Important Quote: "Inadequate calories puts the body in a starvation mode. This induces a rise in blood sugars due to glycogen release by the liver. It also initially stimulates the release of the neurotransmitter seratonin which, unfortunately, is followed by a “crash” -- that is, a "high" or rush followed by an intense deficiency of seratonin, which makes the dieter feel really bad. In addition, it resets the body's caloric thermostat to a lower setting so that the dieter either gains weight or fails to loose weight while restricting themselves to a much lower calorie diet "
Navigational Shortcut: To skip the medical stuff & get right to the heart of the matter
This information may permit us to reduce
the number of neonates
experiencing shoulder dystocia (SD) at birth and associated perinatal
morbidity or mortality. A significant number of SD babies will suffer
from respiratory and cardiac depression, admission to the NICU, or
brachial nerve injury with Erbs palsey. Reduction of macrosomia is a
goal worth pursuing. This new understanding of normal and impaired
carbohydrate metabolism is also useful to the non-pregnant population
(including ourselves, children, spouses and others).
It is an all too familiar story for home birth midwives -- a midwife we know and like and whose experience and skills we consider to be excellent -- had a bad outcome in what should have been a normal low risk home birth. One of the most frequent scenarios of this type is the 9, 10, or 11 pound baby with a pernicious shoulder dystocia, requiring massive intervention by the midwife to resolve and resulting in a baby born with a really low apgar (0 or 1). Resuscitation was necessary, often without success or perhaps the baby was kept on life support for several days before being determined to be in a vegetative state. Everyone involved is just devastated.
A frequent theme of these
stories is that the mother had her last baby/babies at home without incident (good size but not huge) and so the
family and the midwife are all understandably shocked. This shouldn’t
have happened (but it did!). Numerically this is a rare occurrence but of
that small number of adverse events for home birth families, a surprising
number seem to involve macrosomic babies and its subsequent
Obstetrical literature concludes that
shoulder dystocia can not be reliably predicted. More than 50%
of cases occur in normal weight babies. For babies predicted to be macrosomic, more than 90% do not have SD. Ultrasound estimates of fetal
weight can be wrong in both directions, by as much as 15%. This means a
10 pound baby may be estimated to be anywhere between 8 1/2 pounds to 11
and 1/2 pounds. Clearly screening is not able to reliably identify SD
before the fact.
While midwives know many useful techniques for
freeing the baby without damage, a small number of cases cannot be satisfactorily
resolved. Being in the hospital would not have helped.
There is no realistic surgical cure for SD (Zanvanelli maneuver/CS not
more, routine interventions of hospital care may make matters
worse, especially if the mother is given drugs or anesthesia or forced
to deliver on her back. Certainly the Gaskin Maneuver is a useful tool
for resolving SD irrespective of the location of the birth, but it is
not a magic bullet.
Consider what a blessing it would be if we could
rather predictably prevent the very type of macrosomia that seems so
often to be associated with SD. I don’t know for sure that what I am
going to say will be able to live up to that promise but I am convinced
that it has a high likelihood of helping, at the very least, to lower
the number of undiagnosed and/or subclinical GDM macrosomic babies (the group most particularly at risk
for SD). It also would permit us to identify and offer help to mothers
who have impaired carbohydrate metabolism and therefore are at high risk
for developing diabetes and its many complications sometime later in
difficulties and cumulative
dangers of Impaired Carbohydrate Metabolism
The medical and personal consequences of diabetics
are legion. It is the leading cause of blindness in the US and it
contributes to heart disease, kidney disease (and the resulting need for
dialysis), amputation of lower limbs and for men, erectitle dysfunction
and impotence. Childbearing women with insulin-dependent diabetes have
greatly increased stillbirth rates. For women with GDM the major
maternal complication during pregnancy is hypertension. For their babies
it includes a small increase in stillbirth, macrosomia, shoulder
dystocia, brachial nerve injury and higher rate of otherwise sick
neonates. However, better identification of clinical GDM and good management of
it antepartally has improved the circumstances for these babies.
With good care (maintaining of near-normal blood glucose levels)
the rate of stillbirth is now equal for GDM mother to that of
Traditionally all forms of diabetics have been
assumed to arise from insulin insufficiency. In juvenile onset diabetic
this pathological condition is ascribed to the death, dearth or damage
of beta cells in the pancreas.
