5 Steps to prevent Heart Disease

Monday, April 30, 2018

What my ophthalmologist taught me about insulin resistance.

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.











Sunday, April 29, 2018

Eat Rich Live Long Flub #4

  
Abstract below cherry picked in Eat Rich Live Long p 268

"All were put on treatment."  Cummings and Gerber left out 

the treatment was statins.



In 2004 it was not well known that statins increased CAC score with reduced risk with reaching goal of lower LDLc.
Now we know if you adjust the higher calcium score with the calcium volume we find statins did not make the plaque worse. 








"in subjects receiving compared to those not receiving statin therapy (HR) 
were 0.29 (95% CI 0.13 to 0.56, p = 0.001)" 

 2013 Feb 1;111(3):356-61. doi: 10.1016/j.amjcard.2012.09.033. Epub 2012 Dec 1.

Impact of coronary artery calcium progression and statin therapy on clinical outcome in subjects with and without diabetes mellitus.

Abstract

Coronary artery calcium (CAC) is a marker of atherosclerosis, and CAC progression is independently associated with all-cause mortality in the general population but not convincingly in subjects with diabetes mellitus (DM). 
The aim of this study was to ascertain the differences in the
1-  rates of CAC progression,
2- the effect of statin therapy, and 
3-all-cause mortality in subjects with and without DM. 
The study group consisted of 296 asymptomatic subjects with type 2 DM and 300 controls (mean age 59 ± 6 years, 29% women) who underwent baseline and follow-up CAC scans within a 2-year interval. 
Absolute annual CAC score change, percentage annual CAC progression(change in CAC%), event-free survival, and the effect of statin therapy on survival were all assessed. The mean follow-up duration was 56 ± 11 months. 
Absolute annual CAC score change was 81 ± 10 in subjects with DM and 34 ± 5 in controls (p = 0.0001). 
Percentage annual CAC progression was 29 ± 9% in subjects with DM and 10 ± 7% in controls (p = 0.0001). 
The hazard ratios of death in 3 groups of subjects with DM compared to controls without DM were 1.88 (95% confidence interval [CI] 1.51 to 2.36, p = 0.0001) for  change of CAC of 10% to 20%, 2.29 (95% CI 1.56 to 3.38, p = 0.0001) for change of CAC of 21% to 30%, and 6.95 (95% CI 2.23 to 11.53, p = 0.0001) for change of CAC greater than 30%, all compared to change of CAC less than 10%. 
The adjusted hazard ratios of all-cause mortality: 
1-in subjects receiving compared to those not receiving statin therapy were 0.29 (95% CI 0.13 to 0.56, p = 0.001) 
2-in those without DM and without CAC progression, 0.51 (95% CI 0.21 to 0.73, p = 0.001) 
3-in those with DM and without CAC progression 0.71 (95% CI 0.25 to 0.91, p = 0.003) 
 with all 3 groups compared to 1.0 (reference) in those with DM, with CAC progression and without statin therapy.

In conclusion:

CAC progression was greater and event-free survival lower in patients with DM compared to controls in proportion to the extent of CAC progression. These results suggest that CAC progression is an independent predictor of all-cause mortality in patients with DM.

Try niacin low dose if you are statin intolerant

Original article 2011 link

AIM-HIGH: Results Raise Controversy Over Early Stopping

Sue Hughes

November 15, 2011

Highlights of article:

Final results of the AIM-HIGH trial appear to suggest that the signal of increased ischemic stroke with niacin, which was one of the reasons the study was stopped early, could have been the play of chance, with the final p value for ischemic stroke coming in at a nonsignificant 0.11.
This has provoked a backlash from researchers in the field against the National Institutes of Health (NIH) sponsors of the study who made the decision to terminate the trial.

Dr Steven Nissen (Cleveland Clinic, OH), who was not involved in AIM-HIGH but is a key player in lipid research, was particularly vocal on this issue. He commented to heartwire : "I do not agree with the decision to stop this trial. It was completely inappropriate. The NIH sponsors saw a weak signal of stroke and panicked, and when all the data have come in,
this doesn't appear to be an issue. Now we have lost the opportunity to properly answer the very important question of whether niacin adds any benefit in this population with low LDL levels."

The AIM-HIGH trial randomized 3414 patients with established heart disease, low HDL levels,
and raised triglycerides to extended-release niacin (1500–2000 mg per day) or placebo.
All patients also received simvastatin plus ezetimibe if needed to maintain LDL levels
below 80 mg/dL (2.07 mmol/L).
The trial was stopped earlier this year after a mean follow-up of three years.
The statement from the National Heart Lung and Blood Institute at the time said
the trial had been stopped because niacin was showing no additional benefits over placebo and there was also a small, unexplained increase in ischemic stroke in the niacin group.

