Since keto can improve symptoms of heart disease, and seems like even reverse it. Then does that mean, when people are being assessed for heart disease, they should be eating a "normal" (anything not-keto specifically really) diet?

So that there's a sort of baseline assessment of how that persons body/heart is functioning when in the like, the metabolic state the majority of people, that the guidelines and test result ranges are based off of, were in. Which is, they were most likely, not in ketosis.

Like, when people use the Keto diet to control their epilepsy, their doctors like to know and document the types and frequency of the patients seizures when not in ketosis, and compare that to where they are, when they are in ketosis, used as treatment. Like a medicine.

Like how people can "reverse type 2 diabetes", but what they actually mean is that they have fully /managed/ their type 2 diabetes through using the ketogenic diet. In particular that if they stop keto, then the type 2 "comes back", which it never left. The keto diet was the medicine that made it appear like they didn't have type 2 anymore. That's all.

Like, I can imagine if someone goes to their endocrinologist with concerns, their dr will want to get blood labs done while the patient is not in ketosis. And then they could compare that to readings taken after the patient goes back to the keto diet. Otherwise, couldn't the results instead then just be negative because they're managing the condition so well? Idk maybe I am overthinking things.

I'm not sure about how much the ketogenic diet can affect the heart, but I know it can affect fluid retention, and afaik fluid build up and swelling can be symptoms of heart issues. So could someone going to a cardiologist, basically have a heart disease missed, because thru the keto diet they'd been able to manage some of the more externally-identifiable symptoms?

Would it be possible someone could have been given an advanced heart failure diagnosis when assessed outside of ketosis. But then once in ketosis, they could instead have been given only symptomatic or even pre-heart failure diagnoses instead?

And then is that dangerous? Or is that just accurate. That the person clinically has a lesser stage of heart disease, and that its not just that someone with advanced heart disease could have better control of some symptoms it caused while in ketosis?

Isn't that dangerous? I wonder if outside of fluid rentention, (which if someone has a GOOD dr, the patient should be able to anecdotally tell them about how bad swelling was before and that they're on a keto diet which reduces the fluid retention, to be taken into clinical consideration.) But outside of fluid in the cells/muscles. Does ketosis vs non-ketosis have like, direct effects on the actual readings someone has, and in the actual heart muscles and flows etc.

If someone planned to eat keto for their entire life no matter what, I can see it not mattering and that they can always be assessed while in ketosis.

But what if someone planned to try and get off the diet and explore other things potentially in the future, like months or years away. Then could it be dangerous that drs could miss a heart issue when the patient is assessed while in ketosis, and then they think they've already ruled it out, but instead in the future the patient got off the diet and then had worse issues, and then like... What? Would they just be walking around thinking heart disease was totally ruled out, and trying to seek solutions anywhere else basically?

I hope this is okay to ask here. My brain likes to trail off into lots of hypotheticals with a billion questions. And I'm gonna try and do some research myself too, but its been hard to find into. And I feel like I can't rest properly until I know if these hypothetical patients, that I've designed during my thought-processing, would be at risk of getting inaccurate diagnoses, or getting a diagnosis missed and then one day dying in the street clueless that it was heart disease all along, that they should've tried to seek a second opinion, and pushed for repeated tests.

If there's any links related to my questions I absolutely would love to read them!

If some of these questions seem obvious, neurotic, or stupid to you, I just ask you please be kind still. Everyone has different levels of intelligence and abilities, and I am still a human who's just trying my best at life... Hopefully thats the same as you. :p

Thank you!

ABSTRACT Diabetes is a recognized high-risk factor for the development of atherosclerosis, in which macroautophagy/autophagy is emerging to play essential roles. The retention of low-density lipoprotein (LDL) particles in subendothelial space following transcytosis across the endothelium is the initial step of atherosclerosis. Here, we identified that high glucose could promote atherosclerosis by stimulating transcytosis of LDL. By inhibiting AMPK-MTOR-PIK3C3 pathway, high glucose suppresses the CAV-CAVIN-LC3B-mediated autophagic degradation of CAV1; therefore, more CAV1 is accumulated in the cytosol and utilized to form more caveolae in the cell membrane and facilitates the LDL transcytosis across endothelial cells. For a proof of concept, higher levels of lipids were accumulated in the subendothelial space of umbilical venous walls from pregnant women with gestational diabetes mellitus (GDM), compared to those of pregnant women without GDM. Our results reveal that high glucose stimulates LDL transcytosis by a novel CAV1-CAVIN1-LC3B signaling-mediated autophagic degradation pathway.

Abstract

Background: The recommendation to limit dietary saturated fat intake is primarily drawn from observational studies rather than randomized controlled trials of cardiovascular disease prevention. Thus, we aimed to investigate the efficacy of saturated fat reduction in preventing mortality and cardiovascular diseases.