In adult onset diabetes, medical authorities have promoted the theory of
beta cell exhaustion, often due to overweight and an intemperate diet.
In gestational diabetics the pathogenesis is assumed to be, in part, the
result of the hormones of pregnancy which are antitheses to the action
of insulin, in combination with some underlying genetic propensity to
develop non-insulin dependent (NID) diabetics later in life.
The idea that some diabetics in both groups have or
develop “insulin resistance” has been observed but that concept was
poorly understood and thus had little effect on current treatment or
managements of diabetics or its understanding by the public.
Classically midwives do not provide primarily care to
insulin dependent diabetics. Most midwives also do not continue to
provide primary services (planned labor and birth at home) to those
mothers identified as having clinically diagnosed GDM. As for routine screening of all women
for GDM, midwives have had a lot of resistance to doing this routinely,
in part because it seemed to us that its identification resulted in a
form of medical overkill. The definition of GDM appeared rather
arbitrary (diagnosis and treatment for a woman with a postparadial blood
glucose level of 141 but no Tx if her BG was 139 -- only one or two
points lower). Since the
treatment of GDM is primarily calorie restrictions (which can be done
independently of a diagnosis) this category appeared to accomplish
little except to make everybody anxious. In fact, tight caloric
restriction for GDM women often results in small for gestational age
baby at birth and so seems to merely trade one possible problem for
Identification of GDM seemed to provide little
benefit to mother or baby and so midwives have had little
interest in the subject. I’d like propose that new information makes this a topic
one of great interest which may will permit is to make a very
positive contribution to women. This benefit would surpasses the period
of pregnancy and can even be useful to the general population (both male
and female). In particular, this new understanding of non-insulin
difficent diabetes (NIDD) would permit us to substantially reduce the
previlence of macrosomic babies and the complications that accompany
these bigger babies. It would also help is to be assured that a
mother with a big baby is genuienly (ie. genetically) appropriate rather
than reflecting ICM/GDM.
The following information is presented as my personal
opinion (as opposed results of RCT or other forms of research). This
theory and expanded understanding as presented here was developed after
becoming aware of some exciting new research by an endrocrenologist at
Stanford University (Dr. Reagen), in conjunction with other sources of
new material on adult diabetes by physician experts.
Taken together, this material dramatically changes the theory
behind NID diabetes and its management, especially the identification of
imparied carbohydrate metabolism (ICM) and suitable dietary and
life-style recommendations to prevent it from turning into active type
In addition to very different dietary choices i also
recommend the liberal use of self-monitoring of blood sugar levels at
home by women, including antepartum, postpartum and for well-women gyn
clients with risk factors for impared carbodrate metabolism (ICM). The glycometer marked by Bayer (Glycometer Elite) is one of
the best currently available as it requies the least blood and it
calibrates to same numbers as plasma so blood glucose values do not have
to be adjusted.
The consenses of several authors) is a target level
of blood sugars significany lower that those currently used by clinical
labs to define “normal” for GDM screening. Last but not least, to
properly uutilize these suggestions, each midwife must educate herself independently about ICM/GDM and the glycemic index of foods.
A reading list is included at the end of this article. Many
midwives and/or their family members also have characteristics of
ICM. One of the best ways to develop a thourgh understanding of
these principles may be to keep track one’s own blood sugars and
follow the dietary recommendation for 90 days and monitor the effect on
blood glucose levels and general wellbeing. Reports of benefit include
normalized blood sugars and reversale of frequent urination that
accompanies hyperglycemia, weight loss specifically around the middle of
the body (waist and upper hips) without any calorie restriction or
calorie counting, improved health.
Topics to be covered and new information provided:
The story unfolds
~ Some basic background facts
Healthy adults with normal carbohydrate metabolism
will have fasting blood sugars between 75 and 90. Even a high
meal will only raise it by 20-40 points. At 2 hours the blood sugar of
normoglycemic individuals will be under 120. The longer these people
fast (for instance, not eating overnight), the lower their blood sugars
will go but without becoming hypoglycemic (below 70). This occurs
because they have an intact phase I insulin production in which small
quanities of insulin are constantly present in the blood stream. In
response to a carbo load phase II insulin production is triggered to
meet the high need relative to intense carbohydrate metabolism.
