HEART AND HEART HEALTH

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What is a heart attack?

Life style and the heart

What Is a Heart Attack?
Your heart is an extraordinary organ that can function even when detached from your body as long as it is supplied with an adequate amount of oxygen. It works relentlessly to pump blood throughout your body and beats nearly 100,000 times every day, So it is crucial the muscle receives enough oxygenated blood and nutrients or it can die.
Plaque buildup in your arteries or narrowing of arteries, blocking the blood flow to the heart are a common reason to detrimental loss of blood supply to the heart.
Although sometimes used interchangeably, a heart attack and cardiac arrest are two different occurrences. Sudden, unexpected cardiac arrest is the third leading cause of death in the U.S. but it is different from a heart attack.
The most immediate and recognizable difference is that a heart attack victim will remain conscious with their heart beating, while someone who suffers a sudden cardiac arrest will be unconscious with no discernible heartbeat.
While a heart attack affects the oxygen supply to the heart muscle, cardiac arrest affects the electrical impulses. During a heart attack, part of the heart may have a reduction in oxygen supply if the blood is restricted, but the remaining areas of the muscle will continue to beat
Still, a heart attack can easily trigger a cardiac arrest! A loss of oxygen supply to the heart muscle from a heart attack affects the electrical impulses and may trigger a cardiac arrest.
During a cardiac arrest, the electrical system is impacted by physical conditions, such as cardiomyopathy, heart failure or arrhythmias.
This is perhaps the most common reason for a sudden cardiac arrest.

Life style and the heart
The biological aging of the heart is a major risk factor, but what exactly it consists of? Lifestyle-based prediction model for the prevention of CVD (CardioVasearscular Disease) is too "simplistic" as a guide for daily actions. A review at the molecular level -
what exactly is happening in our heart cells that impacts heart aging, brings some very practicals results in terms of what can we do to improve:

Heart Aging and the Role of SIRT2 Protein

A research published in Nature, focuses on the role of a protein called SIRT2 (a member of the sirtuin protein family) in the aging of the heart.

It turns out that as we age, the level of this protein in the heart decreases. The researchers (in the article) showed two things that show how the presence of SIRT2 is related to the aging of the heart:

If you engineer heart cells so that the level of SIRT2 will be lower, you get young cells...with the function of old cells. In other words, lowering the level of this protein is enough to accelerate the aging of heart cells.
If you increase the level of SIRT2 in older heart cells, you reduce the symptoms of aging, even though the cells are already older!!! Consider it as the molecular fountain of youth of the heart!

Raising the level of SIRT2 in the heart.

As it turns out, there are some everyday things that increase the activity of SIRT2:

Fasting: Fasting and caloric restrictions are well-known triggers of several members of the sirtuin family, including SIRT2[1][2].
Turmeric (Curcumin): It turns out that one of the things it does very well is activate the sirtuins. For example, Research on worms showed that turmeric extends their life (the bottom line in improving health), and that this beneficial effect depends on the production of SIRT2.

In relation to turmeric, it is important to note that consuming it with black pepper, improves its absorption significantly, 20 times, so it is recommended to do it

More about SIRT2: It is a protein that regulates the action of other proteins by their deacetylation, namely - "peeling off" of a small molecule called acetyl, a molecule that plays a central role in those protein's cellular metabolism (Read more below), proteins that serve as a key intermediaries in numerous metabolic pathways[1][2]. Its primary functions include:

Energy production: Acetyl-CoA enters the citric acid cycle (Krebs cycle) in mitochondria, where it is oxidized to generate ATP, NADH, and FADH2[1][5].
Lipid synthesis: In the cytoplasm, acetyl-CoA acts as a building block for fatty acid and cholesterol synthesis[2][4].
Protein acetylation: Acetyl-CoA serves as a substrate for histone acetyltransferases (HATs), influencing gene expression through histone acetylation[2][3].
Ketone body production: In the liver, mitochondrial acetyl-CoA is used to synthesize ketone bodies during periods of carbohydrate scarcity[5].
Carbohydrate metabolism: Acetyl-CoA is produced from the breakdown of glucose through glycolysis and pyruvate dehydrogenase complex activity[1][6].
Amino acid metabolism: Acetyl-CoA participates in the metabolism of certain amino acids[4].

