Hardening of Arteries(Atherosclerosis)
1 of the 12 leading causes ofhigh blood pressure, heart attacks and strokes
This may be hard to hear, but Atherosclerosis or hardening of your arteries started happening when you were just a child and just gets worse over time.
What are the stages of Atherosclerosis?
There are several stages of atherosclerosis (described below).
Each stage involves changes in your artery wall. These changes are so tiny that you can’t see most of them without a microscope. But they add up to cause serious damage to your artery.
The stages of atherosclerosis happen over many years. And they often go undetected.
Stage 1: Endothelial damage and immune response
Atherosclerosis begins when damage occurs to the inner layer of your artery wall from things like high LDL (bad) cholesterol, toxins like cigarettes or even just consistently high blood pressure.
Once damaged, cholesterol starts gathering at the site of the injury and becomes oxidized, causing an immune response which leads to inflammation in your artery.
Stage 2: Fatty Streaks
A “fatty streak” is formed when your body tries to repair itself. It sends white blood cells to consume the cholesterol which then take on a foamy appearance and die, which cause more white blood cells to be sent to the area which cause more damage. This is the beginning of plaque formation.
Stage 3: Plaque Growth
As more dead foamy cells build up at the site, the fatty streak gets bigger, forming a piece of plaque.
Your artery’s smooth muscle cells then form a layer over this area called a fibrous cap to help prevent the plaque from breaking off in your blood stream.
Unfortunately, the plaque keeps growing over time and other things like calcium join the plaque causing it to harden.
Your artery expands to accommodate this new plaque but can only expand so far. As the plaque gets too big, it causes narrowing of your arteries which decreases blood flow.
The plaque may stay stable for a long time. But eventually, it can rupture.
Stage 4: Plaque Rupture
In this final stage, the plaque has been in your artery for a long time — perhaps many years. It has grown in size and taken up more space in your artery. But the fibrous cap has kept the plaque from breaking open until this point.
If the fibrous cap breaks, the plaque inside comes into contact with your blood. This can trigger a blood clot to form. This blood clot (known as a “thrombus”) blocks your blood flow and leads to a heart attack or stroke.
What are the symptoms of atherosclerosis?
Atherosclerosis often doesn’t cause any symptoms until an artery is very narrow or entirely blocked. Many people don’t even know they have the condition until a medical emergency, such as a heart attack or stroke.
You may start noticing symptoms if your artery is more than 70% blocked. The blockage causes your blood flow to slow down.
Some early warning signs include:
- Chest pain (angina) while exercising. This pain stops when you rest.
- Leg cramps when walking.
- Transient ischemic attack (TIA). This is a “mini stroke” that has the same symptoms as a stroke. But it goes away within a day and doesn’t damage your brain. If you have a TIA, you’re at risk of having a stroke within days or weeks.
How can I prevent or lessen atherosclerosis?
You can reduce your risk and lessen the effects of the disease.
Some steps you can take include eating a healthy diet, exercising, quit smoking and managing healthy blood pressure, cholesterol and diabetes.
Tikva has 19 nutrients that target atherosclerosis (hardening of the arteries)
Below are clinical trials and research on these nutrients.
1. Pomegranate https://LifeExtension
In an Israeli study, scientists studied patients with atherosclerosis in the carotid arteries in the neck (causing narrowing – major stroke risk) which are responsible for 80% of the blood flow to the brain. In the patient’s given pomegranate juice supplement for one year, there was a 35% decrease in the size of atherosclerotic lesions, while the placebo group increased in size by 9%.
This shows that pomegranate actually reversed existing atherosclerosis.
In addition, total antioxidant activity increased by 130%, and systolic blood pressure fell by 21%.
2. Grape Seed Extract https://www.ncbi.nlm.nih.gov/
In a clinical trial with 287 patients on the effects of grape seed extract on atherosclerosis, researchers found:
- A decrease in the thickening of the artery wall of 4.9% after 6 months and 5.8% after 24 months
- A decrease in plaque score of 10.9% after 6 months and 33.1% after 24 months
Both of these scores stayed the same or increased in the placebo group.
Researchers found that the carotid plaque can disappear after treatments with grape seed extract and the amount of TIA (mini strokes), stenting and hospital readmission for unstable angina was significantly lower.
3. Coenzyme Q10 https://LifeExtension
Multiple studies show that CoQ10 combats many of the risk factors associated with atherosclerosis.
- One study on heart attack survivors who took 120mg of CoQ10 for one year showed the rate of total cardiac events and nonfatal heart attacks decrease by 45% and HDL (good) cholesterol increased.