Results presented today at the American Heart Association (AHA) 2011 Scientific Sessions
and published online simultaneously in the New England Journal of Medicine
show that at two years, niacin therapy had increased HDL levels from a median of 35 to 42 mg/dL,
lowered triglyceride levels from 164 to 122 mg/dL, and lowered LDL levels from 74 to 62 mg/dL.




Focus on the Low LDL Level
Speculation on the reason for the lack of benefit with niacin is focusing on
the low LDL level achieved in the trial.
Lead investigator Dr William Boden (University at Buffalo School of Medicine, NY)
commented to heartwire : "if you are starting off with an LDL of 70,
it may not be possible to show any incremental benefit."
He also pointed out that patients in the trial were very well-treated in terms of other medical therapy,
and many patients had been on statins for several years.
But he said these patients were not representative of the real world,
where only about 15% to 20% of patients actually get their LDL levels down to 70.
"I would urge people not to overreact to these results.
They should not be extrapolated to patients with LDLs of 100 or more,
which is much more the norm. We must not throw the baby out with the bathwater."
But Boden and Nissen both stressed that reducing LDL to 70 with high-dose statins
is still the first priority. Nissen commented:
"I am less likely to use niacin after this trial,
but I would still use it in patients who can't get to LDL goals with statins."
" Dr. Robert Giugliano says, "before holding a final retirement party for niacin,
it would be appear to more prudent
to assign it to part-time work such as in statin-intolerant patients."
Stroke: "A Causal Association or the Play of Chance"?
On the stroke issue, the AIM-HIGH investigators report in the paper
that ischemic stroke occurred as the first event in 27 niacin patients (1.6%) vs
15 placebo patients (0.9%).
However, eight of the strokes in the niacin group occurred
between two months and four years after discontinuation of niacin treatment.
"When all the patients with ischemic stroke were considered,
rather than just those in whom the stroke was the first study event,
a nonsignificant higher trend persisted in the niacin group," they say.
They add: "The overall rate of ischemic stroke was low,
and it is not clear whether the increase seen with niacin reflects a causal association
or the play of chance."
Boden added to heartwire : "When the NIH stopped the trial,
there was an increase in ischemic stroke of borderline significance.
I think they saw neutral outcome data, and because of a potential ethical safety issue
they decided to stop the trial.
But there was no signal of an increase in fatal stroke or of all-cause or cardiac mortality.
And now that we have all the data, the effect is far from significant,
and when we look just at strokes that occurred when the patients were actually on treatment,
we have 21 on niacin vs 18 on placebo.
The earlier numbers were clearly an aberration--just the play of chance."
Boden said he was "disappointed that we couldn't complete the trial as designed,"
especially in view of the previous VA-HIT trial,
which was conducted before statin use became so widespread
and showed a reduced event rate with gemfibrozil (which also raises HDL),
but this didn't start to appear until 18 months into the study.
"We had planned a 4.6-year follow-up, but we only got three years,
so we are unable to know for sure the effect of niacin in this patient group."
Quotes from M Davidson and T Dayspring from 2014 link


I first wrote about low dose, low cost triple therapy to lower non-HDLc in 2010 in my book, The Tubby Theory from Topeka

Steps:
1-Endur-acin (over the counter niacin) is a proprietary wax matrix that does not cause flushing.  Take only 1,000 mg a day. 
2-After a month if not at non-HDLc goal, add one half tab Zetia (now generic  Ezetimibe 10 mg)
3-After another month if non-HDLc not at goal, take full pill of Zetia. 
4- After another month if non-HDLc not at goal get Lipitor 10 mg (now generic atorvastatin) take one half tab a day.
5- Now on triple low dose medications, if non-HDLc not at goal increase to full tablet of Lipitor 10 mg.  

These three medications at low dose have very little side effects. 

The three medications together may only cost about $100 a year. 

Enduracin 500 mg on internet costs $90 for 1,000 tablets. (a two year supply)

Atorvastatin 10 mg is $40 for one year supply. 

Ezetimibe is a new generic and may still be a little costly, but at half a pill a day it is much cheaper than the brand Zetia. 

Saturday, April 28, 2018

Eat Rich Live Long cherry pick old articles of Ridker #3

This is a third blog critical of the use of references in Eat Rich Live Long









In Jupiter, cholesterol efflux capacity was associated with incident CVD in individuals on potent statin therapy but not at baseline.


