One of the most prevalent bone illnesses, Osteoporosis, affects millions globally. Women’s postmenopausal Osteoporosis is a serious health issue.
Osteoporosis is linked to an increased risk of vertebral spine, femoral neck, and distal radius low-trauma fractures that cause significant morbidity.
According to growing scientific research, a diet that encourages atherosclerosis (hardening of the arteries) may also induce Osteoporosis.
Let’s delve deep into the facts that make Cholesterol another causal factor of the common decreasing bone density disease Osteoporosis.
Factors Leading To Osteoporosis On Recent Research
High levels of LDL (“bad”) Cholesterol in the blood are typically thought to increase the risk of cardiovascular disease and clogged arteries.
But current research suggests that elevated blood levels of LDL may also cause thinning and decalcified bones in addition to clogged and calcified arteries.
Numerous epidemiological studies demonstrate a beneficial relationship between the risk of developing cardiovascular diseases and Osteoporosis, pointing to a possible function for hyperlipidemia and/or hypercholesterolemia in controlling Osteoporosis.
According to the vast majority of research, poor bone mineral density, a reliable indicator of Osteoporosis, and high Cholesterol and high LDL-cholesterol levels are related.
The osteoporotic bone matrix makes it more likely for cancer cells to spread via the bone matrix.
To promote or stop bone degeneration, this study emphasizes how cholesterol and cholesterol-lowering medications (statins) control the actions of bone-resident osteoblast and osteoclast cells.
If this hypothesis is confirmed, animal products’ high fat and cholesterol concentrations may be more responsible for this condition’s promotion than their protein level.
How Could High LDL Levels Cause Osteoporosis?
LDL particles have the same ability to travel from the bloodstream and into arteries as they have to enter bones.
These white blood cells develop into macrophages in the arterial wall, which absorbs changed LDL particles and develop into “foam” cells.
These cells build up over time, forming atherosclerotic plaque.
Increased LDL can also draw more monocytes to the bone, which develop into osteoclasts. Osteoclasts consume the nearby bone structure.
The bone-eating action of these macrophages is countered when LDL levels are in the therapeutic range (50-100 mg/dl) by an osteoblast, another bone cell continually generating new bone tissue.
Osteoclast activity increases as LDL levels in the blood and bone rise. Additionally, the development of osteoblasts is hampered by oxidized LDL in bone.
Gross bone mineral density decreases due to elevated LDL levels in the bone. Osteoporosis might develop over time as a result of high LDL levels.
Hyperlipidemia And Bone Regeneration
In the vasculature and bone subendothelial regions, lipid oxidation products that accumulate due to hyperlipidemia are more likely to occur.
Increased quantities of oxidized lipids in the serum from atherogenic high-fat diets slow osteogenesis in culture.
Atherosclerosis and vascular calcification are two detrimental outcomes of hyperlipidemia caused by food consumption or genetic abnormalities in cholesterol uptake and clearance.
The amount of cholesterol-lowering directly impacts the decrease in vascular calcification.
It is unknown if the degree of Cholesterol-lowering affects the decrease in fractures.
It is necessary to do additional research to ascertain whether acute hyperlipidemia dictates the density of bones in animals and if the amount of lipid-lowering impacts the degree of osteoporosis reduction.
Studies are still underway, and scientists are working to understand the relationship between Cholesterol and Osteoporosis in more detail.
Randomized trials with sufficient power are required to assess bone density and fracture in people randomly assigned to take statins against alternative lipid-reducing medications and paired to match equal levels of lipid-lowering.
How To Reduce Cholesterol-Induced Osteoporosis?
Here are a few simple ways and preventive measures that one can implement in their life to avoid Osteoporosis due to high cholesterol levels:
● Drugs and diets that lower LDL have been demonstrated in studies to slow bone loss in both animals and/or people.
● Both beneficial and detrimental impacts on bone health may result from consuming milk and dairy products.
Full and even low-fat dairy products may boost LDL levels to the point where the additional calcium and vitamin D they provide outweighs the positive effects of the additional calcium and vitamin D.
This is due to these foods’ very substantial saturated fat and cholesterol content.
● People susceptible to either atherosclerosis or Osteoporosis should be advised to reduce all nutritional foods that contain saturated and hydrogenated fat and Cholesterol unless LDL is below 100 mg/dl.
Finding out whether osteoporosis medications worsen or improve vascular calcification, and vice versa, is a crucial priority.
It is important to assess the basic mechanisms by which lipids influence the differentiation of mineralizing cells and biomineralization, and understanding the mechanisms by which lipids control atherogenesis is a good place to start.
Both old and intriguing new animal models have promise for uncovering genetic regulatory elements.
A recent NIH Working Group has identified further research objectives at the intersection of vascular and bone biology.
Ultimately, this research should produce fresh, effective methods for the concurrent biological reversal of vascular calcification and Osteoporosis.