- Another study comparing CoQ10 to patients taking statins showed that 60mg of CoQ10 improved multiple atherosclerosis risk factors, such as lipid profiles, platelet clumping and oxidative stress.
- In a different study, people who took a combination of 120mg of CoQ10 and 1200mg of aged garlic extract for one year saw a decrease in the progression of hardening of arteries by 4x those in the placebo group and the amount of inflammation was reduced as well.
CoQ10 has also been shown to help prevent LDL (bad) cholesterol from oxidizing which causes arterial palque formation.
4. Magnesium https://AmericanCollegeofCardiology
In a Framingham Heart Study with 2,695 participants, researchers found that for each 50mg per day increase in magnesium intake, there was a 22% decrease in coronary artery calcification.
They concluded that increased magnesium intake was associated with decreased arterial calcification and has been shown to lower the risk of adverse cardiac events, such as stroke, nonfatal heart attacks, and cardiac death.
The study shows that increased magnesium may slow or prevent arterial calcification and plaque formation.
5. Zinc https://ActaPharmacologicaSinica
A number of studies reported that zinc deficiency can contribute to atherosclerosis. In middle aged and elderly people, low zinc intake showed an increase in carotid intima-media thickness (endothelial lining) and was associated with low HDL (good) cholesterol and in increase in coronary artery disease.
6 & 7. Selenium & Vitamin D https://CambridgeUniversityPress
A recent study on the effects of Selenium and Vitamin D supplements taken together showed that they have a synergistic interaction. When taken together they enhanced both immune and endothelial functions and slowed atherosclerotic development.
8. Manganese https://BriefLands
In a study with 334 subjects, they found that the amount of manganese in patients with atherosclerosis was less than those that were healthy and as the hardening of arteries progressed, the amount of manganese decreased even further.
This finding indicates that as atherosclerosis progresses, manganese levels decrease.
9. Chromium https://SageJournals
There is evidence in some studies that shows that supplementation with chromium decreased the risk of cardiovascular disease, insulin resistance, atherosclerosis, heart attacks and lowered cholesterol levels.
Chromium was shown to lower total serum cholesterol levels, decrease LDL (bad) and increase HDL (good) cholesterol. It is involved in lipoprotein metabolism which helps to promote health and prevent disease such as atherosclerosis and various other cardiovascular diseases. Older people need more chromium in their diet to help with improve lipid metabolism.
10, 11, 12 . Betaine & Vitamin B6 & B12 https://OxfordAcademic
Betaine is also called Trimethylglycine (TMG). Studies suggest that betaine along with Vitamins B6 and B12 help reduce high levels of homocysteine. Some studies show that high levels of homocysteine may encourage atherosclerosis (hardening of arteries).
In a study on betaine reducing homocysteine levels at low dose dietary intake levels, it was shown that after 6 weeks of betaine supplementation, there was a 23% decrease in homocysteine.
13. L-Taurine https://SageJournals
In a study on L-Taurine supplementation in patients with previous heart failure, they found that after 2 weeks there was an anti-atherogenic and anti-inflammatory effect in the taurine group, but not in the placebo group.
14. L-Theanine https://LifeExtension
L-theanine has been shown to prevent lipid peroxidation which can cause cell damage or cell death which can lead to atherosclerosis and cardiovascular disease.
15, 16, 17. L-Citrulline, L-Arginine & Beetroot https://ScienceDirect
L-Citrulline, L-arginine and Beetroot all produce nitric oxide. Nitric Oxide protects in multiple ways against the initiation and progression of atherosclerosis including vasodilation (widening of arteries), preventing adhesion of blood cells and platelets to endothelial cells (making them less sticky) and inhibiting smooth cells from accumulating. Nitric oxide also helps to prevent LDL (bad) cholesterol from oxidizing.
18. Vitamin C https://www.ncbi.nlm.nih.gov/
Vitamin C helps to reduce monocyte adhesion to the endothelium. Adhesion and migration of monocytesoccur at the beginning of atherosclerotic plaque formation.
In addition Vitamin C helps prevent LDL oxidation (which turns into plaque) and has been shown to improve nitric oxide production which increases vasodilation (widening of arteries).
Vitamin C also helps prevent cell death of vascular smooth muscle cells, which helps keep plaques more stable if atherosclerosis has developed.
19. Vitamin D https://www.ncbi.nlm.nih.gov/
Research shows that Vitamin D has a protective effect on atherosclerosis through multiple mechanisms including endothelial dysfunction (narrowing of large blood vessels on the hearts surface), the accumulation of vascular smooth muscle cells, and changes in the immune system and inflammatory response.