Adults with lowered glucose tolerance/or impaired
carbohydrate metabolism do not have or have lost the phase I insulin
production. This results in increasing blood sugars overnite (often
peaking at 4 in the morning) as their livers release the small quanities
of glycogen that are part of normal physiology but the pancreas fails to
do the same for insulin. Their
fasting blood sugars are typically in the high 90s or 100s. After
eating, blood sugar levels rise very rapidly (absent phase I insulin
already in blood stream) to greater than 140 (perhaps 180 or higher) and
do not returned to under the 140 mark for longer than 2 hours.
These abnormal laboratory findings are often accompanied by
carbohydrate craving, the need to urinate more often than “normal” (
>> 8+ times a day, a biological coping mechanism in responce to
hyperglycemia as the body tries to rid itself of excess blood glucose
through increased kidney perfusion), excess weight gain, especially
around the midsection and an inability to lose weight easily despite
caloric restriction. In extreme cases, episode of gastroparesis occur.
Gastroparesis is an autotomic nervous system abnormality (vaso-vagal
reflex) in which the stomach suddenly stops normal parastalsis. It stops
emptying and begins to slowly fill with undigested food and liquids and
gases intil the over-distention mechanically triggers intractable
vomiting. If permicious vomiting continues for a long enough time
(several hours) the patient faces circulatory collapse from dehydration
and IVs will be necessary to prevent unconscienceness. It goes away as
suddenly as it starts and may not reoccur for many months.
Current laborary values for a “normal” GTT are
too high. They are up to 110 mgs for fasting, and 140 mgs for 2 hrs
postprarandial. These upper limits actually represent ICM rather than
healthy metabolism. Ideally fasting levels should be at or under 90
and 2 hr PP at or under 120. It
was recently recommended by the American Diabetic Associaiton that
fasting levels be lowered to 95 and 2 hour to 130. These are more in
line with efficient cargohydrate metabolism but still on the high side.
Reseach done at Stanford Medical School by Dr Reagen:
Dr Reagen’s research project divided test subjects
into four categories -- those with normal glucose metabolism, those with
significantly impaired glucose metabalism (pre-diabetic, very mild
diabetes), diabetics with moderate disease and those with most severe
NID diabetes. Blood was
drawn seven times -- fasting, 1, 2, 3, 4, 5 and 6 hours post prarandial.
It was measured for both glucose and insulin levels.
Values were then graphed by these two parameters, in conjunction
with the times they were drawn.
Conventional wisdom would dictate that normal
subjects experience a rise in blood sugars and insulins levels that are
concordant with BG rise. For those with evidence of diabetic disease,
the insulin levels should fall behind the evidenced need as revealed by
BG (insulin defficiency theory), thereby being lower than the
nomoglycemic individual. According to this theory, it is the lack of
insulin which results in eleavated blood glucose levels. However, Dr
Reagen’s research revealed a startling divergency
from these expectations with regard to insulin levels, especially
for the normal subjects and those with the mildest level of impared
The normal subjests stated out with normal fasting
blood sugars (90 or less), rose to a high of
only 120 at 2 hrs postprarandial and returned the general range
of fasting (under 100) by about 3 hours. The impared glucose/mild
diabetic group followed this same general pattern of blood sugar
elevations but at a higher level of all values and a longer sloop for
recovery. Their fasting blood glucose levels were all slightly higher --
about 100, 2 hour pp was about 130 and it took longer than 3 hours to
return to near fasting levels, which for them were still slightly raised
as compared to normal subjects (>100).
Based on BG level alone, there appeared to be little difference
between these two groups, with the obvious exception that all BG values
However, a dramatic and unanticipated difference was
revealed by the graph representing insulin levels, especialy for these
two categories (normal and mildly impared). For the normal group,
insulin levels pretty much tracted the blood sugar levels,
meaning they began low, rose to the highest point in the same
ratio as the rise in blood sugar, and then returned again to about the
same level as fasting.
According the insulin deficency theory, insulin
levels in mild diabetics should start out even lower than those of
normal subjects (showing deficency), with a very limited (ie.
inadequate) rise as the blood sugars went up postpradially (inability to
meet the increased need). However, that is not what happened at all.
Insulin levels in the ICM/mild diabetic group start at approximately the
same “normal” level and then sky-rocket to 4 or 5 times
that of normoglycemics, slowly returning again to nearly normal.
Graphically represented this is a huge and impressive spike -- like
seeing the Transamerica building in the San Francisco skyline.
