Statins and Dementia studies

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Julie G
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Re: Statins and Dementia studies

Post by Julie G »

A couple of monthes ago I tested it again and LDL was 100. I think it's because I started cooking with saturated fat (ghee). In the past I used olive oil, but I hear more and more doctors (like dr Paul Mason) saying we shouldn't use olive oil to cook because it oxidises easily.
Opinions vary re. using olive oil for cooking. I reserve it to finish vegetables and salads to preserve the healthful polyphenols. That said, it still has a smoke point of 425F. Ghee, surprisingly, has a very low smoke point of 350F, so isn't great for cooking. Avocado oil seems to be the best choice as a cooking oil as it has a very high smoke point of 510F and is great for lipids as well.
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Re: Statins and Dementia studies

Post by Maria4/4 »

Plumster wrote: Tue Feb 20, 2024 8:57 am An LDL of approximately 70 is great, but not particularly low -- except maybe for an e4.

LDL and apoB are the measurements to pay attention to. Optimal apoB is 40-80, ideally below 62.

I would like to discourage you from attempting to raise either LDL or apoB.
Thanks, Plumster for your valuable inputs.

I used to monitor my LDL and apoB, but I don't know anymore if it is relevant. Many doctors now recommend we just monitor the trig/HDL racio which is a good indicator of the presence of oxidized LDL (small particles), like dr Paul Mason in this interesting video: https://www.youtube.com/watch?v=rdgS3PuSuyg. He says "even when total LDL is low, the presence of small dense LDL predicts cardiac risk", which would make total LDL an irrelevant marker.

I also was shocked with this oreo study that proved that eating oreos is more efficient than a statin reducing LDL levels https://www.youtube.com/watch?v=L1mMnnyJrgk. During two weeks Nicholas Norwitz PhD (usually on a keto diet) ate 12 oreo cookies per day. In 16 days, his LDL went from 385 to 111 mg/dl. Does this mean he is healthier?

Honestly, I don t know what to think anymore 🤣 . What are your thoughts on these topics?
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Re: Statins and Dementia studies

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Julie G wrote: Tue Feb 20, 2024 10:58 am
A couple of monthes ago I tested it again and LDL was 100. I think it's because I started cooking with saturated fat (ghee). In the past I used olive oil, but I hear more and more doctors (like dr Paul Mason) saying we shouldn't use olive oil to cook because it oxidises easily.
Opinions vary re. using olive oil for cooking. I reserve it to finish vegetables and salads to preserve the healthful polyphenols. That said, it still has a smoke point of 425F. Ghee, surprisingly, has a very low smoke point of 350F, so isn't great for cooking. Avocado oil seems to be the best choice as a cooking oil as it has a very high smoke point of 510F and is great for lipids as well.
Thanks, Julie G, for your comment. I used to think exactly as you do, but I now hear a lot of doctors saying that the type of fat is the most important characteristic to consider when choosing a cooking fat. They say mono and polyunsaturated fats are very healthy raw. When they are heated, they become unstable. The result? They oxidize easily and inflame our bodies.
In this video [youtube]https://www.youtube.com/watch?v=CSqRqcwVH6E&t=2590s[/youtube] dr Paul Mason, Dr Peter Brukner and the dietary nutrition Nicole Moore explain this process and give several arguments to justify their thinking.
In this very interesting video [youtube]https://www.youtube.com/watch?v=4WPF3RMPI9k[/youtube] Dr Peter Brukner shows the graph below to justify why saturated fat couldn’t be the cause of the rise of heart disease and why vegetable oils could be the ones to blame.

Image

Dr Mark Hyman was the first person I heard say that we shouldn't cook with olive oil. He said he used to do this and had a lot of oxidized LDL (small dense particles). Then he replaced the olive oil with ghee and the oxidized LDL was extremely reduced (it was a maybe a year ago, so I don't remember in which video I saw this information, sorry).

I have to confess I am a little bit confused with all this conflicted information.
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Re: Statins and Dementia studies

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This topic had been very interesting to me for a long time. I am a Type 1 Diabetic that was diagnosed at age 47. When diagnosed, I was immediately put on 10 mg of Pravastatin to protect my heart, even though my cholesterol levels were normal. To protect my kidneys, I was prescribed an Ace Inhibitor (lisinopril) which helps control blood pressure even though my blood pressure was normal. Furthermore, I was told to take 5000 ug Vitamin D even though those levels were normal. In addition, insurance requires endocrinology appointments every 3 months including labs. Fast forward 24 years later, I enjoy excellent health including zero plaque everywhere they look. All of my laboratory parameters remain exactly the same for 24 years. When I asked my GP why I had zero plaque he was sure it was from taking a statin at middle age before there was any time for build up from elevated cholesterol. This made me wonder about using this special cohort of middle age Type 1 diabetics who were put on this same course of preventive medicine. I can imagine that there would be a lot of good info gleaned from this group who were given these meds before ever having the condition the drugs were used for. So far, every study regarding use of statins and its effect on dementia, uses patients who were diagnosed first with high cholesterol (obviously). The same is true for Ace Inhibitors and the studies linking its use to lower dementia rates. If I were wealthy, I would fund a study looking at this group of middle age long term preventive medicine users.
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Re: Statins and Dementia studies