Cholesterol efflux capacity was moderately correlated with
1- HDL cholesterol,  r= 0.39,

2-apolipoprotein A-I, r= 0.48,

3-HDL particle number, r= 0.39

 Baseline HDL particle number was inversely associated with incident CVD (adjusted odds ratio per SD increment [OR/SD], 0.69; 95% confidence interval [CI], 0.56-0.86; P less than 0.001),

 whereas no significant association was found for 
1-baseline cholesterol efflux capacity (OR/SD, 0.89; 95% CI, 0.72-1.10; P=0.28), 

2-HDL cholesterol (OR/SD, 0.82; 95% CI, 0.66-1.02; P=0.08), or 

3-apolipoprotein A-I (OR/SD, 0.83; 95% CI, 0.67-1.03; P=0.08). 

Twelve months of rosuvastatin (20 mg/day) did not change cholesterol efflux capacity (average percentage change -1.5%, 95% CI, -13.3 to +10.2; P=0.80), but increased 

1-HDL cholesterol (+7.7%),

2- apolipoprotein A-I (+4.3%), and

3- HDL particle number (+5.2%). 

On-statin cholesterol efflux capacity was inversely associated with incident CVD (OR/SD, 0.62; 95% CI, 0.42-0.92; P=0.02),
 although HDL particle number again emerged as the strongest predictor (OR/SD, 0.51; 95% CI, 0.33-0.77; P less than 0.001).





Questionable use of Ridker reference in Eat Rich Live Long #2

Reference used on p 262 in Eat Rich Live Long

The data below from the article sited on p262 contradicts the heading of the chapter 
ApoB/ApoA1 had the worse predictive value of the ratios. 

 APOB/APOA1: The MASTER RATIO. 
Conclusion of article:
"NON-HDLc & ratio of TC/ HDLc were as good as or better than apolipoprotein fractions in prediction of future CVE." 

Data from Article
After adjustment for age, smoking status, blood pressure, diabetes, and body mass index, the HRs (hazard ratios)for future cardiovascular events for those in the extreme quintiles were 
1.62 (95% CI, 1.17-2.25) for LDL-C, 
1.75 (95% CI, 1.30-2.38) for apolipoprotein A-I,
 2.08 (95% CI, 1.45-2.97) for total cholesterol,
 2.32 (95% CI, 1.64-3.33) for HDL-C,
 2.50 (95% CI, 1.68-3.72) for apolipoprotein B(100),
 2.51 (95% CI, 1.69-3.72) for non-HDL-C, 
and 2.98 (95% CI, 1.90-4.67) for high-sensitivity CRP (P<.001 for trend across all quintiles).
 The HRs for the lipid ratios were
 3.01 (95% CI, 2.01-4.50) for apolipoprotein B(100) to apolipoprotein A-I,
 3.18 (95% CI, 2.12-4.75) for LDL-C to HDL-C,
 3.56 (95% CI, 2.31-5.47) for apolipoprotein B(100) to HDL-C, and
 3.81 (95% CI, 2.47-5.86) for the total cholesterol to HDL-C (P<.001 for trend across all quintiles). 
The correlation coefficients between high-sensitivity CRP and the lipid parameters ranged from -0.33 to 0.15, and the clinical cut points for CRP of less than 1, 1 to 3, and higher than 3 mg/L provided prognostic information on risk across increasing levels of each lipid measure and lipid ratio.

CONCLUSIONS:

Non-HDL-C and the ratio of total cholesterol to HDL-C were as good as or better than apolipoprotein fractions in the prediction of future cardiovascular events. After adjustment for age, blood pressure, smoking, diabetes, and obesity, high-sensitivity CRP added prognostic information beyond that conveyed by all lipid measures.

Friday, April 27, 2018

The man cheated from the Nobel Prize

1 min 40 second video from HBO: Weight of the Nation

The above video is a talk from Dr. Rudolph Leibel in May 2012.


I first read about the co-discover of Leptin in Gina Kolata's book Rethinking Thin, published 2007.


Presently, I am reading The Hungry Gene: The Science of Fat and the Future of Thin, published 2002, by Ellen Ruppel Shell.


Chapter Five
"(Rudy)Leibel was already thirty-eight years old when he came to Rockerfeller University 1979, a few months before Jeff Friedman arrived"

That sentence begins an amazing story of how Rudolph Leibel M.D. was kept out of a history breaking scientific article.