For the other two categories (moderate & severe
diabetics), insulin level also rose but not as dramatically. None the
less, moderate diabetics still tracked higher than the
normoglycemic level and those of the most severe diabetics matched
those of normoglycemic subjects. What this means is that diabetics
is NOT a disease of insulin difficency
but rather one of insulin resistance. At least one expert on
impared carbodrate metabolism identifies increased abdominal fat
distribution (“spare-tire”) as a marker of insulin resistance.
This is a very different pathogenisis than any of us would have
In addition to its crucial role in carbohydate
metabolism, insulin is also a growth hormone. The unidentified GDM
mother whose body produces 4 or 5 times the normal quanity of insulin
after every meal obviously has a fetus which is regularly flooded with
extremely high levels of growth-inducing insulin.
Furthermore, the women who flunks her 1 hour
screening (blood sugar over 140) then passes her 3 hours GTT is very
likely to be a woman with ICM in the early, “pre-diabetic” phase.
The reason she has normal 3 hours levels is that she still has a massive
production of insulin (4 to 5 times normal) which eventually brings it
down to the “normal” level. While this normalizes the numbers for
her blood glucose (and confuses the issue for her caregiver!), it also
regularly exposes her baby to high level of
growth stimulating insulin and most likely, also triggers insulin
resistance characteristics in the baby such as increase abdominal girth
with a disproportionally large torso and big shoulders -- a setup for
Carbohydrate rich diets (including the so-called
“complex” carbohydrates) have been promoted as superior for both
normal population and as the ideal diabetic diet. However this dietary
regime triggers greatly
increased insulin productions for those with impaired glucose metabloism.
Modern day carbohydrate metabolism and insulin
resistance -- the effects of ancestry and genetic norms for those of
northern European extraction, which consisted of a diet high in raindeer
meat, fish, whale blubber and non-starcher tubers, roots, etc
Carbohydrate metabolism seems to be very specific to
the ethnicity of the individual and reflects the genotype of that
subgroup. The very idea of “impaired” carbohydrate metabolism is a
culturally defined “norm” which reflects a specific cultural bias
relative to major changes in modern-day human diets.
If you trace the history of the “normal” human diet back far
enough you see various versions of
“hunter-gather” populations whose eating pattern could not be
farther from that of the modern day American diet. In this natural world
everything eaten was a “whole food” -- freshly killed small animals,
fresh caught fish, birds, termites, other bugs, nuts, roots, other
tubers and nonstrarchy vegatable, whole fruits (no orange juice!) and
berries . It must be noted here that the human genome was originally
molded by this wholesome diet which never, ever included any significant
amount of refined sugars or starches (so called “complex”
Simply changing to an agricultural-based diet is a
massive change and not everyone’s genone survived this watershed
event. It may be assumed that those individuals which encountered sever
metabolic problems adjusting to agricultural diets became victims of
selective breeding. This would assume that they died before they could
reproduce so that those genes which were straighted jacketed to the
hunter-gather diet died with these unfortunate folks.
However, there are many places in the world with
populations that have survived intact on wholesome food diets. Many
native or “indigeous” populations today get the majority of their
calories from unrefined sources such as whole grains, non-strachy
vegatables, large amount of fish, fish oils, or other animal meats.
Likewise they eat virtually NO refined sugars, starches, stimulants or
alcoholic beverages (potato
chips, candy bars, twinkies, french fries, bread, pasta, crusants,
crackers, ice cream, StarBucks coffee, beer, wine, hard liqour, etc.).
Interestingly enough, the list of those ethnicities who are considered to be “at
risk” for GDM, refects many of these same these populations who have
until very recently enjoyed a “natural” or whole food diet -- Asian, Australian aboriginy, Afro-American, American
Indian, South and Central American
Indian, Hispanic, Pacific Islander, etc.
Specific aspects of the switch to an agricultural
There are many different grains which have been grown
for the last several thousand years. Corn, rye, barley, wheat, oats,
etc. It is from these “cereal” grains that we get breads, baked
goods and pastas. The habit of pouring water over a stale loaf of bread
so as to soften it for eating resulted in the acidental “discovery”
of beer and other alcoholic beverages. The water that ran off each loaf
was caught in a the same bucket and over the course of a few days of
sitting around in the warm ambit air, the yeast naturally present in it
“brewed” itself into an alcoholic drink.
