“ Background— Coronary artery calcium (CAC) has been demonstrated to be associated with the risk of coronary heart disease. The Multi-Ethnic Study of Atherosclerosis (MESA) provides a unique opportunity to examine the distribution of CAC on the basis of age, gender, and race/ethnicity in a cohort free of clinical cardiovascular disease and treated diabetes.
Methods and Results— MESA is a prospective cohort study designed to investigate subclinical cardiovascular disease in a multiethnic cohort free of clinical cardiovascular disease. The percentiles of the CAC distribution were estimated with nonparametric techniques. Treated diabetics were excluded from analysis. There were 6110 included in the analysis, with 53% female and an average age of 62 years. Men had greater calcium levels than women, and calcium amount and prevalence were steadily higher with increasing age. There were significant differences in calcium by race, and these associations differed across age and gender. For women, whites had the highest percentiles and Hispanics generally had the lowest; in the oldest age group, however, Chinese women had the lowest values. Overall, Chinese and black women were intermediate, with their order dependent on age. For men, whites consistently had the highest percentiles, and Hispanics had the second highest. Blacks were lowest at the younger ages, and Chinese were lowest at the older ages. At the MESA public website (http://www.mesa-nhlbi.org), an interactive form allows one to enter an age, gender, race/ethnicity, and CAC score to obtain a corresponding estimated percentile.
Conclusions— The information provided here can be used to examine whether a patient has a high CAC score relative to others with the same age, gender, and race/ethnicity who do not have clinical cardiovascular disease or treated diabetes.”
https://www.ahajournals.org/doi/10.1161/circulationaha.105.580696
I’m 32F, 165cm (5’5”), 54kg (120lbs), caucasian.
Six months ago, I had what seemed like a heart attack and went to the ER. It was determined to be a panic attack, but I was tachycardic and my blood pressure was 150/110. (My typical blood pressure, measured at GP appointments, is somewhere around 110/70.) I was prescribed 50mg metoprolol daily to help control the panic attacks. I have recently been trying to wean myself off of the metoprolol, as it seems to be causing some unfortunate side effects (hair loss). I am also taking hormonal contraceptives.
I had an ultrasound today, to check out my abdominal aorta because I had been feeling a pulsating mass around the umbilical area. I took 50mg of metoprolol this morning, three hours prior to the ultrasound. The aorta was fine, but the velocity of blood moving in the proximal common iliac arteries was DOUBLE that in the distal abdominal aorta. 50% stenosis of the iliac arteries is therefore indicated, and tomorrow I must schedule a CT scan to confirm a diagnosis of atherosclerosis of the iliac arteries.
Wait, what?!
I have no family history of atherosclerosis before age 65. I exercise regularly, eat healthily, have never been overweight, and don’t have high cholesterol, diabetes, or high blood pressure. I smoked cigarettes for a bit in college, but quit many years ago. My dad, a lifelong pack-a-day smoker in his fifties, has no atherosclerosis. My mother has none either. I don’t drink alcohol, nor partake of recreational drugs.
The blockage has caused no noticeable symptoms, and my leg strength and stamina are as good as always. I don’t get any pain in my legs unless I have spent the day in high heels (I have flat feet, so that’s to be expected). I run, hike, and walk quite a lot, and haven’t noticed any of those things getting harder over the years. My weight has been stable. The only thing I noticed was different was the sudden anxiety and panic, which I figured was brought on by some stressful life circumstances.
My GP is utterly perplexed and rather concerned, which of course has me freaking the heck out. So I was hoping that maybe some of you wonderful folks would have some ideas of what might be going on here. I know I have to wait for the CT (and probably an angiogram too) to get any real answers, but I’m painfully curious as to what the possibilities might be. I can’t find any information online about this kind of thing afflicting otherwise healthy 30-somethings, so I haven’t a clue. Why the heck
... keep reading on reddit ➡https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/
Characteristics of herbivores and carnivores, causes of atherosclerosis, serum cholesterol and atherosclerosis, reductions in LDL from reduction in fat in diets, and statins.
I was curios about the life expectancy on ZC. So I looked into the health of the eskimo before they were influenced by modern culture and found this paper from 1993 by M R Zimmerman MD PhD
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC325106/?page=1
While doing an autopsy on Alaskan mummies they found atherosclerosis and severe osteoporosis. Of course they blame their diet.