Page 90
"Leibel says he approached Friedman with the ob proposal in the spring of 1986.  Friedman recalls this episode differently insisting it was he who approached Leibel"

"Leibel understood the physiology of obesity"
"Friedman had the tools of molecular biology"

Page 98
The article was published by Friedman in Nature on Dec. 1, 1994 titled "Positional Cloning of the Mouse obese Gene and Its Human Homologue.. precisely one day after Friedman had filed for a patent....Leibel and Bahary were acknowledged in the fine print at the end of the paper as 'important contributors to the early phases of the work,' as was Lily, Freidman's fiancee, who was not a scientist.
Leibel was flabbergasted."




How To Break Out a story of important information. Struggling for the Tipping Point


I have been using twitter and my blog to get some attention in the media and public.  I have 74,400 hits on my blog as of this morning.  

I am hoping to get some response from these reporters.  I have tweeted them before. I have never had a response from Gina Kolata over the years.  

I basically want my original idea of The Sponge Syndrome to be recorded in the media and internet as I feel my theory of the billions of fats cells that never go away in the reduced obese acting like a sponge that cause weight gain because of the great number of cells sending out the starvation message(via the episomes called MiRNA) of low leptin to all the other cells in the body. 

The greater the number of fat cells the greater the number of episomes sent out.

Second point for campaign: There is no other book on The Chronic Disease of Obesity.  It is the second unique aspect of my book. 

Third point for campaign: The suggestions in my 2010 book The Tubby Theory from Topeka have been accepted in terms of advising non-HDLc as a biomarker instead of LDLc and the routine screening use of CAC CT scan in people with a calculated 5% risk of a cardiovascular event. 

Fourth Point: My idea of the multiplier effect of treating high LDLc  very early with statins has since been advanced by major Lipidology leaders. 

Weight Loss Maintenance=Sisyphean Task

In 2012 I published the hard news of the difficulty of weight loss maintenance. I espoused that the Sponge syndrome (80 billion fat cells that never disappear) causes the problem.

I echoed Gina Kolata's book

Rethinking Thin: The New Science of Weight Loss--and the Myths and Realities of Dieting  link


 when she discussed the false hope of diet and exercise in April 2008.

Kolata wrote a NYT article called

After ‘The Biggest Loser,’ Their Bodies Fought to Regain Weight  link in May 2016

Now in Feb. 2018, I wrote about maintaining weight loss in:

The Chronic Disease of Obesity: How Sponge Syndrome Causes Repeated Weight Gain link



As a great author and reporter I hope Ms. Kolata writes a book titled:

The Sisyphean task of maintaining weight loss

After 10 years it is time to teach the science of obesity, leptin and hyperplasia of adiopocytes.

It's time to get the message out.

Wednesday, April 25, 2018

Eat Rich Live Long not accurate on reference for ApoB/ApoA1 ratio #1

I looked up Eat Rich and Live Long reference on
 p 262 and 263. Ridker et.al.  July 2005

Eat Rich Live Long: "In this study... the ApoB/ApoA1 ratio put in a great performance, trumping ApoB alone.   Interestingly, the total (cholesterol?) ratio put in a great performance, trumping ApoB alone...the total (cholesterol?)/HDL ratio did even better"
The authors, Cummings & Gerber seem to have mischaracterized the conclusion above: "Non-HDLc and the ratio of total cholesterol to HDLc were as good or better than apoB."

Confusion over MESA CAC scores

Dr Eades has used a formula with calcium score and volume to determine if the increase in CAC calcium score is significant.  Statins now are well known to increase CAC calcium score but decrease CVD and LDLc and non-HDLc.  This throws off the conclusions of MESA.

 My CAC scores have been 9, 20,  8, 144 after many years of statins and low non-HDLc
 This is my risk with a calcium score of 144 but no mention of CAC calcium volume. Note non-HDLc is used in MESA calculation.
 This is my risk with an earlier CAC score of 8.  Quite significant. Despite DM2 in both calculations, my risk is half at the lower CAC score.  Because the volumes were not taken into account I believe this calculation is flawed with people on statins.  16% of people in MESA were on statins.  They probably had lower LDLc but with higher calcium score thus distorting the results. 
The National Lipid Association came out with new guidelines advising cheap non-HDLc to follow rather than apoB(which requires expensive advanced lipid testing).  

Dr Sniderman objects with this tour de force review here.  

Thus CAC score and LDLc data is often simplified to the point of being wrong.  Must look more closely at these numbers. 

Monday, April 23, 2018

How I got fired by my Endocrinologist.

