Lets talk about eggs
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Re: Lets talk about eggs
I don't think the apoe4 gene is the cause, but rather that they have another gene that causes the lipid problem with cholesterol. That it is the genotype that is paired together often but not always? Just my observational thoughts.
- Gilgamesh
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Re: Lets talk about eggs
Richard, thanks for your efforts.RichardS wrote:This looks to me to be an excellent, if not dated review (1998). Are there any newer studies to be added to this collection of human dietary cholesterol studies by apoe status?
I try to find newer studies often by looking at the "Cited by" items in PubMed, but this study is an orphan:
http://www.ncbi.nlm.nih.gov/pubmed/9507235
And Tso did only one more study looking explicitly at APOE status, though it's in children with type 1 diabetes:
http://www.ncbi.nlm.nih.gov/pubmed/?ter ... or%5D+apoe
GB
Re: Lets talk about eggs
Thanks Richard. I'm having trouble interpreting the chart. It seems they don't say whether the effect is favorable or unfavorable for which variable in the far right columns? I can guess, but am I missing something?
ApoE 3/4 > Thanks in advance for any responses made to my posts.
Re: Lets talk about eggs
Understandable. Hidden at the bottom of the table is the footnote that says entries marked with "a" show E4 with the significantly greatest response.circular wrote:Thanks Richard. I'm having trouble interpreting the chart. It seems they don't say whether the effect is favorable or unfavorable for which variable in the far right columns? I can guess, but am I missing something?
The Lehtimaki et al 1992 paper, which was not well controlled but specifically aimed at only manipulating egg yolks, showed 4/4's (only 3 subjects) with a 2.3-fold greater increase in total cholesterol compared to 3/2, 3/3 and 3/4. What it did to LDL-C, I can't tell. Even with my university library access, I can't get this old paper and am relying on the abstract. FWIW, the total cholesterol response for 3/4's was non-significantly less than the 3/3's.
Re: Lets talk about eggs
Thanks again Richard. I saw that superscript "a" note too but they didn't clarify whether the response was good up or down and for which variable.
In the Lehtimaki study one wonders what else and in what quantities the 4/4s were eating with the same constituents as the egg yolks.
Since E4 is supposed to increase dietary cholesterol absorption (if I got that right), if some E4s hyper-absorb more than others, I wonder what other genes might be influencing this.
In the Lehtimaki study one wonders what else and in what quantities the 4/4s were eating with the same constituents as the egg yolks.
Since E4 is supposed to increase dietary cholesterol absorption (if I got that right), if some E4s hyper-absorb more than others, I wonder what other genes might be influencing this.
ApoE 3/4 > Thanks in advance for any responses made to my posts.
Re: Lets talk about eggs
From the footnote in the table: "[superscript]a ApoE phenotype showing the significantly greatest response."circular wrote:Thanks again Richard. I saw that superscript "a" note too but they didn't clarify whether the response was good up or down and for which variable.
In the Lehtimaki study one wonders what else and in what quantities the 4/4s were eating with the same constituents as the egg yolks.
Since E4 is supposed to increase dietary cholesterol absorption (if I got that right), if some E4s hyper-absorb more than others, I wonder what other genes might be influencing this.
Just a reminder that the Lehtimaki study had a tiny 4/4 group and that we see no mention of the food being provided to the subjects like we see in many of the other studies. Lots more chance for confounding variables, so I give more weight to the other 4 studies I quoted.
Re: Lets talk about eggs
Neither cholesterol, nor egg intake, was associated with a higher risk of dementia. Conversely, moderate egg intake was associated with improved cognitive performance. This held true for E4 carriers. I'm unable to find full-text to learn more.
Association of dietary cholesterol and egg intakes with the risk of incident dementia or Alzheimer disease: the Kuopio Ischaemic Heart Disease Risk Factor Study.
https://www.ncbi.nlm.nih.gov/pubmed/28052883
Association of dietary cholesterol and egg intakes with the risk of incident dementia or Alzheimer disease: the Kuopio Ischaemic Heart Disease Risk Factor Study.
https://www.ncbi.nlm.nih.gov/pubmed/28052883
Abstract
BACKGROUND:
There is little information about the associations of intakes of cholesterol and eggs, a major source of dietary cholesterol, with the risk of cognitive decline in general populations or in carriers of apolipoprotein E ɛ4 (APO-E4), a major risk factor for dementia.
OBJECTIVE:
We investigated the associations of cholesterol and egg intakes with incident dementia, Alzheimer disease (AD), and cognitive performance in middle-aged and older men from Eastern Finland.
DESIGN:
A total of 2497 dementia-free men, aged 42-60 y in 1984-1989 at the baseline examinations of the prospective, population-based Kuopio Ischaemic Heart Disease Risk Factor Study, were included in the study. Information on the apolipoprotein E (Apo-E) phenotype was available for 1259 men. Data on cognitive performance tests at the 4-y re-examinations were available for 480 men. Dietary intakes were assessed with the use of 4-d food records at baseline. Dementia and AD diagnoses were based on Finnish health registers. Cox regression and ANCOVA were used for the analyses.