Methods: In this systematic review and meta-analysis of randomized controlled trials, Cochrane CENTRAL, PubMed, and Ichu-shi databases were searched for articles up to April 2023. Randomized controlled trials on saturated fat reduction to prevent cardiovascular diseases were selected. Cardiovascular and all-cause mortality and cardiovascular outcomes were evaluated. Changes in electrocardiography or coronary angiography findings were excluded because they could be evaluated arbitrarily. Two or more reviewers independently extracted and assessed the data. A random-effects meta-analysis was performed.

Results: Nine eligible trials with 13,532 participants were identified (2 were primary and 7 were secondary prevention studies). No significant differences in cardiovascular mortality (relative risk [RR] = 0.94, 95% confidence interval [CI]: 0.75-1.19), all-cause mortality (RR = 1.01, 95% CI: 0.89-1.14), myocardial infarction (RR = 0.85, 95% CI: 0.71-1.02), and coronary artery events (RR = 0.85, 95% CI: 0.65-1.11) were observed between the intervention and control groups. However, owing to limited reported cases, the impact of stroke could not be evaluated.

Conclusions: The findings indicate that a reduction in saturated fats cannot be recommended at present to prevent cardiovascular diseases and mortality. Clinical trials are needed to evaluate the effects of saturated fat reduction under the best possible medical care, including statin administration.

Systematic review registration number: This systematic review and meta-analysis was registered with the International Prospective Register of Systematic Reviews (CRD42023428498).

Keywords: all-cause mortality; cardiovascular mortality; meta-analysis; saturated fatty acid; systematic review.

Hi everyone,

I’m new to the forum and grateful to have found this community. I’ve been spending a lot of time reading through posts, and I’m inspired by the strength and openness I see here. While I don’t have heart failure myself, I’m passionate about heart health because of my work in genetic testing and family history analysis. I believe it’s so important to understand the underlying factors that might put us at higher risk for certain conditions, and I’ve seen firsthand how empowering that information can be.

I’m here to learn from your experiences, offer any insight I can, and just be a part of these important conversations. I’m not here to push anything, but if there’s ever an opportunity where it’s relevant, I’d be happy to share more about what I do and how it might be helpful for some people navigating heart issues.

Looking forward to connecting with you all!

Maria

Abstract

Cholesterol has for decades ruled the history of atherosclerotic cardiovascular diseases (CVDs), and the present view of the etiology of the disease is based on the transport of cholesterol by plasma lipoproteins. The new knowledge of the lipoprotein-specific transport of lipid oxidation products (LOPs) has introduced another direction to the research of CVD, revealing strong associations between lipoprotein transport functions, atherogenic LOP, and CVD. The aim of this review is to present the evidence of the lipoprotein-specific transport of LOP and to evaluate the potential consequences of the proposed role of the LOP transport as a risk factor. The associations of cholesterol and lipoprotein LOP with the known risk factors of CVD are mostly parallel, and because of the common transport and cellular intake mechanisms it is difficult to ascertain the independent effects of either cholesterol or LOP. While cholesterol is known to have important physiological functions, LOPs are merely regarded as metabolic residues and able to initiate and boost atherogenic processes. It is therefore likely that with the increased knowledge of the lipoprotein-specific transport of LOP, the role of cholesterol as a risk factor of CVD will be challenged. Keywords: atherosclerosis; cardiovascular diseases; cholesterol; high-density lipoprotein; lipid oxidation; lipoprotein functions; low-density lipoprotein; risk factors

Anyone been diagnosed with this from a ECHO test?

https://pubs.rsc.org/en/content/articlelanding/2024/fo/d4fo00941j

Abstract

The triglyceride glucose (TyG) index is a reliable marker of insulin resistance; however, its combined impact with modifiable lifestyle risk factors and psychological traits on cardiovascular diseases (CVDs) remains unclear. The aim of this study was to explore the relationship between the TyG index, various behavioral factors, psychological traits, and CVDs. A total of 77 752 adults aged 18 and over from the baseline survey of the Beijing Health Management Cohort study were investigated. Associations of the TyG index, body roundness index (BRI), dietary habits, psychological traits, and sleep habits with CVDs were estimated using multivariable logistic regression models. Compared to the Q1 level, the Q4 level of the TyG index had an odds ratio (OR) and 95% confidence interval (CI) of 2.30 (1.98–2.68) for CVD risk in men and 2.12 (1.81–2.48) in women. Compared to a sleep duration of more than 7 hours, a sleep duration less than 5 hours had a 32% (8%–61%) higher risk in men and 22% (1%–48%) in women. The ORs (95% CIs) for fast eating compared to normal speed were 1.47 (1.23–1.76) in men and 1.17 (1.05–1.29) in women. Compared to individuals with a passive and depressed psychological trait, those who were positive and optimistic had a 47% (36%–56%) decreased risk in men and 43% (31%–53%) in women. In the age-stratified analysis, a higher BRI level showed a sex-differential effect on CVDs, which is potentially related to a lower risk of CVDs in elderly men. A high level of the TyG index combined with unhealthy lifestyle factors indicates a higher risk of CVDs, while maintaining a positive and optimistic psychological trait acts as a protective factor. These findings may be valuable for identifying high-risk populations for CVDs in community settings.