Lipids and Insulin

Discussion in 'Health and medical' started by Jim Dumas, Mar 4, 2004.

  1. Willbill

    Willbill Guest

    Jim Dumas wrote:

    > willbill wrote:

    >> if you've never looked at that book by Parsons, it's
    >> worth looking at coz it gives detailed info on how to
    >> possibly work around "flushing"
    >>
    >> also, drink dry red wine. :)

    > I may try niacin if I can't lower total cholesterol with
    > my current approach.

    imo your total cholesterol number isn't that high. what you
    need is a higher HDL number, and niacin therapy and alcohol
    are #1 and #2 for higher HDL

    > I used to drink half a 750 ml bottle of California Merlot
    > or Cabernet each day at dinner. But my metabolism changed
    > and I found that it dehydrated me too much. So I now drink
    > alcohol only on special occasions. The problem with using
    > wine medicinally is the potential for excessive use. So I
    > find I'm better off not to tempt myself.
    >
    > On the basal NPH front: I added a 6U NPH bumper dose to my
    > morning 16U ultralente (separate injections) to see if it
    > will lower my high morning triglycerides. These were left
    > over from a HIGH (off scale) bedtime reading so I could
    > not accurately dose for them. The cause was too much
    > cheese at dinner. So I'm now testing the hypothesis that
    > NPH is better than ultralente, as a variable basal,
    > because of its shorter tail. The objective is to minimize
    > hypoglycemia and triglycerides during the day. The method
    > corrected a morning Humalog dose for the NPH taken, as
    > done in the bedtime examples in this thread. So it should
    > be interesting today.
    >
    > In any case, thanks for the suggestions,

    you're welcome

    here's another one:

    get pure beef-Lente from CP and dose it 1x at sometime
    in the evening/bedtime (as part of an MDI/DAFNE
    routine for you)

    (and given your high early morning basal needs, an
    evening 1x of beef-lente is by far better for you than 1x
    of beef-PZI)

    this assumes that you've never used beef-insulin

    (i think that that's what you've said, but am not totally
    sure. main thing that i'm aware of is your weird focus on
    "studies" and antibodies)

    iow, just do it and find out

    my hunch is that you will be pleasantly (!) surprised

    bill t1 since '57, ex 8-yr pumper, pork/beef-L 2x,
    simple MDI/DAFNE
     


  2. Jim Dumas

    Jim Dumas Guest

    willbill wrote:

    > imo your total cholesterol number isn't that high. what
    > you need is a higher HDL number, and niacin therapy and
    > alcohol are #1 and #2 for higher HDL

    It turns out that as triglycerides fall, the carrier protein
    VLDL is converted into HDL via the enzyme lipoprotein lipase
    that's under control of insulin. So I can raise my HDL by
    keeping my TGs low. There is also a direct correlation of
    LDL with BG. So I can keep LDL (bad cholesterol) low by
    keeping BG under tight control. LDL is also lowered, as VLDL
    is converted into HDL instead of LDL via lipoprotein lipase
    that's produced by basal insulin. I can see these minor
    movements in the bedtime to morning lipid assays.

    Next, the effects of exercise have not "kicked in." So I
    should see HDL increase and LDL decrease as I exercise more.
    So I'll wait for these effects to play out before I get
    excited about niacin.

    Next, yesterday's 6U NPH piggybacked on the 16U ultralente
    in the morning did not produce hypoglycemia during the day.
    But unfortunely we went out to dinner unexpectedly, and that
    blew my TGs off the scale (HIGH assay) at bedtime. The
    morning TGs were 188 mg/dl so my extra 8U NPH at bedtime
    (26U NPH basal dose) worked well and no nocturnal
    hypoglycemia occurred. Morning BG was 118 mg/dl and bedtime
    BG was 149 mg/dl. The bedtime dose was 6R+26N with lower R
    from the shift to higher basal NPH. The dinner was at a
    local micro brewery and I had two large dark beers with
    scallops, baked potato and sour cream. So TGs were in
    trouble. I'll have to do this morning NPH again when I'm not
    busy so I can monitor it closely.

    Lastly, please note that I'm trying to cut beef out of my
    diet!

    BTW, I read something about T1s using mixed beef-pork Lilly
    Iletin having higher anti-insulin antibody concentrations,
    (synergy of two antigens are more potent than each one
    separately). It was this group of T1s that have difficulty
    transferring to human rDNA insulins because their antibodies
    bind easily to human rDNA insulin. The article mentioned
    that monocomponent insulin produces lower respective
    antibody titers with less cross-binding to human rDNA
    insulin. But I can't remember were the article is and have
    been looking for it. In any case, T1s should pick an insulin
    molecule species and stick with it to keep antibody titers
    to a miminum. I've picked human and plan to stick with it
    (so no Lantus either). When my therapy fails, then I'll
    consider a change in insulin preparations.

