new danger proposed
Peter C
after the ingestion of foods with a large content of fat.
Lipemia being "The presence of an abnormally high concentration of lipid in
the blood. Called also hyperlipemia, hyperlipidemia, hyperlipoidemia,
lipidemia, lipoidemia."
Postprandial lipemia now recognised as "an independent risk factor for
coronary artery disease."
And who are prone to postprandial lipemia - you guessed it - YOU - "Type 2
diabetes mellitus and insulin resistance are associated with enhanced
postprandial lipemia".
Luckily diabetic medications help reduce postprandial lipemia - especially
Analogue insulins, acarbose and metformin.
But is this another test we need to do, testing lipids pp ??? Or should we
just control fat levels and take the meds ?
Anybody know WHICH research has established "Postprandial lipemia ... as an
independent risk factor for coronary artery disease."
The effects of medications used for the management of diabetes and obesity
on postprandial lipid metabolism.
Eleftheriadou I, Grigoropoulou P, Katsilambros N, Tentolouris N.
Curr Diabetes Rev. 2008 Nov;4(4):340-56.
PMID: 18991602 [PubMed - in process]
Michelle C
"Peter C" <espr...@europe.com> wrote in message
news:ggpado$vcl$1...@aioe.org...
Lipemia after eating is due to excess carbs. Insulin instructs the body to
store excess carbs as fat so the body changes excess carbohydrate into
triglycerides causing the lipemia.
This is just the same information about Type 2 diabetics being susceptible
to heart disease, but in a new form.
--
Best regards,
Michelle C., T2
diet & exercise
BMI 21.5
Peter C
"Michelle C" <bookb...@yahoo.com> wrote in message
news:ggpbpg$7t2$1...@news.motzarella.org...
>
>
> Lipemia after eating is due to excess carbs. Insulin instructs the body
> to store excess carbs as fat so the body changes excess carbohydrate into
> triglycerides causing the lipemia.
>
of it - postprandial lipemia.
Postprandial or alimentary lipemia is defined as ..."Transient lipemia
occurring after the ingestion of foods with a large content of fat. Also
called postprandial lipemia."
Carbs are not implicated in it.
Ozgirl
> Postprandial lipemia ( alimentary lipemia) - Transient lipemia
> occurring after the ingestion of foods with a large content of fat.
> Lipemia being "The presence of an abnormally high concentration of
> lipid in the blood. Called also hyperlipemia, hyperlipidemia,
> hyperlipoidemia, lipidemia, lipoidemia."
>
> Postprandial lipemia now recognised as "an independent risk factor for
> coronary artery disease."
> And who are prone to postprandial lipemia - you guessed it - YOU -
> "Type 2 diabetes mellitus and insulin resistance are associated with
> enhanced postprandial lipemia".
> Luckily diabetic medications help reduce postprandial lipemia -
> especially Analogue insulins, acarbose and metformin.
> But is this another test we need to do, testing lipids pp ??? Or
> should we just control fat levels and take the meds ?
>
> Anybody know WHICH research has established "Postprandial lipemia ...
> as an independent risk factor for coronary artery disease."
Is this what you are looking for?
http://www.lipidworld.com/content/4/1/21
Andrew B. Chung, MD/PhD
> Peter C wrote:
>
> > http://groups.google.com/group/alt.support.diabetes/msg/78829bf1e1ad19db?
> >
> > The research is not talking about lipemia in general but one particular type
> > of it - postprandial lipemia.
> > Postprandial or alimentary lipemia is defined as ..."Transient lipemia
> > occurring after the ingestion of foods with a large content of fat. Also
> > called postprandial lipemia."
> > Carbs are not implicated in it.
> >
>
Not for folks low-carbing via a high fat diet.
Thus, it remains wiser to simply eat less, down to the right amount to
avoid over-eating either carbs or fat:
http://groups.google.com/group/sci.med.cardiology/msg/3558812d72ab4e17?
Nicodemus
news:52efc273-0c81-4dd6...@v4g2000yqa.googlegroups.com:
Hello Again Dr. Chung
May I suggest that you engage into your soul and everlasting membership,
the body and flesh, do you ever wonder about the jews?