RESULTS:
During the 21.9-y follow-up, 337 men were diagnosed with dementia, and 266 men were diagnosed with AD. Neither cholesterol nor egg intake was associated with a higher risk of incident dementia or AD. For example, when evaluated continuously, each intake of 100 mg cholesterol/d was associated with a multivariable-adjusted HR of 0.90 (95% CI: 0.79, 1.02) for incident dementia, and each additional 0.5 egg (27 g)/d was associated with an HR of 0.89 (95% CI: 0.78, 1.01). However, egg intake was associated with better performance on neuropsychological tests of the frontal lobe and executive functioning, the Trail Making Test, and the Verbal Fluency Test. The Apo-E4 phenotype did not modify the associations of cholesterol or egg intake (P-interactions > 0.11).
CONCLUSIONS:
Neither cholesterol nor egg intake is associated with an increased risk of incident dementia or AD in Eastern Finnish men. Instead, moderate egg intake may have a beneficial association with certain areas of cognitive performance.
- Hepoberman
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Re: Lets talk about eggs
For years and years (decades) I ate bacon an eggs for breakfast. My wife, before we were married, tended to skip breakfast altogether.
While neither breakfast may be ideal, I wonder who would get dementia first? I don't think much can be learned with this type of observation. I do know that eating eggs instead of oats noticeably raises my total cholesterol and I believe lower is better.
While neither breakfast may be ideal, I wonder who would get dementia first? I don't think much can be learned with this type of observation. I do know that eating eggs instead of oats noticeably raises my total cholesterol and I believe lower is better.
- LillyBritches
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Re: Lets talk about eggs
Hi, girly! I know...I just read this. Veggie omelettes, anyone?Juliegee wrote:Neither cholesterol, nor egg intake, was associated with a higher risk of dementia. Conversely, moderate egg intake was associated with improved cognitive performance. This held true for E4 carriers. I'm unable to find full-text to learn more.
Immediately after my stepdad's heart attack at age 57 (about 13 years before he developed AD), and his subsequent quadruple-bypass cardiac surgery, my mother and he completely overhauled their diets. In particular, they ate only oatmeal and Eggbeaters (egg whites) for breakfast. For YEARS. They did all the "right" things that cardiologists advised in the 80s: low/no fat, no butter, chicken and fish only, egg whites only, and lots and lots and lots of grains. Oh, and we can't forget that margarine jam-packed with trans-fats.
My poor Mother said if she ate one more piece of chicken she was sure to morph into one.
They also exercised like mad...well...especially Phil. He became a master mall-walker, lifted free weights, and they went dancing every weekend. Additionally, they were forever engaged in crossword puzzles, seeing friends, traveling, etc. Very active people.
They never, ever deviated from their prescribed diet.
Then the ball dropped, and it dropped hard: circa age 70, Phil was diagnosed with AD. After genetic testing (pretty damned new in the early 90s), it was discovered he was 3/4 and his status was used as confirmation for his AD diagnosis. So, of course, that low/no fat diet and all those egg whites did very little to ward off the beast. Phil passed at 77 from complications due to AD...pretty standard cause of death for an AD victim.
Fast forward even further: my beloved Mother started having memory issues around age 89-90. Then movement issues. Yada, yada, yada - "they" think she has Lewy Body but not AD. Then a cerebral CT scan shows only minor brain atrophy...but also indicates cerebral small vessel disease. During this time, I discovered 23andme and both Mother and I spit in the tube. My ApoE results were 4/4 and hers were 3/4 just like her husband Phil's.
He and she ate the same diet. For YEARS. They kept their minds active with the same types of cognitive stimulation and levels of physical activity. Both were pretty fit elderly folks.
Big difference? LOAD ran in Phil's immediate and extended family - three of his siblings developed it around the same age as did he. The fourth sibling never did get AD; however, he had massive cardiac issues beginning in middle age and, of course, he died from them in his early 80s. To make this family's history even more maudlin: Phil's sweet son David, a Pharmacist, passed three years ago from early-onset AD. He was only 61.
My Mother's family? Longevity abounded. No dementia other than some paternal Aunts becoming slightly dotty as they approached 90, 95, and 99, respectively. The 99-year-old was only starting to become forgetful right before she passed. And my sweet Mother died this past October at age 96. She was sleeping more this past year and seemed to get infection after infection (that, too, is just disease progression), but her mental status was, well, status quo.
Two 3/4s - two very different experiences.
My point? Oh, yes. Eat eggs. Lots of eggs. Omelettes are fabulous at Sunday brunch.
Love, and hope everyone is doing well,
Lillianne
I'm just a oily slick in a windup world with a nervous tick.
Re: Lets talk about eggs
Welcome back dear LB! I think of you often while caring for my elderly mom as you remained so faithfully by her side.
Both my 3/4 mother & 3/4 brother are long-term egg eaters. Prior to Julie's posting the Finnish study & prompted by Dr. Geiger's egg indictment, I halved by intake. Likely to be psychological, but I feel sharper eating those fresh, runny pastured eggs. My 69 y/o brother does everything wrong with the exception of daily eggs & golf.
Both my 3/4 mother & 3/4 brother are long-term egg eaters. Prior to Julie's posting the Finnish study & prompted by Dr. Geiger's egg indictment, I halved by intake. Likely to be psychological, but I feel sharper eating those fresh, runny pastured eggs. My 69 y/o brother does everything wrong with the exception of daily eggs & golf.