I'm a big fan of ZC but this information has me a bit worried. Any thoughts on the topic? Thanks
I'm on day two of working on a lady with horrific atherosclerosis (hardening of the arteries). It's a six point, but it's so bad that when I've tried to inject the femoral, the fluid shoots back up. There's very little drainage, etc. And of course this is a body that is going to be shipped internationally, so a quick burial is not happening. First time I've cried in the prep room in awhile... yay. I guess I'm just looking for a little empathy from some others who have been there, because this royalty sucks...
https://youtu.be/alZ47dgu3LU
I found this a very insightful talk on the pathogenesis of atherosclerosis. It certainly filled in some gaps in my understanding and put other information in perspective. Worth a watch for those interested.
Basic idea: Instead of AS being caused by high blood LDL levels increasing LDL transport from the lumen into the intima (inside out) where it gets stuck and oxidized, AS is caused by endothelial damage which leads to thickening of the wall which triggers vaso vasorum proliferation into the intima where LDL can now infiltrate. Consequently the root cause of AS is not blood LDL levels but IR, hypertension, systemic inflammation, etc.
Factors that can be improved on a ketogenic diet.
Edit: I think this is the relevant article: https://www.sciencedirect.com/science/article/pii/S1359644616301921?via%3Dihub
What are your opinions on the theory that well-intentioned calcium supplementation has actually caused vascular calcification and thereby a significant amount of strokes, heart attack and dementia?
https://doi.org/10.1002/advs.202003410
https://pubmed.ncbi.nlm.nih.gov/33977048
Abstract
Atherosclerosis is a chronic inflammatory disease that can cause acute cardiovascular events. Activation of the NOD-like receptor family, pyrin domain containing protein 3 (NLRP3) inflammasome enhances atherogenesis, which links lipid metabolism to sterile inflammation. This study examines the impact of an endogenous metabolite, namely ketone body 3-hydroxybutyrate (3-HB), on a mouse model of atherosclerosis. It is found that daily oral administration of 3-HB can significantly ameliorate atherosclerosis. Mechanistically, 3-HB is found to reduce the M1 macrophage proportion and promote cholesterol efflux by acting on macrophages through its receptor G-protein-coupled receptor 109a (Gpr109a). 3-HB-Gpr109a signaling promotes extracellular calcium (Ca^(2 ) ) influx. The elevation of intracellular Ca^(2 ) level reduces the release of Ca^(2 ) from the endothelium reticulum (ER) to mitochondria, thus inhibits ER stress triggered by ER Ca^(2 ) store depletion. As NLRP3 inflammasome can be activated by ER stress, 3-HB can inhibit the activation of NLRP3 inflammasome, which triggers the increase of M1 macrophage proportion and the inhibition of cholesterol efflux. It is concluded that daily nutritional supplementation of 3-HB attenuates atherosclerosis in mice.
------------------------------------------ Info ------------------------------------------
Open Access: True
Authors: Shu‐jie Zhang - Zi‐hua Li - Yu‐dian Zhang - Jin Chen - Yuan Li - Fu‐qing Wu - Wei Wang - Zong Jie Cui - Guo‐Qiang Chen -
Additional links:
https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/advs.202003410
https://www.nature.com/articles/s41598-021-86324-w
- Article
- Open Access
- Published: 12 April 2021
Intake of food rich in saturated fat in relation to subclinical atherosclerosis and potential modulating effects from single genetic variants
- Federica Laguzzi,
- Buamina Maitusong,
- Rona J. Strawbridge,
- Damiano Baldassarre,
- Fabrizio Veglia,
- Steve E. Humphries,
- Rainer Rauramaa,
- Sudhir Kurl,
- Andries J. Smit,
- Philippe Giral,
- Angela Silveira,
- Elena Tremoli,
- Anders Hamsten,
- Ulf de Faire,
- Bruna Gigante,
- Karin Leander &
- IMPROVE Study group
Scientific Reports volume 11, Article number: 7866 (2021) Cite this article
Abstract
The relationship between intake of saturated fats and subclinical atherosclerosis, as well as the possible influence of genetic variants, is poorly understood and investigated. We aimed to investigate this relationship, with a hypothesis that it would be po
... keep reading on reddit ➡I want to take calcium supplements, but I'm afraid of atherosclerosis. Because my father has a history of heart attack. Is there anything you could recommend to avoid atherosclerosis while taking calcium supplements? Does using only K2 work?
Bad diet for a decades and cleaned up and quit eating fried foods and so on, now I am curious if there are any atherosclerosis reversing peptides. Thanks.
Sek Kathiresan discusses his research on "The Long Run" podcast with Luke Timmerman:
The NYT wrote about the research last summer:
https://www.nytimes.com/2020/06/27/health/heart-disease-gene-editing.html