Amazing Grace
Hi Dan, May You Find Complete Place in that keypress
May You Become The Most Complete
May You Cast Your Vision On The Most Complete World
It Sounds Like Hallelujah
In a twinkle it Becomes
Michelle C
"Ozgirl" <are_we_t...@maccas.com> wrote in message
news:6pb769F...@mid.individual.net...
Thanks Jan. I would dearly love to know what constituted the "fatty meal".
Was it just fat? Or was it the typical high carb diet plus copious fat?
Very pertinent facts left out of their data.
bgl
>
>> The research is not talking about lipemia in general but one
>> particular type of it - postprandial lipemia.
>> Postprandial or alimentary lipemia is defined as ..."Transient
>> lipemia occurring after the ingestion of foods with a large content
>> of fat. Also called postprandial lipemia."
>> Carbs are not implicated in it.
"Susan" <su...@nothanks.org> wrote in message
news:6patrbF...@mid.individual.net...
>
> Carbs, as Michelle said are the cause of post prandial lipemia.
>
Maybe it's the bug I'm cultivating & my mind is mushy, but it looks like
these both can't be true.
If ppl is *defined* as related to fat intake, how can carbs be "the
cause"?
Unless maybe it requires lots of both?
bj
GysdeJongh
news:ggpado$vcl$1...@aioe.org...
> Anybody know WHICH research has established "Postprandial lipemia ... as
> an independent risk factor for coronary artery disease."
Maybe this ?
Diabetes Res Clin Pract. 2008 Jun;80(3):380-5. Epub 2008 Mar 5.
Postprandial lipaemia in patients with impaired fasting glucose, impaired
glucose tolerance and diabetes mellitus.
AIMS: To compare the postprandial lipid responses in subjects with
prediabetes (IFG and IGT), newly detected diabetes mellitus (NDDM) and
normal glucose tolerance (NGT). METHODS: Postprandial lipid responses to a
standard oral fat challenge was studied in forty-four subjects who were
divided after an OGTT into NGT, pure impaired fasting glucose (PIFG), pure
impaired glucose tolerance (PIGT) and NDDM. RESULTS: There was a
significantly higher postprandial triglyceride (PPTg) response with a higher
PPTg area under curve (p=0.004) and peak PPTg levels (p=0.003) in patients
with NDDM but not with either PIFG (p>0.05) or PIGT (p>0.05) when compared
with NGT. Overall, PPTg responses correlated significantly with fasting
plasma glucose (p=0.001) and 2h plasma glucose (p=0.001) but not with age,
sex, body mass index, waist, or insulin resistance. CONCLUSION: Subjects
with newly detected diabetes mellitus displayed postprandial
hypertriglyceridemia after a standard oral fat meal challenge while no such
abnormality could be demonstrated in subjects with IFG or IGT. This defect
is probably related to glycemic status and insulin resistance.
PMID: 18321605
Review :
J Am Coll Cardiol. 2008 Jan 22;51(3):249-55.
Dietary strategies for improving post-prandial glucose, lipids,
inflammation, and cardiovascular health.
The highly processed, calorie-dense, nutrient-depleted diet favored in the
current American culture frequently leads to exaggerated supraphysiological
post-prandial spikes in blood glucose and lipids. This state, called
post-prandial dysmetabolism, induces immediate oxidant stress, which
increases in direct proportion to the increases in glucose and triglycerides
after a meal. The transient increase in free radicals acutely triggers
atherogenic changes including inflammation, endothelial dysfunction,
hypercoagulability, and sympathetic hyperactivity. Post-prandial
dysmetabolism is an independent predictor of future cardiovascular events
even in nondiabetic individuals. Improvements in diet exert profound and
immediate favorable changes in the post-prandial dysmetabolism.
Specifically, a diet high in minimally processed, high-fiber, plant-based
foods such as vegetables and fruits, whole grains, legumes, and nuts will
markedly blunt the post-meal increase in glucose, triglycerides, and
inflammation. Additionally, lean protein, vinegar, fish oil, tea, cinnamon,
calorie restriction, weight loss, exercise, and low-dose to moderate-dose
alcohol each positively impact post-prandial dysmetabolism. Experimental and
epidemiological studies indicate that eating patterns, such as the
traditional Mediterranean or Okinawan diets, that incorporate these types of
foods and beverages reduce inflammation and cardiovascular risk. This
anti-inflammatory diet should be considered for the primary and secondary
prevention of coronary artery disease and diabetes.
