High levels of low-density lipoprotein (LDL) cholesterol that haven’t responded to diet, exercise, or medication have been linked to hypothyroidism. Elevated levels of the “bad” cholesterol can be caused by an underactive thyroid. Untreated hypothyroidism can lead to heart problems, including an enlarged heart and heart failure.
LIPID PEROXIDATION
Another result of free radical activity is lipid peroxidation which can yield the toxic compound, 4-‐hydroxynonenal (4-‐HNE).
4-‐ Hydroxynonenal can increase the neurofibrillary tangles as seen in Alzheimer’s disease.
4-‐HNE is a compound that reacts with a protein and is a major player in the type of neurodegeneration seen in Alzheimer’s disease, Parkinson’s disease and ALS.
4-‐HNE can rapidly inactivate glutathione reductase (the B2-‐dependent form), which is a key protective antioxidant.
LDL (low density lipoproteins) and HDL (high density lipoproteins) both exist in the brain BUT only LDL is a transporter of cholesterol and phospholipids to the central nervous system.
Cholesterol and phospholipids are important for “nerve conductivity” or in other words, they help increase the nerve firing.
Both HDL and LDL can be readily oxidized in the presence of inorganic iron such as found in “enriched” white flour products. Oxidized LDL can induce cell death which closely parallels the cell deaths seen in excitotoxicity.
Buildup of oxidized LDL represents a possible link to ALS and other neurodegenerative diseases.
Oxidized HDL can also cause neuronal death.
In Alzheimer’s disease as well as Parkinson’s disease and ALS, we also see an increase in disordered protein transporters which can be triggered by viral infection, mercury exposure, oxidative stress and/or hereditary S.O.D. (super oxide dismutase) mutants.
In every single cell of the body, both the cell nucleus and the mitochondrial DNA are vulnerable to free radical damage. As a matter of fact, mitochondrial DNA is 10 times more sensitive to free radical damage. The good news is that this extreme vulnerability of mitochondrial DNA can be protected by targeted nutraceutical agents! The most profound of which is DHLA (dihydrolipoic acid), the reduced form of alpha lipoic acid, which is now available in stable form for the first time in history. DHLA promotes a dramatic increase in cellular ATP (energy) and quenches every known free radical (both RNS and ROS species) that can occur in living tissue.
Never forget that your body can produce Vitamin D naturally if your cholesterol levels are normal and your liver, kidneys, and gut are all functioning normally.
Cholesterol is good for you.
When sunlight comes into contact with your skin, it actually converts cholesterol into Vitamin D.
Eating cholesterol and saturated fat does not increase cholesterol levels in the blood for most people.
On any given day, we have between 1,100 and 1,700 milligrams of cholesterol in our body.
25% of that comes from our diet, and 75% is produced inside of our bodies by the liver.
Much of the cholesterol that’s found in food can’t be absorbed by our bodies, and most of the cholesterol in our gut was first synthesized in body cells and ended up in the gut via the liver and gall bladder.
The body tightly regulates the amount of cholesterol in the blood by controlling internal production; when cholesterol intake in the diet goes down, the body makes more. When cholesterol intake in the diet goes up, the body makes less.
In some people, dietary cholesterol does modestly increase both LDL (“bad cholesterol” and HDL (“good cholesterol”), but it does not affect the ratio of LDL to HDL or increase the risk of heart disease.
Cholesterol is not technically a fat; rather, it’s classified as a sterol, which is a combination of a steroid and alcohol. It’s crucial to understand that you don’t have a cholesterol level in your blood. Cholesterol is fat-soluble, and blood is mostly water. In order for cholesterol to be transported around the body in the blood, it has to be carried by special proteins called lipoproteins. These lipoproteins are classified according to their density; two of the most important in cardiovascular disease are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).
As an analogy to make this more clear. Imagine your bloodstream is like a highway. The lipoproteins are like cars that carry the cholesterol and fats around your body, and the cholesterol and fats are like passengers in the cars. Scientists used to believe that the number of passengers in the car (i.e. concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies, however, suggest that it’s the number of cars on the road (i.e. LDL particles) that matters most.
The significance of this in terms of determining your risk of heart disease is profound.
When you go to the doctor to get your cholesterol tested, chances are he or she will measure your total, LDL and HDL cholesterol. This tells you the concentration of
cholesterol (passengers) inside of the lipoproteins (cars), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood.
it’s possible to have normal or even low cholesterol, but a high number of LDL particles. (12) If this person only has their cholesterol measured, and not their particle number, they will be falsely led to believe they’re at low risk for heart disease.
the patients that are the most likely to present with this pattern are among the highest risk patients: those with metabolic syndrome or full-fledged type 2 diabetes.
The more components of the metabolic syndrome that are present—such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL—the more likely it is that LDL particle number will be elevated.
On the other hand, patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease.
What Causes Elevated LDL Particle Number?
LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.
As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry.
Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.
Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides.
The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.
Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (22) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.).
Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.)
Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol.
Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone.
Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori,
which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (27) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL.
Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens.
One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as
lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation.
Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins.
Some foods help your digestive tract absorb less cholesterol. For example:
•oats, barley, and other whole grains
•fruits such as apples, pears, bananas, and oranges
•vegetables such as eggplant and okra
•beans and legumes, such as kidney beans, chickpeas, and lentils