My Cholesterol is 3.8 nmol/l
HDL 2.1 nmol/l
LDL 0.8 nmol/l
Cholesterol / HDL ratio 1.81
Perfect readings ?
So why is my Triglyceride up at 1.9 nmol/l ?
Where is it coming from ? Is it probable to undo the beneficial effects of my accurate cholesterol profile and lead to arteriosclerosis ?
And why doesn't LDL + HDL add on up to Total Cholesterol ?
Answers: Triglycerides are chemically distinct from the sterols (i.e. derivatives of cholesterol such as sex hormones, glucocorticoids and mineralocorticoids). They are formed by a glycerol molecule bound by fatty acid chains (drawn schematically, they look more approaching tadpoles compared to the ring-like structure of sterols).
Hence, triglycerides may be elevated primarily without any abnormality of cholesterol. The treatment is beside drugs known as fibrates (such as clofibrate), to lessen synthesis of triglycerides. This is a different family of drugs to those used to treat cholesterol (the HMG-CoA reductase inhibitors, such as simvastatin).
It is endogenous (diet plays a small chunk in it but your body depends outstandingly on fatty acids for energy and stores these within adipose tissue. We all differ surrounded by our capacity to mobilise fatty acids for metabolism).
Hypertriglyceridaemia wants treating because it does increase risks of arterial disease except it is athersclerosis NOT arteriosclerosis which these lipids increase the risk of (including cholesterol in the definition of lipid).
Hypertriglyceridaemia can also motive pancreatitis, eruptive xanthomata and xanthelasma, pseudohyponatraemia and other health problems but it is treatable (see above).
LDL + HDL do not make a payment up to Total Cholesterol as they are not the only forms of cholesterol transport within the blood. The terms HDL and LDL stand for High Density and Low Density Lipoproteins respectively. These are protein and lipid complexes which emulsify cholesterol (itself lipophilic and hence insoluble within water) and transport it around the body in blood. The LDL represents plausible excess cholesterol and is crudely understood as conferral vectors of cholesterol TO body tissues from liver, hence it is labelled the impossible cholesterol. HDL on the other hand seem to transport cholesterol back to the liver from lateral tissue for either recycle or excretion (in bile, the human body cannot itself destroy the sterol ring although it can convert fatty acids into sterols if involve be).
The missing story: chylomicrons and some other lipoproteins also exist, they help transport lipids within the diet from gut to lymphatics and hence through the circulation and eventually to the liver for processing and distribution elsewhere via LDL.
Hope this helps.
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Getting your blood drawn?
HDL 2.1 nmol/l
LDL 0.8 nmol/l
Cholesterol / HDL ratio 1.81
Perfect readings ?
So why is my Triglyceride up at 1.9 nmol/l ?
Where is it coming from ? Is it probable to undo the beneficial effects of my accurate cholesterol profile and lead to arteriosclerosis ?
And why doesn't LDL + HDL add on up to Total Cholesterol ?
Answers: Triglycerides are chemically distinct from the sterols (i.e. derivatives of cholesterol such as sex hormones, glucocorticoids and mineralocorticoids). They are formed by a glycerol molecule bound by fatty acid chains (drawn schematically, they look more approaching tadpoles compared to the ring-like structure of sterols).
Hence, triglycerides may be elevated primarily without any abnormality of cholesterol. The treatment is beside drugs known as fibrates (such as clofibrate), to lessen synthesis of triglycerides. This is a different family of drugs to those used to treat cholesterol (the HMG-CoA reductase inhibitors, such as simvastatin).
It is endogenous (diet plays a small chunk in it but your body depends outstandingly on fatty acids for energy and stores these within adipose tissue. We all differ surrounded by our capacity to mobilise fatty acids for metabolism).
Hypertriglyceridaemia wants treating because it does increase risks of arterial disease except it is athersclerosis NOT arteriosclerosis which these lipids increase the risk of (including cholesterol in the definition of lipid).
Hypertriglyceridaemia can also motive pancreatitis, eruptive xanthomata and xanthelasma, pseudohyponatraemia and other health problems but it is treatable (see above).
LDL + HDL do not make a payment up to Total Cholesterol as they are not the only forms of cholesterol transport within the blood. The terms HDL and LDL stand for High Density and Low Density Lipoproteins respectively. These are protein and lipid complexes which emulsify cholesterol (itself lipophilic and hence insoluble within water) and transport it around the body in blood. The LDL represents plausible excess cholesterol and is crudely understood as conferral vectors of cholesterol TO body tissues from liver, hence it is labelled the impossible cholesterol. HDL on the other hand seem to transport cholesterol back to the liver from lateral tissue for either recycle or excretion (in bile, the human body cannot itself destroy the sterol ring although it can convert fatty acids into sterols if involve be).
The missing story: chylomicrons and some other lipoproteins also exist, they help transport lipids within the diet from gut to lymphatics and hence through the circulation and eventually to the liver for processing and distribution elsewhere via LDL.
Hope this helps.