PMID: 18206731
hth
Gys
GysdeJongh
news:ggpado$vcl$1...@aioe.org...
> Anybody know WHICH research has established "Postprandial lipemia ... as
> an independent risk factor for coronary artery disease."
Maybe this ?
Alan S
That is a review, not a study. Here it is:
The effects of medications used for the management of
diabetes and obesity on postprandial lipid metabolism.
Eleftheriadou I, Grigoropoulou P, Katsilambros N,
Tentolouris N.
33 Lakonias Street, 115 27 Athens, Greece.
nte...@med.uoa.gr.
Postprandial lipemia has emerged as an independent risk
factor for coronary artery disease. In this systematic
review we examined the effect of the medications used for
the management of diabetes, obesity and dyslipidemia on
postprandial lipemia. It should be mentioned that no
standardization exists for a test meal and for the duration
of observation postprandially to allow for direct
comparisons between the published studies. Type 2 diabetes
mellitus and insulin resistance are associated with enhanced
postprandial lipemia. Insulin is effective in reducing both
fasting and post prandial total triglyceride levels as well
as triglycerides contained in the triglyceride-rich
lipoprotein sub-fractions. Additionally, the newer
rapid-acting insulin analogues seem to be more effective in
the reduction of postprandial lipemia than the short-acting
human insulins. Acarbose ameliorates postprandial lipemia
and reduces the atherogenic chylomicron and very low density
lipoprotein remnants. Metformin reduces both fasting and
postprandial triglyceridemia, fasting and post-prandial free
fatty acids and may increase the concentrations of the high
density lipoprotein cholesterol. Sulfonylureas reduce
fasting and postprandial triglyceride levels while data on
the effect on high density lipoprotein levels are
inconsistent. The effect of meglitinides on postprandial
lipid metabolism is neutral. Rosiglitazone decreases fasting
and postprandial free fatty acids but has no significant
effect on fasting and postprandial triglycerides.
Pioglitazone has additional beneficial effects on lipid
metabolism because it reduces postprandial free fatty acids,
fasting and postprandial triglycerides and increases high
density lipoprotein cholesterol levels. Limited available
data suggest that glucagon-like peptide-1 analogues and
vildagliptin reduce postprandial lipemia through reduction
of intestinally-derived triglycerides. No data exist on the
effect of sitagliptin on postprandial lipemia. Orlistat
improves postprandial lipemia by reducing the absorption of
the dietary fat; no data exist on the effect of sibutramine
and rimonabant on the metabolism of lipids in the
postprandial state.
Cheers, Alan, T2, Australia.
--
d&e, metformin 2000 mg
Everything in Moderation - Except Laughter.
http://loraldiabetes.blogspot.com (Analysis of a Day's Meals)
http://loraltravel.blogspot.com (Two Indian Hotels: to Sleep, Perchance...)
Alan S
<espr...@europe.com> wrote:
>
>"Michelle C" <bookb...@yahoo.com> wrote in message
>news:ggpbpg$7t2$1...@news.motzarella.org...
>>
>>
>> Lipemia after eating is due to excess carbs. Insulin instructs the body
>> to store excess carbs as fat so the body changes excess carbohydrate into
>> triglycerides causing the lipemia.
>>
>The research is not talking about lipemia in general but one particular type
>of it - postprandial lipemia.
Which research? urls or pubmed details please.
>Postprandial or alimentary lipemia is defined as ..."Transient lipemia
>occurring after the ingestion of foods with a large content of fat. Also
>called postprandial lipemia."
>Carbs are not implicated in it.
>
What are you quoting that from?
Alan S
Thanks, Jan
Alan S
<are_we_t...@maccas.com> wrote:
The first thing that jumps out is that they appear to have
only used a high-fat meal for their study. There doesn't
seem to be any comparison with a high-carb meal. But I've
only skimmed it so far.
This is one of the references to that, which is given as the
basis of the high-fat meal; still reading it:
Relation of Triglyceride Metabolism and Coronary Artery
Disease Studies in the Postprandial State
Full text:
http://atvb.ahajournals.org/cgi/reprint/12/11/1336
GysdeJongh
news:7221j4l2aop6khril...@4ax.com...