(an intereting historical
aside -- the letter “B” in Indo-Europen languages reflects the fact
that bread, brew, beer and breasts all reflect some physical &
visual aspect of a “bubble” or “bump” . In fact, most of our
“B” words reflect that physical or visual quality -- band, beets,
burr, barrel, body, back, belt, bend, bar, barf, ball, ballon, bomb,
boat, bottle, barque??)
Agriculture gave rise to the mass production of
cereal grains which were then ground into flours and used in a variety
of breads, crackers and cereals. Refinement of cereal grains
dramatically increases their glycemic index. Of all the grains
commonally grown in the northern hemisphere, wheat flour is capable of
the most refinement. This is why it is used for delicate pasties and why
its added expenses denies it to very poor populations. It also has the
highest glycemic index of all grains.
There is very little difference, glycemic index wise, between
whole wheat flours and breads baked with them and those made with white
flour. Both have equally astronomically high glycemic indices.
One way to think about this propensity for a high
glycemic index based on how fine the flour is ground. Consider the
difference between dipping our hand in water and “sprinking” water
about (in rather big drops), versus a shaker bottle used to sprinkle
clothes for ironing, versus a spray bottle such as used to spray Windex
versus the water vabor truned into steam in our modern irons. Grinding
wheat flour produces the dietary equlvilent of
a fine mist (whole wheat) or water vapor as steam (white pastry
flour). Obviously the abilllity of the body to extract carbohydrate is
maximized many times by this phenomon
which produces a
rapid extraction of glucose.
Glycemic index theory and meaning - the glycemic
index of a food is how quickly it is converted to blood glucose. The
index uses the conversion of 50
grams IV glucose as the bench mark a glycemic index of 100. Other
foods/fluids are measured against that number (only dates exceed
glucose, with a number of 106). Those with rates under 50 are considered
to be “low” and those over 55 are considered relatively high.
Examples are of differing glycemic indices are table sugar at 55,
potatoes 93, lentils 30 and dahl (the germ part of lentils with the
outer covering removed) are only 8. The higher the glycemic index of
foods or beverages, the greater the stimulation of insulin production.
Liquids invaribly have a faster absorption rate than solids,
ground grains higher than whole grains.
Glycemic index of an entire meal can be lowered by
mixing low GI foods with those that are, by themselves, unacceptably
high. For instance, a protein food (meat /fish/ cheese) a salad and
non-starchy vegatable eaten with a starchy vegatable like mashed
potatoes or white rice will have a moderate glycemic index and therefore
is kind to the individual with ICM.
Most American diet experts at present recommend that
we consume about 50-60% complex carbodrates, not more than 30%
fats/oils and about 20% proteins. Physician experts on ICM suggest a
“balanced diets, in which these three elements are much more closely
carbohydrate - cholesteral connection:
A number of authors have observed a connection between high
complex/low fat diets and abnormal cholesterol production. Dr
Swartzbein’s has a whole chaper (ch. 6) in her book explaining
the normal mechanism of cholesterol production. Acording to this
information, the precursor dietary event to abnormal cholesterol levels
are excess dietary carbohydrates. Among her diabetic and prediabetic
patients, cholesterol levels fell when they stopped eating high levels
of complex carbos (50/30/20) and switched to her recommendations for a
“balanced” eating plan. In this instance, the word “balance”
refers to an equal division of calories between the three major food
types -- 40% carbohydrates, 35% healthy fats and oils and 25% protein.
Insulin resistance -- an imperfect definition of an
imperfectly understood phenonem
This is a leading edge discussion as the current
understanding of insulin resistance is imperfect and still evolving.
At present it is unable to be “treated” with any
pharmiseutical agent which reverses the pathology as such as the way
that insulin reverses diabetic hyperglycemia. The classical explaination
focuses on the biological activity of insulin which is a hormone used by
the body to “unlock” the cells so that glucose can be moved out of
the blood stream and into the intracellar storage space to be available
for future use.
Insulin resistance appears to reflect a situation in
which the carbohrdrate storage is already at maximum capasity. In an
effort to overcome this problem the body continues to pump out more and
more insulin in a futile attemt to “unlock” this normal carbohydrate
storage mechanism. If this continues on long enough, the pancreas seems
to wear out. Also, the unconverted blood sugars eventually are converted
to fat and stored as periumbilical deposits of adipose tissue.