A healthy diet - protecting and improving the gut microbiota we already discussed at length the importance of our diet as a preventive measure. "Taking care" of our heart is no exception. These two scientific articles are just another corroboration of this element:

The Role of Gut Microbiota on Insulin Resistance

Role and Effective Therapeutic Target of Gut Microbiota in Heart Failure,

Additional parameters:

Normal body mass index (BMI)
Getting at least 2.5 hours of exercise each week and watching television seven or fewer hours per week
Avoiding smoking

Limiting alcohol to one drink or less per day.

Heart Aging and the Role of SIRT2 Protein

A Healthy Diet

Cholesterol and heart condition

Cholesterol and heart conditions:
Cholesterol has been a highly publicized "scapegoat" for causing heart disease for decades. As a result, many have diligently cut all cholesterol-rich foods (which are often also nutrient-rich foods) from their diets.
As precautionary measure, more than 1 in 4 Americans over 45 take cholesterol-lowering statin drugs at the behest of their physicians, despite their lengthy list of side effects and dubious effectiveness. and the underlying question that is: do we really need to be worried about cholesterol?

The problem is not cholesterol levels but rather the development of insulin resistance (IR)!
Insulin resistance is strongly associated with cardiovascular diseases (CVD). Insulin resistance, characterized by the body's decreased response to insulin, leads to several metabolic alterations that contribute to the development of CVD. IR is a condition encompassing hyperglycemia and compensatory hyperinsulinemia. It occurs when insulin is not capable of exerting its maximum effects on target tissues, including skeletal muscles, liver and adipose tissue. This alteration of insulin signaling pathways results in the development of cardiometabolic disorders, including obesity, dyslipidemia, low-grade inflammation, endothelial dysfunction and hypertension, all of which are predisposing factors for atherosclerosis and CVD.

Some facts about cholesterol:
Cholesterol is important to our body! our liver makes about three-quarters or more of your body's cholesterol—that's how important it is.
Many of the healthiest foods happen to be rich in cholesterol (and saturated fats), yet cholesterol has been demonized since the early 1950s following the popularization of Ancel Keys' flawed research.
Is high total cholesterol and/or elevated low-density lipoprotein (LDL) cholesterol indicative of elevated heart disease risk? With regard to total cholesterol, as far back as 1977, with the publication of the Framingham Study, no correlation between heart disease and total cholesterol could be found.
Further research showed that the problem is not cholesterol but oxidized LDL.

“Is the oxidized LDL a bad player?” Ali asks, “[or] is it there to protect us from oxidative injury? Rather than letting the important cells get oxidized, is the LDL sacrificing itself in protecting the body? Then, your whole paradigm changes ...

LDL is not a bad player — it’s trying to protect us. What I need to figure out is how do I prevent this oxidative injury in the first place, and an argument that should surface is that, maybe I should have more LDL around so that oxidative injury can be ... prevented, rather than having less LDL? These are the kinds of fundamental questions that science should be asking.”

Note the link between polyunsaturated fats (PUFAs), lipoprotein(a) [Lp(a)], and oxidized low-density lipoprotein (LDL) - the higher PUFA level in the blood, the higher the levels of arachidonic acid in plasma, which is linked to elevated Lp(a) concentrations.

"The primary way to prevent atherosclerosis, then, is to radically reduce your LA (Linoleic Acid) intake by eliminating seed oils from your cooking, and avoiding processed foods (which are loaded with seed oils) and restaurant foods (as most are cooked in seed oils)."

Cholesterol has many health benefits. It plays a key role in regulating protein pathways involved in cell signaling and may also regulate other cellular processes, for instance.
It's already known that cholesterol plays a critical role within your cell membranes, but research suggests cholesterol also interacts with proteins inside our cells.
Cholesterol is one of the molecules that allow for these interactions to take place. For example, cholesterol is the precursor to bile acids, so without sufficient amounts of cholesterol, your digestive system can be adversely affected.
It also plays an essential role in our brain, which contains about 25 percent of the cholesterol in our body. It is critical for synapse formation, i.e. the connections between your neurons, which allow us to think, learn new things, and form memories.

Some facts about cholesterol

Cholesterol and our diet

Cholesterol blood Level and our diet

Cholesterol level is not the result of what we eat! The regulation of HDL and LDL cholesterol levels involves several interconnected body mechanisms:

The biggest factor in cholesterol is not diet but genetics or heredity. Our liver is designed to remove excess cholesterol from our body, but genetics play a large part in our liver's ability to regulate cholesterol to a healthy level.