    Thanks again,
    --
    Jim Dumas T1 4/86, background retinopathy, rarely
    hypoglycemic: <1/mo. lispro+R+U+NPH daily, moderate
    exercise, typically <6% HbA1c
     
  3. Jim Dumas

    Jim Dumas Guest

    Jim Dumas wrote:

    > It turns out that as triglycerides fall, the carrier
    > protein VLDL is converted into HDL via the enzyme
    > lipoprotein lipase that's under control of insulin. So I
    > can raise my HDL by keeping my TGs low. There is also a
    > direct correlation of LDL with BG. So I can keep LDL (bad
    > cholesterol) low by keeping BG under tight control. LDL is
    > also lowered, as VLDL is converted into HDL instead of LDL
    > via lipoprotein lipase that's produced by basal insulin.

    Before this thread ends I just want to point out that
    Joslin's Diabetes Mellitus, 13th ed., p.374 under the lipid
    disorders chapter 21 states:

    "VLDL production is influenced by glucose, fatty acids and
    insulin. ... Insulin is required for VLDL production, both
    for apoprotein synthesis and because it regulates several
    enzymes involved in lipogenesis. On the other hand,
    increases in insulin have been shown to inhibit VLDL
    secretion in hepatocytes by phosphorylating apoB, which
    impedes the assembly of apoB with lipids."
    ---

    This suggests too little as well as too much insulin keeps
    triglycerides high thereby pointing to basal insulinemia as
    the key to controlling hypertriglyceridemia. This is alittle
    scary as you could be well controlled but have low basal
    insulinemia with high VLDL triglycerides (major CVD risk).
    The same is true if you are over-insulinated with
    hypoglycemic events too often. So there is some middle
    ground insulinemia that disposes of VLDL and triglycerides
    properly that is not handled by the prandial insulin dose.
    This is where intermediate-acting NPH or lente really shine.

    The VLDL transport protein is produced and destroyed or
    converted by the liver. After the liver makes triglycerides
    they are transported via VLDL to the fat cells. The VLDL is
    then removed from circulation under insulin control by the
    liver. Albumin is used to transport triglycerides (FFA) from
    fat cells back to the liver and muscles. But VLDL moves TGs
    from liver to fat cells. VLDL is implicated in CHD/CVD so by
    lowering TGs, I also lower VLDL and my CVD risk.

    ASIDE: The death of T1 Dave Groves with his double bypass
    got me off my duff to look at this problem. I could have
    gone for years thinking I was fine with only BG assay data.
    But when you add bedtime triglycerides to your control
    strategy, you see hypertriglyceridemia is a major problem
    (for all DMs per Joslin's DM text). If you don't add basal
    insulin to counter this, it will remain high through the
    night and increase your CVD risk.

    In any case, this suggests CHD/CVD is a basal insulinemia
    issue and could be iatrogenic via improper basal insulin
    therapy. Moreover, it surprises me how subtle changes in my
    R+NPH bedtime ratio manages to control both BG (100-150
    mg/dl) and TGs (100-200 mg/dl) without increasing rates of
    nocturnal hypoglycemia.

    Now all I need is a cheap triglyceride assay method with
    broader assay range to about 700 mg/dl. (Guyton's Med
    Physiology text says the average plasma lipoproteins sum to
    700 mg/dl! So an assay range to 500 mg/dl is too low.)

    So IMO, BGs+TGs are the future for insulin therapy
    management,
    --
    Jim Dumas T1 4/86, background retinopathy, rarely
    hypoglycemic: <1/mo. lispro+R+U+NPH daily, moderate
    exercise, typically <6% HbA1c
     
  4. Jim Dumas wrote:
    >
    snipped
    > So IMO, BGs+TGs are the future for insulin therapy
    > management,
    > --
    > Jim Dumas T1 4/86, background retinopathy, rarely
    > hypoglycemic: <1/mo. lispro+R+U+NPH daily, moderate
    > exercise, typically <6% HbA1c

    Jim, I have to thank you for posting your experiences. I
    have been following this thread with great fascination.

    Your information is another valuable tool in the health
    maintenance kit.

    Vicki
     
  5. Jim Dumas

    Jim Dumas Guest

    Vicki Beausoleil wrote:

    > Jim, I have to thank you for posting your experiences. I
    > have been following this thread with great fascination.
    >
    > Your information is another valuable tool in the health
    > maintenance kit.

    You're welcome, Vicki. Diabetic dyslipidemia (generally as
    hypertriglyceridemia and elevated LDL) has been known to
    exist for years. There is even one of the heart arteries
    known to have high plaque for DMs that the normal population
    doesn't have. I was just reading a Diabetes Care article
    from 1992 that investigated T2 dyslipidemia that concluded
    tight BG control wasn't enough to prevent CVD. T1 CVD is
    almost the same as T2 CVD so all of the results apply. But
    the current prevention starts with normalization of BGs
    before adding other meds.

    On the variable NPH dosing front: I had my typical fat-
    ladened 1/2 pizza yesterday but preemptively took 26R+10N
    before dinner (5pm) to see if bedtime (1am) TGs would be
    lower. They were still off the scale (HIGH >500
    mg/dl) but my bedtime NPH was held to 17U (vs. 18U normally)
    and TGs came in at 188 mg/dl (<=200 is good). I had
    no nocturnal hypoglycemia but morning BG was 174
    mg/dl. So under did it alittle. But still learning
    and experimenting.

