I remember a conference when a lipid specialist said, if the dyslipidemia (TG/HDLc) of DM was found before the high glucose DM might now be considered mostly a lipid disorder.
On my dilated eye exam today my ophthalmologist said I had no vascular disease in my fundus. This is surprising because I had diabetes mellitus type 2 diagnosed in 1998.
I didn't know it at the time but I probably had insulin resistance since 1993 when I had
LDLc of 97,
Total cholesterol 149,
Triglycerides 157,
HDLc 33,
non-HDLc was 149-33= 116 (which is high but it was not on the Sequoia Advanced Lipid report and I never heard of it.)
Dr Robert Superko wrote that my LDL subclass was pattern B (small LDLc ) in 1998 and first therapy was exercise, appropriate diet and weight loss. Secondary therapies include nicotinic acid (niacin) and gemfibrozil. At that time Niacin caused flushing (I didn't know about Endur-acin) and Gemfibrozil caused constipation so I didn't take them. Hell my LDLc was normal at 96. I didn't know about the discordance of LDLc in metabolic syndrome and did not know I could check that with non-HDLc which was high.
Exercise: I always have done that.
Appropriate diet: I have gained and loss weight all my life and I tried to avoid fats.
Weight loss: done only to always regain (I had not yet elucidated the Sponge Syndrome)
NOW I KNOW ATKINS OR LOW CARBOHYDRATE HIGH FAT DIET IS WHAT I SHOULD HAVE DONE.
I now realize I should have had a fasting glucose with a insulin level and then a 2 hour Post prandial glucose with insulin level.
I would probably would have seen I was pre-diabetic with insulin resistance.
Yet UpToDate and guidelines still do not get routine insulin levels. No fault of Dr. Superko.
I had a waist greater than 40" and my Triglyeride/HDLc ratio was 157/33= 4.75. More than 3.0 suggests the dyslipidemia of insulin resistance.
Thus insulin resistance for at least 25 years.
Yet no vascular disease in the eye.
My last Hgb A1c was 7.7 and has been as high as 10 when I stopped Actos.
More than 10 years ago my ophthalmologist found early Age related Macular Degeneration(AMD).
Now in 2018 he said there was no increase in the Macular Drusen he had found before. He attributed it to my
LDLp 666 and
non-HDL cholesterol of 84,
LDLc 66,
HDLc 60,
Remnants 18,
Triglyceride 144 non-fasting.
He knows I am a lipidologist and told me to look it up. I found this:
"Unesterified cholesterol controls the fluidity, permeability and electrical properties of eukaryotic cell membranes. Consequently, cholesterol levels in the retina and the brain are tightly regulated whereas depletion or oversupply caused by diet or heredity contribute to neurodegenerative diseases and vision loss."
Lakk 2018 Feb
By tight control of my lipids with low dose atorvastatin 10 mg and Endur-acin (niacin) 1,000 mg I have maintained great Lipid levels documented here
My glucose control has not been so good but my lipid levels have been very low, thus I have the following CIMT and CAC results not due to low HgbA1c but due to low lipids.
My calcium score did finally go up on atorvastatin and niacin but when calculated with the calcium volume it is not a high score as give by a formula from Dr Eades from Colorado.
In Eat Rich Live Long Feb 2018, Ivor Cummings and Jeffrey Gerber MD claim insulin resistance is the root cause of everything.
I must respectfully disagree, I think increased visceral fat is the cause of insulin resistance due to low adiponectin.
Dr. Dayspring did not like my term of Tubby Factor for non-HDLc as 20% of people with metabolic syndrome are not obese.
I believe many people have increased visceral fat and that insulin resistance needs to be checked with fasting glucose and/or 2 hour postprandial glucose both with insulin levels will bring attention to insulin resistance in people who do not have a waist of 40" but do have excess visceral fat.
Thus it is increased visceral fat that is the root of everything leading to insulin resistance.
On my dilated eye exam today my ophthalmologist said I had no vascular disease in my fundus. This is surprising because I had diabetes mellitus type 2 diagnosed in 1998.
I didn't know it at the time but I probably had insulin resistance since 1993 when I had
LDLc of 97,
Total cholesterol 149,
Triglycerides 157,
HDLc 33,
non-HDLc was 149-33= 116 (which is high but it was not on the Sequoia Advanced Lipid report and I never heard of it.)
Dr Robert Superko wrote that my LDL subclass was pattern B (small LDLc ) in 1998 and first therapy was exercise, appropriate diet and weight loss. Secondary therapies include nicotinic acid (niacin) and gemfibrozil. At that time Niacin caused flushing (I didn't know about Endur-acin) and Gemfibrozil caused constipation so I didn't take them. Hell my LDLc was normal at 96. I didn't know about the discordance of LDLc in metabolic syndrome and did not know I could check that with non-HDLc which was high.
Exercise: I always have done that.
Appropriate diet: I have gained and loss weight all my life and I tried to avoid fats.
Weight loss: done only to always regain (I had not yet elucidated the Sponge Syndrome)
NOW I KNOW ATKINS OR LOW CARBOHYDRATE HIGH FAT DIET IS WHAT I SHOULD HAVE DONE.
I now realize I should have had a fasting glucose with a insulin level and then a 2 hour Post prandial glucose with insulin level.
I would probably would have seen I was pre-diabetic with insulin resistance.
Yet UpToDate and guidelines still do not get routine insulin levels. No fault of Dr. Superko.
I had a waist greater than 40" and my Triglyeride/HDLc ratio was 157/33= 4.75. More than 3.0 suggests the dyslipidemia of insulin resistance.
Thus insulin resistance for at least 25 years.
Yet no vascular disease in the eye.
My last Hgb A1c was 7.7 and has been as high as 10 when I stopped Actos.
More than 10 years ago my ophthalmologist found early Age related Macular Degeneration(AMD).
Now in 2018 he said there was no increase in the Macular Drusen he had found before. He attributed it to my
LDLp 666 and
non-HDL cholesterol of 84,
LDLc 66,
HDLc 60,
Remnants 18,
Triglyceride 144 non-fasting.
He knows I am a lipidologist and told me to look it up. I found this:
"Unesterified cholesterol controls the fluidity, permeability and electrical properties of eukaryotic cell membranes. Consequently, cholesterol levels in the retina and the brain are tightly regulated whereas depletion or oversupply caused by diet or heredity contribute to neurodegenerative diseases and vision loss."
Lakk 2018 Feb
By tight control of my lipids with low dose atorvastatin 10 mg and Endur-acin (niacin) 1,000 mg I have maintained great Lipid levels documented here
My glucose control has not been so good but my lipid levels have been very low, thus I have the following CIMT and CAC results not due to low HgbA1c but due to low lipids.
My calcium score did finally go up on atorvastatin and niacin but when calculated with the calcium volume it is not a high score as give by a formula from Dr Eades from Colorado.
In Eat Rich Live Long Feb 2018, Ivor Cummings and Jeffrey Gerber MD claim insulin resistance is the root cause of everything.
I must respectfully disagree, I think increased visceral fat is the cause of insulin resistance due to low adiponectin.
Dr. Dayspring did not like my term of Tubby Factor for non-HDLc as 20% of people with metabolic syndrome are not obese.
I believe many people have increased visceral fat and that insulin resistance needs to be checked with fasting glucose and/or 2 hour postprandial glucose both with insulin levels will bring attention to insulin resistance in people who do not have a waist of 40" but do have excess visceral fat.
Thus it is increased visceral fat that is the root of everything leading to insulin resistance.
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