Take, for instance, people with genetic familial hypercholesterolemia. This is a condition characterized by abnormally high cholesterol, which tends to be resistant to lowering with lifestyle strategies like diet and exercise.

Further, eating nutritious cholesterol-rich foods is not something we should feel guilty about; they're good for us and will not drive up our cholesterol levels as we may have been told.

To date, extensive research did not show evidence to support a role of dietary cholesterol in the development of CVD. It is worth noting that most foods that are rich in cholesterol are also high in saturated fatty acids and thus may increase the risk of CVD due to the saturated fatty acid content.

What is the "Right" Cholesterol Level:

In recent years, there is a growing number of studies that show that higher cholesterol levels of both HDL and LDL types are associated with prolonged life expectancy [REF1], [REF2]. Not only that cholesterol levels of 252 mg/dl were found to be associated with prolonged life expectancy, but there are many articles [REF3], [REF4], [REF5] that presents the rational for these findings.

Bottom line, cholesterol level is a body "built in" response to various nutritional and other health conditions (like chronic inflammation, insulin resistance and more) and therefore it makes no sense to take medications to lower the cholesterol level (which impedes the body's positive reactions), rather than dealing with the issues that triggered this reaction.

Insulin Resistance

"Multiple studies have demonstrated that insulin resistance is a strong predictor of atherosclerotic cardiovascular (CV) disease (ASCVD) and have been summarized in a recent meta-analysis by Gast et al".

Insulin resistance (IR) has profound implications for vascular health, contributing to both functional and structural damage in blood vessels. Below is an overview of its effects:

Impaired endothelial function (the control of blood fluidity, platelet aggregation and vascular tone): Insulin resistance is associated with endothelial dysfunction, which is characterized by reduced production of nitric oxide, increased inflammation, and oxidative stress in the endothelial cells lining blood vessels. Endothelial dysfunction limits the ability of the blood vessels to repair damage caused by blood vessels inflammation, as it interferes with the normal processes of the widening of blood vessels (vasodilation) and the recruitment of repair cells to damaged areas.
Decreased nitric oxide production: Insulin resistance can lead to decreased production of nitric oxide, a molecule that plays a key role in maintaining the health and function of blood vessels. Nitric oxide helps to regulate vascular tone, inhibit platelet aggregation, and prevent leukocyte adhesion to the endothelium (a single layer of cells, called endothelial cells, which line all your blood vessels and lymphatic vessels). Reduced nitric oxide levels impair the ability of blood vessels to respond to injury and promote repair processes.
Pro-inflammatory state: Insulin resistance is associated with a chronic low-grade inflammatory state characterized by elevated levels of inflammatory cytokines and chemokines. This systemic inflammation can further damage the endothelium and impair repair mechanisms in response to inflammation induced injury. Additionally, inflammation promotes the development and progression of atherosclerosis, further compromising vascular repair.
Hyperglycemia-induced damage: Insulin resistance is often associated with hyperglycemia (high blood sugar levels), which can lead to the formation of advanced glycation end products (AGEs). AGEs contribute to endothelial dysfunction, oxidative stress, and inflammation, all of which impair the ability of the cardiovascular system to repair damage caused by inflammation.

Overall, insulin resistance contributes to a pro-atherogenic environment characterized by endothelial dysfunction, inflammation, dyslipidemia, and hyperglycemia, which collectively limit the ability of the cardiovascular system to repair damage caused by blood vessels inflammation, and promote the progression of atherosclerosis and cardiovascular disease.

"The molecular etiology (etiology = attribution of the cause or reason for something) of the insulin resistance directly contributes to the development of atherosclerotic cardiovascular disease by inhibiting nitric oxide production (endothelial dysfunction) and stimulating the MAPK pathway".

In conclusion of the above section, lowering insulin resistance is the most important action to reduce CHD risk! Our recommended diet, that includes intermittent fasting and physical exercises is most likely to provide the desired results.

STATINS

"Of note despite the ability of statins to lower LDL-C, non-HDL-C, and apolipoprotein B levels, statins do not lower Lp(a) (Lipoprotein (a)) levels and may even increase levels (10,11). Finally, statins modestly increase HDL-C levels (8,12,13). In most studies HDL-C levels increase between 5-10% with statin therapy".