    One interesting result for pumpers is the observation of
    lower TGs than normals typically achieve, (Joslin's DM, 13th
    ed., lipid disorder chapter). That's quite interesting and
    is a major reason to pump, IMO. I'd like to see some
    clinical trial for MDI vs. pumpers vs. normals (controls)
    for CVD. That would really be interesting.

    In any case, I guess I'll know in 20 years if I'm right,
    --
    Jim Dumas T1 4/86, background retinopathy, rarely
    hypoglycemic: <1/mo. lispro+R+U+NPH daily, moderate
    exercise, typically <6% HbA1c
     
  6. On Mon, 22 Mar 2004 19:00:40 GMT, in misc.health.diabetes Jim Dumas
    <[email protected]!mindspring.com> wrote:

    >>> with regard to improving your cholesterol levels, i
    >>> suggest you look into niacin therapy.
    >>
    >>That's a good suggestion. Joslin's DM, 13th ed., p.386,
    >>mentions >=3D =
    1=20
    >>gm/day of nicotinic acid is necessary to see "profound lipid-
    >>lowering=20 effects." Unfortunately, I have rosacea and
    >>the "flushing" effect of=20 niacin will increase the
    >>facial vasodilation and make the condition =
    worst. =20
    >>So niacin is not good for me.

    You might ask about Niaspan (or, though I don't know the
    name, similar = other prescription versions). this is a long
    acting/delayed acting niacin = form, unlike the over the
    counter delayed acting ones (which i'm told can be = toxic
    to the liver). While I got some flushing the first few weeks
    I took it, = especially at the beginning lower doses, I'm
    now up to a two gram per day dose, = taken at bedtime. Even
    when I then get up at 3 am to check an overnight bg, I've
    detected no remaining flushing effect, and certainly, none
    while normally= awake during the day. Apparently, with
    Niaspan, many patients find the = flushing effect goes away
    in a few weeks, as the body adjusts. That, at least, = has
    been my experience, and it seems worth it, as my HDL levels
    went up from = around 35 to 45 just on half the dose I'm
    taking now. A worthwhile difference, my cardiologist feels
    (and so do I). =20

    Peter
     
  7. Jim Dumas

    Jim Dumas Guest

    Peter W. Rowe wrote:

    > You might ask about Niaspan (or, though I don't know the
    > name, similar other prescription versions). this is a long
    > acting/delayed acting niacin form, unlike the over the
    > counter delayed acting ones (which i'm told can be toxic
    > to the liver). While I got some flushing the first few
    > weeks I took it, especially at the beginning lower doses,
    > I'm now up to a two gram per day dose, taken at bedtime.
    > Even when I then get up at 3 am to check an overnight bg,
    > I've detected no remaining flushing effect, and certainly,
    > none while normally awake during the day. Apparently, with
    > Niaspan, many patients find the flushing effect goes away
    > in a few weeks, as the body adjusts. That, at least, has
    > been my experience, and it seems worth it, as my HDL
    > levels went up from around 35 to 45 just on half the dose
    > I'm taking now. A worthwhile difference, my cardiologist
    > feels (and so do I).

    Hi Peter,

    That's good info, thanks.

    My HDL averages 39 mg/dl before exercise effects. I've had a
    55-60 mg/dl HDL when I was running every other day before I
    hurt my knee. I now ride a road racer bicycle and will try
    to build up to 20 miles in 1 hour every other day. Since I
    now live in Florida, I can exercise all year (but in the
    mornings in the summer heat, of course). So I plan to use
    exercise, diet and insulin (variable basal insulinemia
    clearly lowers triglycerides in my samples: ex. pizza
    dinner, usual bedtime NPH gives 183 mg/dl in the morning
    fast, pizza dinner +8U extra NPH gives 93 mg/dl next
    morning, pizza dinner + 3U NPH + 16 miles/hour exercise
    before pizza gives 67 mg/dl fasting triglycerides the next
    morning), thereby pushing HDL higher via triglyceride
    depletion (VLDL is converted into HDL under these low TG
    conditions). But I haven't exercised enough yet to lower
    HDL. However, I have measured a 46 mg/dl HDL in my quest to
    lower TGs. But I have not duplicated this again (diet
    dependent, it was a low fat dinnner).

    In any case, I'll try to use a "natural" method first and in
    a year reevaluate. If it fails, I'll start some
    pharmacological intervention.

    Nobody in my family dies from heart attacks. We all seem to
    expire with a cerebral hemorrhage at 95-100 years old. My 79
    yo mother has had a 240
    mg/dl total cholesterol for years. She tosses her Lipitor in
    the trash that her Doc forces on her then goes out and
    pushes a snow shovel or push mower around the yard in
    Rhode Island. Her face gets bright red and she runs over
    any of us children that get in her way. (OK Mom! Watch my
    feet please!)

    So I'll follow her lead and exercise too. Thanks again,
    --
    Jim Dumas T1 4/86, background retinopathy, rarely
    hypoglycemic: <1/mo. lispro+R+U+NPH daily, moderate
    exercise, typically <6% HbA1c
     
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