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JulieAnnie wrote: Wed Feb 28, 2024 10:40 am This topic had been very interesting to me for a long time. I am a Type 1 Diabetic that was diagnosed at age 47. ... Fast forward 24 years later, I enjoy excellent health including zero plaque everywhere they look. All of my laboratory parameters remain exactly the same for 24 years. When I asked my GP why I had zero plaque he was sure it was from taking a statin at middle age before there was any time for build up from elevated cholesterol. This made me wonder about using this special cohort of middle age Type 1 diabetics who were put on this same course of preventive medicine. I can imagine that there would be a lot of good info gleaned from this group who were given these meds before ever having the condition the drugs were used for. So far, every study regarding use of statins and its effect on dementia, uses patients who were diagnosed first with high cholesterol (obviously). The same is true for Ace Inhibitors and the studies linking its use to lower dementia rates. If I were wealthy, I would fund a study looking at this group of middle age long term preventive medicine users.
The South Koreans looked at this for you in a national cohort. Although they don't distinguish between Type 1 and Type 2 diabetes, the results suggest you and your doctors made a great team 24 years ago.
We explored the association between cholesterol levels and dementia risk according to the presence of diabetes and statin use. In this population-based longitudinal cohort study, the Korean National Health Insurance Service datasets (2002–2017) were used. Among individuals aged ≥ 40 years who underwent health examinations in 2009 (N = 6,883,494), the hazard of dementia was evaluated according to cholesterol levels...It is reassuring that the lack of increase in the risk of dementia with LDL-C level in the lowest quartile or quintile was consistently observed in statin users, also in those with diabetes. In those with diabetes, moderate- or high-intensity statins would have been more frequently used than in the general population because recent guidelines have recommended statin therapy with adequate intensity regardless of baseline LDL-C level in people with diabetes. In this study, statin users with diabetes and LDL-C level in the lowest decile (LDL-C < 75 mg/dl) did not present increased risks of all-cause dementia.
Charts show benefits for risk of AD, vascular dementia and all-cause dementia by deciles (i.e the lowest 10% to the highest 10%)
Association between cholesterol levels and dementia risk according to the presence of diabetes and statin use: a nationwide cohort study
Image 2-28-24 at 1.55 PM.jpeg
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Re: Statins and Dementia studies

Post by Plumster »

Maria4/4 wrote: Sun Feb 25, 2024 1:24 pm
I used to monitor my LDL and apoB, but I don't know anymore if it is relevant.



Hi again Maria4/4, here is a reason to monitor LDL and ApoB:
Mendelian randomization reveals apolipoprotein B shortens healthspan and possibly increases risk for Alzheimer’s disease

Leah Martin, Brian B. Boutwell, Carmen Messerlian & Charleen D. Adams

Communications Biology volume 7, Article number: 230 (2024)


Abstract

Apolipoprotein B-100 (APOB) is a component of fat- and cholesterol-transporting molecules in the bloodstream. It is the main lipoprotein in low-density lipoprotein cholesterol (LDL) and has been implicated in conditions that end healthspan (the interval between birth and onset of chronic disease). However, APOB’s direct relationship with healthspan remains uncertain. With Mendelian randomization, we show that higher levels of APOB and LDL shorten healthspan in humans. Multivariable Mendelian randomization of APOB and LDL on healthspan suggests that the predominant trait accounting for the relationship is APOB. In addition, we provide preliminary evidence that APOB increases risk for Alzheimer’s disease, a condition that ends healthspan. If these relationships are causal, they suggest that interventions to improve healthspan in aging populations could include strategies targeting APOB. Ultimately, given that more than 44 million people currently suffer from Alzheimer’s disease worldwide, such interventions are needed.
Open access: https://www.nature.com/articles/s42003-024-05887-2
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Re: Statins and Dementia studies