Statins May Make Heart Health Worse

There is evidence showing that statins may worsen heart health, and only appear effective due to statistical deception. One scientific study concludes: "Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms". Another study brings this conclusion: "How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease"
This study shows that "Use of the statin medications routinely result in lower coenzyme Q10 (CoQ10) levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies." "Myopathies are a heterogeneous group of disorders primarily affecting the skeletal muscle structure, metabolism, or channel function. They usually present with muscle weakness interfering in daily life activities. Muscle pain is also a common finding and some myopathies are associated with rhabdomyolysis".

CoQ10 is crucial for efficiently transferring electrons within the mitochondrial oxidative respiratory chain and producing adenosine triphosphate (ATP). ATP is a coenzyme used as an energy carrier in every cell of our body. When we consider that our heart is the most energy-demanding organ in our body, we can surmise how potentially devastating it can be to deplete our body's main source of cellular energy.

So while one of statins' claims to fame is warding off heart disease, scientific studies show that they actually increase our risk of depleting our body of CoQ10.

The depletion of CoQ10 caused by the drug is why statins can increase our risk of acute heart failure.

Statins, Cholesterol Reduction and Myelin

Given the discussion in this section about the importance of cholesterol for the production of myelin, and the importance of myelin to cognitive functioning, it is not surprising that dementia and altzheimer disease rapidly increased with the expansion of statins usage as shown by these numbers from QuickStats: "Age-Adjusted Death Rates for Alzheimer Disease Among Adults Aged ≥65 Years, by Sex — National Vital Statistics System, United States, 1999–2019. The age-adjusted death rate for Alzheimer disease increased from 128.8 per 100,000 in 1999 to 233.8 in 2019.23 (Apr 2021)"

Anyone who takes a statin drug, MUST take Coenzyme Q10 as a supplement. For those who are over 40, it is strongly recommend to take ubiquinol (CoQ10's reduced form) instead of CoQ10, as it's far more effectively absorbed by our body.

What is the "right" Cholesterol Level

Statins May Make Heart Health Worse

Insulin Resistance

Statins, Cholesterol Reduction and Myelin

Inflammation and Heart Desease

Thyroid Health and Heart Disease

Additional indicators to assess heart disease risk:

Fasting insulin level test: The normal fasting blood insulin level after a night of fasting varies, but generally falls within the range of 2-12 μU/mL (or μIU/mL) for the general population.
Excess fat, particularly around our belly, is one of the major contributors to heart disease,
Fasting blood sugar level test: This test measures your blood sugar after an overnight fast (not eating). The normal blood sugar level after a night of fasting (typically 8 hours or more) is between 70 to 99 mg/dL (3.9 to 5.5 mmol/L)
"Coronary-heart-disease (CHD) mortality was approximately doubled for subjects with inpaired glucose tolerance (IGT), defined as a blood-sugar above the 95th centile (greater than or equal to 96 mg/dl)".
Iron level: Iron can be a very potent oxidative stress, excess iron levels can damage blood vessels and increase the risk of heart disease. Ideally, ferritin levels should be monitored to make sure that they are not much above 80 ng/ml. The simplest way to lower elevated iron level, is to donate blood. If that is not possible, a therapeutic phlebotomy can effectively eliminate the excess iron from our body.

Inflammation and Heart Disease

Inflammation may promote the growth of plaques, loosen plaque in your arteries and trigger blood clots — the primary cause of heart attacks and strokes. When a blood clot blocks an artery to the heart, you have a heart attack.

Thyroid Health and Heart Disease

Thyroid hormone (TH) has a fundamental role in cardiovascular homeostasis in both physiological and pathological conditions, influencing cardiac contractility, heart rate, diastolic function and systemic vascular resistance through genomic and non-genomic mediated effects. In heart failure the main alteration of thyroid function is referred to as "low-triiodothyronine syndrome" characterized by decreased total serum (T3) and free T3 with normal levels of thyroxine and thyrotropin.

Patients with baseline or new-onset abnormal thyroid function had a higher mortality than those with normal thyroid function, even after controlling for other known mortality predictors.

Vascular oxidative stress and inflammation are major determinants of endothelial function. "Endothelial dysfunction is an early predictor of atherosclerosis and future cardiovascular events"! Endothelial dysfunction is a type of non-obstructive coronary artery disease in which there are no heart artery blockages, but the large blood vessels on the heart's surface constrict (narrow) instead of dilating (opening). This condition tends to affect more women than men and causes chronic chest pain.

Patients with baseline or new-onset abnormal thyroid function had a higher mortality than those with normal thyroid function, even after controlling for other known mortality predictors.

Additional indicators to assess heart disease risk