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Posts Tagged ‘vldl’

I’m trying to get  a right  answer for this question for quiet some time. The literature on lipids is so vast  , one can never finish reviewing it.There are   nearly two dozen journals that  deal with lipids ,Atherosclerosis, obesity ,and vascular biology .

Yet  , the answer to this simple question is elusive to us .The Irony is complete when we have evidence for   two diagonally  opposite responses 4 and 5 .

My interpretation of the issue

Any lipid molecule if exceeds a critical  level ( Only  if   . . . associated with hypertension, or diabetes or smoking ) can penetrate the vascular endothelium. ( HT-pressure injury , Smoke- Endothelial dysfunction  due to Nitric oxide depletion) DM -Glycation of cell membrane  , finally some  unknown inflammatory component )

Though evidence  for direct endothelial  injury is more for LDL ,  less for TGL (Almost nil  for VLDL , but  TGL has more VLDL in it !)

Strangely ,these molecules , express a mob psychological behavior .In isolation they appear innocuous. But ,in an  unfavorable   setting it shows signs of  revolt. If a group of  LDL molecule start attacking a  dysfunctional segment  of endothelium , the other molecules  like TGL and VLDL fractions would love to join the crowd  and inflict further  damage . (Of course ,the lonely HDL may watch the chaos silently !)

Questions to ponder

If LDL is a sharp knife like molecule  trying to injure the blood vessel , every normal human being is potentially threatened  by this  lipid fraction . Mind you,  this is a physiological molecule  traversing the human vascular system  at concentration  of 130mg/dl  at the  velocity of blood .

So it is  foolish  to blame this  physiological molecule for all our ignorance.

I recall one recent definition for hyperlipidemia

The lipid levels at which a patient develops vascular injury is considered high for him !

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We know diabetes, smoking, hyperlidemia, hypertension are major risk factors for progressive vascular disease. They damage the vascular endothelium either directly or indirectly ,   by aggravating the atheroscelortic process .  Diabetes apart from affecting the medium sized arteries , also affect the microvasculature.  Smoking  has a direct effect on endothelial function .It depletes vascular nitric oxide. High levels of circulating lipids injures the sub endothelial structures and invades the media by entering macrophages .So , all these 4 risk factors either operate independently or interact with each other and result in progressive vascular    disease.

While we  believe  , these risk factors do not have any bias in attacking the human vascular  tree, in the real world it is observed they have their own  behavior pattern and  have unique predilection and a deadly alliance .

For example , in  chronic smokers TAO is the commonest manifestation , thrombo angitis is far too less common to occur in the coronary arteries.

Similarly  hypertension  per se  rarely results in an acute coronary syndrome while it is  the  single  important  cause for cerebro vascular  disease. Diabetes especially in women has very strong predilection for CAD , while diabetic per se is a lesser risk for stroke. Hyperlipedimia may be the one which has fairly even risk throughout the vasculature. Similarly there is  a difference in renal and   carotid arterial involvement with reference to  the conventional  risk factors .

SHT diabetes dyslipidemia coroanry risk factor

Why this apparent difference ?

We are unlikely  to get an answer to this question in the near future .  Left to the youngsters  . . . of tomorrow !

* Note of  clarification

The source for the above chart is collected from various studies and also a huge observational data from our hospital. There could be some geographical variation , a given individual may respond differently to these risk factor depending upon his genetic predisposition and susceptibility . So the above data can be applied to general population and not to a individual.

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