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JulieAnnie wrote: Wed Feb 28, 2024 10:40 am This topic had been very interesting to me for a long time. I am a Type 1 Diabetic that was diagnosed at age 47. When diagnosed, I was immediately put on 10 mg of Pravastatin to protect my heart, even though my cholesterol levels were normal. To protect my kidneys, I was prescribed an Ace Inhibitor (lisinopril) which helps control blood pressure even though my blood pressure was normal. Furthermore, I was told to take 5000 ug Vitamin D even though those levels were normal. In addition, insurance requires endocrinology appointments every 3 months including labs. Fast forward 24 years later, I enjoy excellent health including zero plaque everywhere they look. All of my laboratory parameters remain exactly the same for 24 years. When I asked my GP why I had zero plaque he was sure it was from taking a statin at middle age before there was any time for build up from elevated cholesterol. This made me wonder about using this special cohort of middle age Type 1 diabetics who were put on this same course of preventive medicine. I can imagine that there would be a lot of good info gleaned from this group who were given these meds before ever having the condition the drugs were used for. So far, every study regarding use of statins and its effect on dementia, uses patients who were diagnosed first with high cholesterol (obviously). The same is true for Ace Inhibitors and the studies linking its use to lower dementia rates. If I were wealthy, I would fund a study looking at this group of middle age long term preventive medicine users.
Thank you so much for posting this, JulieAnnie. I am so happy for you that the strategies are working so well and for so long. The proactive treatment strategy, your adherence to it, and the results are very heartening. Thanks again for sharing.
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Re: Statins and Dementia studies

Post by JulieAnnie »

Somehow I'm not surprised that it was the South Koreans that looked at this group of diabetics on long term prevention protocols. My endocrinologist is South Korean and she runs of very tight ship in her practice. She also ran NMR Lipoprofile lab tests as soon as they became available in 2007. Thanks Plumster for finding the research study that confirmed my theory.
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Re: Statins and Dementia studies

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Statin Initiation and Risk of Incident Alzheimer Disease and Cognitive Decline in Genetically Susceptible Older Adults
is an online pre-print of an article in the April 9, 2024 edition of the journal Neurology that looked at whether starting statins in late-life for participants with both genetic risk (Apoe4) and historic risk as a racial group (61% non-Hispanic Black) makes a difference in changes on multiple cognitive assessments over time. Spoiler alert: It does; possibly also for the 39% who were not Black participants.

This is important, because most studies have very few participants from Black communities. The Rush Institute for Healthy Living in Chicago has a long-standing commitment to partnering with local communities of color to improve lifestyle prevention and identify risk and resilience factors for these communities, which may be applicable to other racial/ethnic groups as well.

Here is the abstract; the entire article is behind a paywall.
[Emphasis added]
METHODS: This population-based longitudinal cohort study was conducted in 4 urban communities in Chicago, IL, United States, consisting of 4,807 participants. Statin initiation is based on the inspection of medications during home assessments. Clinical diagnosis for incident AD used the NINCDS-ADRDA criteria, and longitudinal measurements of global cognition consisted of episodic memory, perceptual speed, and the Mini-Mental State Examination tests.

RESULTS: The study participants had a mean age of 72 years, consisting of 63% female individuals and 61% non-Hispanic Black individuals. During the study period, 1,470 (31%) participants reported statin initiation. In a covariate-adjusted competing risk model, statin initiation was associated with a reduced risk of incident clinical AD [hazard ratio (HR) 0.81 (95% CI 0.70-0.94)] compared with nonusers. This association was statistically significantly lower (p interaction = 0.015) among participants with the APOE ε4 allele [HR 0.60 (95% CI 0.49-0.74)] compared with those without the APOE ε4 allele [HR 0.96 (95% CI 0.82-1.12)]. The annual decline in global cognition (β = 0.021, 95% CI 0.007-0.034) and episodic memory (β = 0.020, 95% CI 0.007-0.033) was also substantially slower among participants with the APOE ε4 allele after statin initiation compared with nonusers. However, the association of statin initiation with cognitive decline was not significant among those without the APOE ε4 allele.

DISCUSSION: Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE ε4 allele. The benefits of statin therapy need further consideration in randomized clinical trials, especially among those with the APOE ε4 allele.
CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that among those aged 65 years or older, statin initiation was associated with a reduced risk of Alzheimer disease, especially in the presence of an APOE-e4 allele.
For those wondering what "Class II evidence" is, it refers to the need for evidence-based studies and criteria used to determine the strength of any study. Class II is the second best, per this source: Definition of Classes of Evidence (CoE) and Overall Strength of Evidence (SoE)
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Re: Statins and Dementia studies

Post by sahara »

new study:
Statin Initiation and Risk of Incident Alzheimer Disease and Cognitive Decline in Genetically Susceptible Older Adults
https://www.neurology.org/doi/10.1212/W ... 0000209168
Discussion: "Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE ε4 allele."
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