Hi Alan,
the full text of the article is here, but you have to click in a few
unexpected places to download it :
http://www.ncbi.nlm.nih.gov/pubmed/18991602?dopt=Citation
Curr Diabetes Rev. 2008 Nov;4(4):340-56.
The effects of medications used for the management of diabetes and obesity
on postprandial lipid metabolism.
Eleftheriadou I, Grigoropoulou P, Katsilambros N, Tentolouris N.
PMID: 18991602
hth
Gys
Alan S
<bjon...@verizon.net> wrote:
>
>Maybe it's the bug I'm cultivating & my mind is mushy, but it looks like
>these both can't be true.
>
>If ppl is *defined* as related to fat intake, how can carbs be "the
>cause"?
>
>Unless maybe it requires lots of both?
>bj
That is something Taubes comments on. I am coming to the
realisation that there seems to be a trigger threshold for
lipids, where fat and carbs both need to be ingested
together in certain quantities to lead to bad results.
The paper I am reading at the moment (mentioned in another
threadlet) is a case in point.
http://atvb.ahajournals.org/cgi/reprint/12/11/1336
They used a meal described as "high-fat" to produce
excessive post-prandial triglyceride levels, but it is only
in the fine detail that you find that the meal also included
25gms carb as well as 65gms fat after a 14hr fast.
We see the ultimate version of this in the BGs "Pizza
Effect" we experience; the same sort of long, slow rise and
fall occurs for triglycerides after mixed high carb+fat
meals.
The other fascinating thing in the paper I am reading is
that high post-prandial trigs are not necessarily reflected
in increased fasting trigs. The post-prandial trigs were a
better predictor of CAD than fasting lipids.
I haven't finished digesting the study yet.
Alan S
From the references to the paper:
"The standardized fatty meal whose ingredients have been
described27 contained 729 kcal per square meter of body
surface and consisted of 5.3 g protein, 24.75 g
carbohydrate, 240 mg cholesterol, and 65.2 g fat (from heavy
whipping cream) with a polyunsaturated to saturated fat
ratio of 0.06."
Ozgirl
> x-no-archive: yes
>
> bgl wrote:
>
>> Maybe it's the bug I'm cultivating & my mind is mushy, but it looks
>> like these both can't be true.
>>
>> If ppl is *defined* as related to fat intake, how can carbs be "the
>> cause"?
>>
>> Unless maybe it requires lots of both?
>
> fat would increase it, at most, from my understanding.
>
> Lipemia means fat in the blood, and is not defined in terms of where
> it's from, so I'd argue such a def would be presumptive and wrong.
Well according to the study in my link it said that the PP lipemia was worse
in those whose fasting trigs were higher... it is still the carbs.
Peter C
That's just common sense and probably doesn't need a research paper to
show it.
if your lipids are lower to start with the peak of the transient
postprandial spike caused by a high fat meal will be lower. Same as if
your pre-meal Bg is 4.0 a 5 point spike will take it to 9 pp. If it is
6.0 a 5 pt spike will take it to 11 pp.
All the research seems to be suggesting, without stating it
explicitly, that carbs are responsible for the long term secular
problems with lipemia while a high fat content in a meal will cause a
short term postprandial/alimentary spike in lipids.
I doubt if any of us have had lipids tested at 30 mins, 1 hour, 2
hours after a meal so we wouldn't know whether or not we were
esperiencing transient postprandial lipemia.
I still can't find in any of the links thus far provided any proof
that transient postprandial/alimenatry lipemia "is an independent
marker" for cvd. All the papers put up so far in this thread seem to
take it as a proven premise.
Peppermint Patootie
Alan S <loralgtwei...@gmail.com> wrote:
Once they mention triglycerides, you know they must be talking about
lots of carbs, since that's what drives up tris.
PP
Peter C
"Peppermint Patootie" <Peppermin...@yahoo.com> wrote in message
news:Peppermint_Patootie->> >> Luckily diabetic medications help reduce
postprandial lipemia -
>
> Once they mention triglycerides, you know they must be talking about
> lots of carbs, since that's what drives up tris.
Too simplistic .... trigs are also driven up by high fat meals ( the
transient postprandial/alimenatry lipemia under discussion.)