So it appears that is not the insulin itself that is
“resistant” but rather a storage mechanism which is already at
capasity. (An alternative theory is the possibility
that in some cases the “lock” cells have become resistant to
the biochamical effect of insulin). What is unknown but can be
theorecially proposed is a probablity the each individual’s capasity
for carbohydrate storage reflects both current dietary habits and
their genotype. This may well be a place where genotyping can add
valuable information for people in preventing chronic and debilitating
For people from genomic groups which have, until the
last 100 years or so, eaten a “wholesome” diet, it seems likely that
they have a carbohydrate storage capasity that is “normal” (ie very
small!) for a wholesome diet which
has little or no refined foods, especially grains and sugars. However
exposure to high level of refined foods fills up this small capasity and
ultimatley we define them to have an “impaired” carbohydrate
metabolism (in fact it is the diet and not the person who is faulty!).
This would apply to populations whose ancestors lived
in non-agriculturally-based areas of the world (arctic/ antarctic
circles), very cold regions such as the scandinavian countries,
who would naturally eat a large proportion of fish, fish oils
(whale blubber!), meats, dairy products, etc). Many subgroups from these
regions moved into more southern climes (Ireland, Scotland, Wales,
England) a few hundred years ago and are in fact the antecedent
population for the US. They surplanted a high protein/high fish oils
diet for one that was very low protein and depended on potatoes, rye and
other grains as the core food. In addition, lots of alcohol (often
called “liquid bread”) is often consumed within these groups. It
should be not a surprize that pregnant women from these ethnic groups
have a much increased risk for babies with neural tube defects. Many in
the general populations suffer from alcoholism.
A marker for ICM is a cultural propensity for
alcoholism. Biochemically speaking, alcohol is a carbohydrate molecule
with an extra atom on the molecular structure which increases its rate
of absorption and its calorie count (carbohydrates are 4 per gram
whereas alcohol is 7 per gram). Again one sees the association between
populations that have relatively recent roots in wholeseome diets
(Asian, Australian aboriginy, Afro-American, American Indian, Hispanic,
South and Central American
Indian, Pacific Islander, etc) and alcoholism after adopting the typical
western european diet of refined foods and easy access to alcohol.
Unfortunately, not all grains are equal in regard to
the load they puts on charbodrate metabolism. This occurs because of the
extremely high glycemic index of wheat flours.
Wheat flours and starchy vegatables vs simple sugars
(candy, etc). Recent recommendations for a “healthy” diet have
focused on a theorectical superiority of “complex” carbohydrates and
a low fat, low protein diet which exchews free or simple sugars. The
rationale for this has been the reduction of heart disease through
lowered cholesterol levels. Many of the research finding which this
advise was predicated on were arrived at before the distinction between
high and low density lipids was made.
As an aside, the place in the world that has the lowest heart
attack rate is also the place with the highest per capita rate of olive
oil consumption (the island of Crete).
Whatever its origins and perceived benefits, it
appears that the idea of a “complex” carbohydrate is a meaningful
distinction only in the laboratory and only for chemists. For humans who
chew and swallow foods, all of them (complex starches and simple sugars)
are equal by the time they hit the stomach
-- that means that potatoes, white rice, pasta, whole wheat bread
has as high (actually higher) glycemic index as table sugar. It is not
the teaspoon of sugar added to the breakfast cereal that is the issue,
it is the cereal itself that is high carbohydrate/high glycemic index.
For the same reason, using Sweet and Low instead of real sugar is of no
help and many think aspartame use creates problems of its own.
Also, when the total intake of carbohysrates is
lowered, one must increase other sources of calories -- protein and oils
being a rich source that is in alignment with the “wholesome” eating
patterns of our northern European ancestors and indigenous peoples
around the world.
Recommendations for community-based midwives:
Pay very close attention to body tpye and ethnicity
in your client population. Follow the recommendation to have everyone
screened for DGM (except for that tiny fraction of women with absolutely
NO risk factors -- under 25 y/o, normal pre-pregnancy weight and normal
pregnancy weight gain, AGA
fetus, no direct relative with known to have ICM/diabetes and not of the
above listed ethnicities at increased risk - Asian, Austrailian
aboriginies, Afro-American, American indian (north, south or central
America), Hispanic, and Pacific Islanders).
Pay close attention to the results of GDM screening,
using the tighter criteria of under 95 fasting and under 120 at 2 hours.
