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Drug shown to block artery fat takes a major step forward | News | The University of Aberdeen
In the latest study, funded by the University of Aberdeen’s Development Trust, researchers tested the success of Trodusquemine, on white blood cells taken from 30 healthy volunteers and 30 volunteers with coronary artery disease and atherosclerosis.
They were able to see the same biochemical changes in the cells taken from people as they did in mice after the use of PTP1B inhibitor.
When PTB1B levels are increased in the body, a series of events occur leading to white blood cells taking up oxidised cholesterol, which then turn them into foamy cells, that lead to fatty deposits within arteries and cause even more inflammation.
Five Year Outcomes in Men Screened for Carotid Artery Stenosis at 65 Years of Age: A Population Based Cohort Study - European Journal of Vascular and Endovascular Surgery
All cause mortality in the cohort attending the five year follow up scan was 3.4%. The five year mortality rate was 3.3% (95% CI 2.8–3.9) among men with normal carotid arteries at age 65, 3.5% (95% CI 2.5–4.7) among those with carotid plaques, and 6.6% (95% CI 2.6–15.7) when a 50–79% carotid stenosis was present (p = .428). None of those with severe stenosis died. Only two subjects had stroke listed as the primary cause of death. All cause mortality among those who did not attend the five year follow up scan was 13.0% (95% CI 11.3–14.9), significantly higher than for attendees (p < .001).
General use of medical therapy was higher at rescreening (70 years of age) compared with primary screening (65 years). At age 65 years, 433 subjects (14%) were treated with antiplatelet agents, 694 (22%) with statins, and 1,321 (43%) with antihypertensive medication, while at age 70 years, 657 subjects (22%) were treated with antiplatelet agents, 890 (29%) with statins, and 1,692 (55%) with antihypertensive medication (p < .001). Among those with progressive disease, 123 (23%) had antiplatelet agents, 175 (33%) had statins, and 301 (57%) had antihypertensive medication. Details of use of statins, antiplatelet agents, and antihypertensive medication in subgroups are presented in Table 4.
Five Year Outcomes in Men Screened for Carotid Artery Stenosis at 65 Years of Age: A Population Based Cohort Study - European Journal of Vascular and Endovascular Surgery
Among men participating in carotid screening at age 65, 3,057 were re-screened at age 70. In those with normal carotids (n = 2,318), 23 (1.0%) progressed to a moderate stenosis, and four (0.2%) to a symptomatic severe stenosis. Among those with plaque (n = 696), 25 (3.6%) progressed to moderate stenosis, and eight (1.1%) to severe stenosis, of whom four (0.6%) had symptoms. Of 31 men with 50–79% stenosis, four (12.9%) had progressed to a severe stenosis, of whom two (6.5%) developed symptoms. Five of twelve subjects (42%) with 80–99% stenosis developed symptoms. Disease regression was present among 289/692 plaque (41.7%) and 16/33 stenosis (48.4%). In multivariable analysis, smoking, coronary artery disease and hypercholesterolemia were associated with disease progression. The proportions of antiplatelet, statin, and antihypertensive treatment in the population at age 70 were 22%, 29%, and 55%, respectively.
Carbohydrate Restriction-Induced Elevations in LDL-Cholesterol and Atherosclerosis: The KETO Trial | JACC: Advances
Coronary plaque in metabolically healthy individuals with carbohydrate restriction-induced LDL-C ≥190 mg/dL on KETO for a mean of 4.7 years is not greater than a matched cohort with 149 mg/dL lower average LDL-C. There is no association between LDL-C and plaque burden in either cohort. (Diet-induced Elevations in LDL-C and Progression of Atherosclerosis [Keto-CTA]; NCT057333255)
How this Guy Cut His Cholesterol in Half Without Drugs and Got Ripped
No one could explain why my LDL cholesterol was so high. The most logical explanation—a condition called familial hypercholesterolemia (FH)—wasn’t comforting: It was genetics, and research shows that people with very high LDL and FH have a 22 times greater risk of developing coronary artery disease.
My triglycerides are very low
Triglycerides are a type of fat (lipid) found in your blood.
When you eat, your body converts any calories it doesn't need to use right away into triglycerides. The triglycerides are stored in your fat cells. Later, hormones release triglycerides for energy between meals.
If you regularly eat more calories than you burn, particularly from high-carbohydrate foods, you may have high triglycerides (hypertriglyceridemia).
What's considered normal?
A simple blood test can reveal whether your triglycerides fall into a healthy range:
Normal — Less than 150 milligrams per deciliter (mg/dL), or less than 1.7 millimoles per liter (mmol/L)
My non-HDL is below 130
An optimal level of non-HDL cholesterol for most people is less than 130 milligrams per deciliter (mg/dL), which is 3.37 millimoles per liter (mmol/L). For people with a history of heart attack, the desired level may be lower. Higher numbers mean a higher risk of heart disease.
Lipoprotein (a) Meaning and How Does it Impact My Heart Health? | American Heart Association
High Lp(a) numbers of 50 mg/dL (125 nmols/L) or higher promote clotting and inflammation, significantly increasing risk of heart attack, stroke, aortic stenosis and peripheral artery disease. This is especially true for those with coronary heart disease or familial hypercholesterolemia, or FH, an inherited condition that affects the body’s ability to process LDL “bad” cholesterol.
Lp(a) can accumulate in the walls of blood vessels, forming plaques similarly to LDL cholesterol. These plaques can block blood flow to vital organs such as the heart, brain, kidneys, lungs, and other parts of the body, leading to conditions like heart attacks, strokes, and other cardiovascular diseases.