Just a selection of research papers dealing with OFTTs ( Oral Fat Tolernace
Tests ) show this ....and it seems to be a particular danger for diabetics
after a high fat meal....
http://lib.bioinfo.pl/pmid:17362944
http://www.ncbi.nlm.nih.gov/pubmed/2038874
http://care.diabetesjournals.org/cgi/content/full/24/7/1299-a
http://www.omafra.gov.on.ca/english/research/new_directions/projects/2004/sr9160.htm
Nicky
wrote:
>Too simplistic .... trigs are also driven up by high fat meals
I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
formed when carbs are present.
Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.4% BMI 25
Nicky
wrote:
>Luckily diabetic medications help reduce postprandial lipemia - especially
>Analogue insulins, acarbose and metformin.
Hmmm. All those ones that work by tucking away excess carbs.
>But is this another test we need to do, testing lipids pp ???
Well, would certainly be interesting.
Michelle C
Thanks Alan!
Peter C
"Nicky" <ukc802...@btconnect.com> wrote in message
news:4pr2j49miat0q9rrj...@4ax.com...
> On Sat, 29 Nov 2008 16:21:07 -0000, "Peter C" <espr...@europe.com>
> wrote:
>
>>Too simplistic .... trigs are also driven up by high fat meals
>
> I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
> formed when carbs are present.
>
here's a ducky little simulation, press the "play" button.
http://www.tvdsb.on.ca/westmin/Science/sbioac/biochem/triglyc.htm
Nicky
wrote:
>
>"Nicky" <ukc802...@btconnect.com> wrote in message
>news:4pr2j49miat0q9rrj...@4ax.com...
>> On Sat, 29 Nov 2008 16:21:07 -0000, "Peter C" <espr...@europe.com>
>> wrote:
>>
>>>Too simplistic .... trigs are also driven up by high fat meals
>>
>> I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
>> formed when carbs are present.
>>
>but they need fatty acids to be formed .
>here's a ducky little simulation, press the "play" button.
>
>http://www.tvdsb.on.ca/westmin/Science/sbioac/biochem/triglyc.htm
You don't get the glycerol without the carb, it's formed from glucose.
Nicky
Peter C
>>> I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
>>> formed when carbs are present.
>>>
>>but they need fatty acids to be formed .
>>here's a ducky little simulation, press the "play" button.
>>
>>http://www.tvdsb.on.ca/westmin/Science/sbioac/biochem/triglyc.htm
>
> You don't get the glycerol without the carb, it's formed from glucose.
>
When you play the simulation is it suggesting that you need molecules of
saturated fatty acids and glycerol in the proportion of 3 to 1 to create one
triglyceride ?
If that is the case then starving the glycerol of saturated fatty acids will
lower the postprandial lipemia caused by a high fat meal that these
researchers have collared as an independent risk factor in cvd.
When I have my lo/no carb high/moderate fat breakfasts am I jumping out of
the fire into the frying pan ?
Am I keeping bgs in check but experiencing a potentially dangerous lipid
spike that as so far remained under the radar ?
Should T2 diabetics have their lipid panels checked after a relatively high
fat meal to check for postprandial lipemia ?
Answers on a postcard please.
_______________________________________________________________
Come in Ancel Benjamin Keys and your "relatively low fat" diet - nearly all
is forgiven.
Alan S
<espr...@europe.com> wrote:
I gave the meal proportions. Although they describe it as a
"fatty" meal (and it is) it was also moderate to high in
carbs and rather low in protein. Read the detail in the
paper I supplied.
http://atvb.ahajournals.org/cgi/reprint/12/11/1336
It is surprisingly old, from 1992.
"The standardized fatty meal whose ingredients have been
described27 contained 729 kcal per square meter of body
surface and consisted of 5.3 g protein, 24.75 g
carbohydrate, 240 mg cholesterol, and 65.2 g fat (from heavy
whipping cream) with a polyunsaturated to saturated fat
ratio of 0.06."
They are not clear about the components of the control diet,
but they note that the past diet of all subjects was:
"Dietary habits were indistinguishable between cases
and control subjects. The diet of cases and control
subjects consisted, on the average, of 12% and 12% of
calories from protein, 42% and 43% from carbohydrates,
and 46% and 45% from fat, with a polyunsaturated
to saturated fat ratio of 0.59 and 0.55, respectively.
Mean daily cholesterol intake was 442 mg and 466 mg,
respectively. Thus, the diet of the study subjects closely
reflected that reported for the Austrian population.32
Regarding exercise, a majority of subjects in both"
Unfortunately they aren't specific about the actual meal for
the control subjects.