Also note if fasting BG is under 70 as these women are at risk for SGS
babies. Downs is also associated with chronically low BG levels.
Dietary teaching for ICM/GDM moms is essential.
Total calories for a pregnant woman of normal weight
would be at least 2100/kal per day.
A most useful skill is the habit of reading labels of packaged
foods for the quanity of carbohydrates. It is shocking to realize just
how many grams are in the typical “complex” carbohydrate (bread - 14
grams, potatoes, pasta, rice, etc). The grams of carbohydrate in junk
food such as coke (41 gms), cookies, candy bars) is truly shocking.
It is my personal bias that self-monitoring of BG
level is necessary so that people can see for themselves the correlation
between unwise consumption of starchy carbohydrates, the feeling of
being unwell, high BG levels, (or hypoglycemia) and how long it takes to
normalizing these cirsumstances after intemporate eating.
One of the major resistance to doing this is the
fear/pain associated with blood drawing. However, new home monitoring
systems which use a finger stick devise actually (really, cross my
heart!) don’t hurt. Yes, it is a finger prick but not one that rises
to the level one would consider “pain”. Bayer Glycometer Elite is
the one i have had the best experience with. It uses the least amont of
blood and beeps when has siphoned right amount of blood for test.
It is important to
wash one’s hands before doing a finger stick as any carbohydrate on
the finger will skew the results (perhaps by double!).
Any reading that is abnormally high or low it should always be
repearted. Occassionally an inadequate amount of blood will give a false
reading of hypoglycemia. Make NO management determinations on a single
high or low reading.
The typical diatary recommendations relative to a
diet-related condition usually focus on percentages for each food group,
permissable total of calories per day and perhaps, a set quanity of
grams of each type of nutrients. I have choosen not to do that for a
couple of reason. First, the information that i am communicating is not
the end product of a research process. No RCT have ever been done (nor
will they in all likelihood), nor are there any other types of level 1
or 2 studies. Quite the
contrary, this is a
“leading edge” in our understanding of ICM and at present, no hard
and fast numbers for pregnancy are avaialbe. Equally important, a tight
regeime of specific number for each type of food is not the way people
think food or the way they eat on a regular and daily basis.
So what i am about to describe is a general theory relative to
developing an improved (or normalized) dietary plan and the life-long
process of changing one’s eating pattern to be more in alignment with
Anyone interested in checking out these theories must
do for themselves (or have done) a initial GTT (50 gm load if pregnant,
75 gram if not), followed by a week or 10 days of checking BGL.
Follow your “regular” eating pattern and do BG determinations
every third day for morning fasting level, PPs (Xs 3) and one at
bedtime. Only after establishing a base line for you and your regular
diet can you reasonably access the effects of any changes.
One of my favorite authors is Christianne Northrup, a
woman OB who lectures extensively on related dietary topics. Her
recommendation is to consume what she describs as colored or
“rainbow” foods -- red, green, yellow and organge vegatables,
brown rice, red, white and blue fruits, etc.
She shows a slide of what she calls the “white foods” --
white flour, sugar, rice, potatoes, pasta, etc”. What she says is
“Now friends, think of these as condiments”. This is a point well
taken. No food (with the exception of alcohol during pregnancy) should
be completely eliminated from the diet.
However the relative ratio and quanities of food groups are
significantly differnent. Favorite
foods which have high glycemic index or number of grams of carbohydrates
can be eaten as a few bites. Early on one learns not to waste carbo
calories on true junk foods -- save then for really good chocolates and
a small piece of birthday cake.
Hunger prevention -- perhaps the most important topic
of all. The
best way to prevent intemporate eating is neither fasting, rigid regimes
(the “Food Nazi” syndrome!) or caloric restrictions. Fasting
stimulates glycogen release by liver --
meaning that it does NOT normalize (lower) blood sugars. Eating
regular meals, (including planned snacks during
pregnancy), is necessary to help reduce hyperglyceria.
So the so-called “secret” or trick to normalizing
the diet is eating lots of the right foods (those with a low to moderate
glycemic index) so that one does not suffer the hunger and anxiety of
rapidly rising and falling blood sugar levels. Not surprizing, breakfast
is the place to start. The plan is to eat a relatively high protein
breakfast so that you have a nice slow release of nutrients
and sustained blood glucose level over the next many hours. