significant association between APOE Īµ2 and CAA.
Do your best.
Make good choices. Nothing in life is guaranteed, but making choices to do the right things for oneās health leads to a positive outlook for the future, give a person a feeling of empowerment of not being a helpless victim, and certainly lowers the risk of prospective health concerns.
We're here for you. Theresa.J gave you a good intro to this site. NF52 also posted some wonderful information. Since she wrote as I was writing this I may be repeating, but for search results from this site on APOPE 2/4
search.php?keywords=%2BApoE2%2F4&terms= ... mit=Search and for search results on CAA
search.php?keywords=CAA&terms=all&autho ... mit=Search
Also, if unfamiliar with Dr Bredesen, you may want to get acquainted with him.
We have an introductory wiki
Bredesen Protocol and his second book,
The End of Alzheimerās Program offers practical information and steps to implement his protocol to reduce your chances of dementia.