The subjects in that referenced study were all non-diabetic,
but even so I would consider 25gms carb after a 14hr fast a
high load. That combination of carbs and fat and low protein
definitely worked to raise the trigs on the day, but did not
seem to raise the fasting trigs.
In that paper they also formed the conclusion that:
"The findings support the concept that the negative
association between HDL cholesterol levels and CAD actually
originates in part from a positive relation between CAD and
plasma triglycerides, as ascertained in the postprandial
state."
and
"The evidence we present establishes by statistical
criteria that triglyceride metabolism is a risk factor for
CAD."
and
"The evidence we present establishes by statistical
criteria that triglyceride metabolism is a risk factor for
CAD. Global postprandial lipemia was higher in cases
than in control subjects, and single triglyceride levels 6
or 8 hours postprandially that caused the difference in
lipemia were strong predictors of disease (Table 3 and
Figure 1)."
Peter C
> On Sat, 29 Nov 2008 16:21:07 -0000, "Peter C"
> the control subjects.
>
> The subjects in that referenced study were all non-diabetic,
> but even so I would consider 25gms carb after a 14hr fast a
> high load.
The load for a OGTT after fasting is 75g of glucose. So the 25g looks
quite moderate. The normal diet was roughly 40% - 40% carbs to fat and
the high fat test meal was something like 68 - 28 fat to carb.
That combination of carbs and fat and low protein
> definitely worked to raise the trigs on the day, but did not
> seem to raise the fasting trigs.
One of the diagrams shows that plasma trigs doubled in the first two
hours from the fasting baseline and had doubled again at 4 hours.
Thereafter the controls declined but the CAD subjects had risen again
at 6 hours.
Unfortunately they did not test at 30 mins, 1 hour etc, 90 mins so the
rise to 4 hours looks smooth. It would have been interesting to know
if there was actually a sharp spike in plasma trigs quite quickly
after the high fat meal, say at 30 mins or 1 hour.
Ozgirl
> "Nicky" <ukc802...@btconnect.com> wrote in message
> news:2c23j41c6kauk8b6a...@4ax.com...
>>>> I don't see how they can be, Peter - tri-GLYCERIDE? - they can
>>>> only be formed when carbs are present.
>>>>
>>> but they need fatty acids to be formed .
>>> here's a ducky little simulation, press the "play" button.
>>>
>>> http://www.tvdsb.on.ca/westmin/Science/sbioac/biochem/triglyc.htm
>>
>> You don't get the glycerol without the carb, it's formed from
>> glucose.
>
> When you play the simulation is it suggesting that you need molecules
> of saturated fatty acids and glycerol in the proportion of 3 to 1 to
> create one triglyceride ?
What is the diet most commonly given to type 2's? last time I looke dit was
low overall fat carb. where's the ratio come into it then?
Did we ever find out what the dietary intake of the subjects was?
Peter C
> On Sat, 29 Nov 2008 18:06:49 -0000, "Peter C" <espre...@europe.com>
>>
> >>>Too simplistic .... trigs are also driven up by high fat meals
>
> >> I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
> >> formed when carbs are present.
I wonder where the term "triglyceride" came from.
It seems to be a misleading because the true name for what are
generally
called "triglyceride" is actually Triacylglycerol.
Which literally means "Three Fatty Acids and One Glycerol" but
effectively
seems to mean "Three Fats and One Carb".
It's true you need carb to create "triglyceride (?)" but you
definitely
need three fats also.
So what's that telling us - that fat is three times as important as
carb in
the creation of trigs ? Dunno.
What are the implications - you need a bit of carb and lot of fat to
make
postprandial lipema ( basically a trig spike )
i.e. a low carb-high fat breakfast ?
And it seems axiomatic in the papers quoted in this thread that...
1. High fat meals produce postprandial lipemia.
2. Postprandial/alimenatry lipemia is associated with cvd.
Nicky
<peter.c...@btinternet.com> wrote:
>What are the implications - you need a bit of carb and lot of fat to
>make
>postprandial lipema ( basically a trig spike )
>i.e. a low carb-high fat breakfast ?
>And it seems axiomatic in the papers quoted in this thread that...
>1. High fat meals produce postprandial lipemia.
>2. Postprandial/alimenatry lipemia is associated with cvd.
But in the papers quoted, they were going with 25g carb - certainly
not what I'd eat for breakfast (although I might for supper). Does a
high fat, truly low carb meal produce a spike? - not proven. Does a
high fat meal produce cvd when you're not carb loading alongside it? -
again, not proven. Lipid panels tend to move in the right directions
with low carb; whilst I agree with you that testing pp lipemia might
be interesting, I just don't think we know enough about its dangers.
However, we know plenty about the dangers from carbs.
Nicky.
Trinkwasser
wrote:
>Am I keeping bgs in check but experiencing a potentially dangerous lipid
>spike that as so far remained under the radar ?
>Should T2 diabetics have their lipid panels checked after a relatively high
>fat meal to check for postprandial lipemia ?
>Answers on a postcard please.
My GP did a non-fasting lipid panel at one stage.
Not much difference, the trigs went from ridiculously low to just very
low.
Would be interesting to see an immediate postprandial result for
comparison I admit, but my lipids were so utterly dangerously crap on
the Low Fat High Carb diet and are now by her admission better than a
lot of nondiabetics that I suspect any postprandial spikes would have
to be really severe to do much harm.
The Accountants now try to limit us to one TChol/year, lipid panels
are too expensive.
Maybe someone else with a less cash-strapped health service could get
one done as a comparison.
Trinkwasser
wrote:
>The highly processed, calorie-dense, nutrient-depleted diet favored in the
>current American culture
Well that's pretty much all the bases covered
Peter C
> On Sat, 29 Nov 2008 16:21:07 -0000, "Peter C" <espr...@europe.com>
> wrote:
>
>>Too simplistic .... trigs are also driven up by high fat meals
>
> I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
> formed when carbs are present.
>
I wonder where the term "triglyceride" came from.
It seems to be a misnomer because the true name for what are generally
called "triglyceride" is actually Triacylglycerol.
Which literally means "Three Fatty Acids and One Glycerol" but effectively
seems to mean "Three Fats and One Carb".
It's true you need a carb to create "triglyceride (?)" but you definitely
need three fats also.
So what's that telling us - that fat is three times as important as carb in
the creation of trigs ? Dunno.
What are the implications - you need a bit of carb and lot of fat to make
postprandial lipema ( basically a trig spike )
i.e. a low carb-high fat breakfast ?
And it seems axiomatic in the papers quoted in this thread that...
1. High fat meals produce postprandial lipemia.
2. Postprandial/alimenatry lipemia is associated with cvd.
So when my Doc tells me my lipid panel is "like a baby's" ( a very healthy
baby I assume ) that might be hiding lots of undetected but damaging
postprandial lipemia.
Kurt
> "Nicky" <ukc802466...@btconnect.com> wrote in message
>
> news:4pr2j49miat0q9rrj...@4ax.com...
>
> > On Sat, 29 Nov 2008 16:21:07 -0000, "Peter C" <espre...@europe.com>
> > wrote:
>
> >>Too simplistic .... trigs are also driven up by high fat meals
>
> > I don't see how they can be, Peter - tri-GLYCERIDE? - they can only be
> > formed when carbs are present.
>
> I wonder where the term "triglyceride" came from.
> It seems to be a misnomer because the true name for what are generally
> called "triglyceride" is actually Triacylglycerol.
> Which literally means "Three Fatty Acids and One Glycerol" but effectively
> seems to mean "Three Fats and One Carb".
> It's true you need a carb to create "triglyceride (?)" but you definitely
> need three fats also.
> So what's that telling us - that fat is three times as important as carb in
> the creation of trigs ? Dunno.
> What are the implications - you need a bit of carb and lot of fat to make
> postprandial lipema ( basically a trig spike )
> i.e. a low carb-high fat breakfast ?
> And it seems axiomatic in the papers quoted in this thread that...
> 1. High fat meals produce postprandial lipemia.
> 2. Postprandial/alimenatry lipemia is associated with cvd.
> So when my Doc tells me my lipid panel is "like a baby's" ( a very healthy
> baby I assume ) that might be hiding lots of undetected but damaging
> postprandial lipemia.
Hi Peter,
From what I've read in your posts, I get the feeling that your doctor
would find you a good patient based on your proactive approach to
health.
The terms low-carb and low-fat really need to be defined by the
healthcare community because they don't seem to have any standard
ranges. Therefore, when we discuss things in this newsgroup and use
those terms we could all be talking about different things. For many
many years studies have shown the dangers of eating a high fat diet,
but did they just examine diets with lots of bad transfats and
saturated fats? I'm not sure. Also, how much is too much fat? How much
is too much carb? Too little carb? These are questions that may never
be answered since we are all different and factors such as height,
weight, genetics, age, disease, and activity levels make coming up
with a specific RDA almost impossible. That's why it's imperative that
we all work with a healthcare professional to help determine our
specific needs, taking in all of those factors..
Low-fat diets in this newsgroup are bashed on a regular basis and seem
to always carry the additional tag of high-carb by the bashers. I
don't eat high carb at all, or really low-fat either...only low in
terms of the bad fats.
As far as your concerns about a spike in fats and its subsequent
effect on CVD, etc. I think your interpretation of the findings is
spot on. But, you know what they say...people only hear what they want
to hear. Personally, I consider this an important and educational
thread worth reading and discussing. Thanks for starting it.
Kurt
Chris Malcolm
> x-no-archive: yes
> bgl wrote:
>> Maybe it's the bug I'm cultivating & my mind is mushy, but it looks like
>> these both can't be true.
>>
>> If ppl is *defined* as related to fat intake, how can carbs be "the
>> cause"?
>>
>> Unless maybe it requires lots of both?
> It doesn't require fats, but it does require carbs. Eating a lot of fat
> would increase it, at most, from my understanding.
> Lipemia means fat in the blood, and is not defined in terms of where
> it's from, so I'd argue such a def would be presumptive and wrong.
A lot of people suppose that fat in the body must mean that fat must
have been eaten to get it in there, i.e. fat makes you fat. They
forget that cows get fat eating grass. Or to be more general, fat is
manufactured in the body, mostly from carbohydrates. In fact in the
animal world the fattest tend to be the vegetarians, and the thinnest
those who eat the most fat.
--
Chris Malcolm
GysdeJongh
> You don't get the glycerol without the carb, it's formed from glucose.
Hi Nicky,
like Chris says somewhere else you don't need to ingest all kind of
things.The human body is a survival machine.The blue print of how it must
function is in the DNA of each of its cells.It can synthesize all it needs
from remarkable different and simple things.Everything you eat is first
ripped apart and then converted to what is needed.To make glycerol it does
not need glucose.Here is a free example :
http://www.jbc.org/cgi/reprint/242/11/2746
J Biol Chem. 1967 Jun 10;242(11):2746-50.
Phosphoenolpyruvate carboxykinase and the synthesis of glyceride-glycerol
from pyruvate in adipose tissue.
PMID: 6027245
In the end about everythig you eat and is not needed right away is converted
to fat and stored.Also protein.Because fat is a survival factor.It can be
stored for times when food becomes scarce.Your body can store 1 day energy
in the form of glycogen but easily a month in the form of fat.If this amount
of energy had to be stored as glycogen our body had to weight about 60 kg
more !
Gys
GysdeJongh
news:ggs6pg$d9u$1...@aioe.org...
> When you play the simulation is it suggesting that you need molecules of
> saturated fatty acids and glycerol in the proportion of 3 to 1 to create
> one triglyceride ?
The simulation is far too simple.Both the fatty acid and glycerol can and
will be synthesized themselves from other things.What things ? Well even
that depends on what your body needs at the moment and what it can choose
from at the moment.Have a look here and be baffled.....
http://www.expasy.ch/cgi-bin/show_thumbnails.pl
hth
Gys
Trinkwasser
wrote:
Putting my cynical head on, IF it was dangerous (bearing in mind that
things from our diet get turned into other things and transported
around by the blood anyway) one might have expected the manufacturers
of Crestor and Lipitor to have been trumpeting from the rooftops in
their quest to get statins marketed to everyone, or put in the
drinking water.
Nicky
wrote:
>Have a look here and be baffled.....
>
>http://www.expasy.ch/cgi-bin/show_thumbnails.pl
LOL! and blinded...
Nicky.
Robert Miles
I thought practically any fats you eat were already triglycerides.
http://en.wikipedia.org/wiki/Triglyceride
Robert