During Christmas holidays I had a fasting glucose of 240 once when I when I reported my levels on Dec. 21, 2017.
 I was surprised my endocrinologist gave me a pass.
Four months later right after a cataract surgery after fasting but getting IV Ringer's Lactate and then post op I had a small muffin, my glucose was  248 and insulin level 8.4.
My endocrinologist  immediately wanted me to add a  sulfonylurea such as glipizide. 
 I said to her, when I was practicing I got away from sulfonylureas because they eventually milked the liver dry of insulin and the patient had to go on insulin injections.  She agreed that was true. 
I said I would be willing to go on Actos (Pioglitazone) at low dose as it seems to be the best drug for insulin resistance.  She doesn't like Actos and said it has been associated with Osteoporosis and I already have osteopenia.  I remembered thinking that I was surprised to have osteopenia as I have always been heavy and always lifted weights over the years.  However, I had been on Actos.  I went to lunch with Eric Westman MD and he suggested I stop Actos to help my weight loss on Atkins.  Thus a few years ago I stop Actos.  I quickly loss 10 lbs., but my fasting glucose shot up to 300! I said to my endocrinologist that of course that weight loss is just water which is probably why you have to be careful giving it to borderline heart failure patients.  She said no, it was lipid weight.  I'm not sure what that means and I was pretty sure she was wrong but I moved on.  
We agreed that I do 3 or 4 hour post-prandial glucose.  If I was running greater than 180, we would start Actos.  I thought after discussion we reached a good compromise. 
I asked if we should get another DEXA scan as it has been 3 years.  She said she wasn't certain medicare would pay for it.  I said if she wrote that she wanted to make certain I didn't develop osteoporosis by stopping testosterone IM, the DEXA scan would be approved.  She wanted to look it up. 
I asked her if she thought that getting insulin levels with fasting glucose to pick up insulin resistance early in people with FBG of less than 100 is a good idea.  She said "yes" Then I asked can I have an insulin level with my next fasting glucose.  She said no.  I said I have an insulin level of 8.4 with a glucose of 248 after fasting and IV Ringer's lactate for my cataract surgery.  She said I have DM2, I didn't need an insulin level.  I said if I take Actos I want to know if my insulin level will get lower with better glucose control. 
I said my HDLc/triglyceride ratio was less than 3.  My non-fasting TG was 99. 
My systolic BP is 116 on ramipril for DM2 and Diltazem for atrial fibrillation. My waist is 41.5" and I want to try to get it under 40".  My bioelectrical impedance scale says my visceral fat is 14? 
When I do my Liposcience Advanced Lipid Study by NMR, my IR score is in the middle in the 40's.  Not a strong score for IR even though my VLDL was a little high because it was non-fasting.

I know I am DM2, I know am IR even though my insulin level was normal. 
I think I have lost enough beta cells in the pancreas that I can't muster a high insulin level a younger person with IR would have.  DM1 may have a zero insulin level.  I don't want to get there.  I hope by losing more visceral fat, I can increase my adiponectin to help my IR.

I told my Endocrinologist I was in Asia and Hawaii from Jan. 11 to March 18, 2018 and I was running in the high 170's FBS even though I was walking at least 10,000 plus steps a day.  When I came home my Hgb A1c was 7.7.  I tried to stay on Atkins but on vacation I was probably not in NK. I was not taking my serum ketone levels so I can't know for certain.

I have been in Topeka for a month and have had fasting serum ketone greater than 0.4 every day except for O.2 and 0.4 on two separate mornings. My fasting glucose has been in the 140's.

Thus I told my Endocrinologist I thought my Hgb. A1c to be back at 6.5.

We compromised and I would start doing post prandial glucoses as I mentioned above but no insulin levels.   

I told her I knew I maintained my low carb diet because I was in serum NK(nutritional ketosis) each morning in the last month.  She was surprised there was a serum finger stick home test for ketones and didn't know anything about it.  This is a young Endocrinologist out of training a year ago? 

She wanted to fire me because she felt I didn't trust her as I was asking questions.  I said I wanted her to be my Doctor.  I told her I liked and trusted her.  She relented.  

When I got home her nurse called and said she transferred me to another physician.  

Update

4-2-18: 2.5 hours after 3 tacos for lunch: 166 glucose
              
4-25-18: 3.0 hours after 3 eggs/3 slices bacon for breakfast: 149 glucose

             4.0 hours after  Mexican Lamb soup and Premium Clear Protein drink 20 g protein, no carbs for lunch: 145 glucose

Thus on strict low carbohydrate diet I am good on my post-prandial glucose and so far do not need to go on Actos.  My AM ketone level on 4-25-18 was 1.1 

I would still like to get a couple of Insulin levels with fasting glucose.  I hope my next Endocrinologist will allow it.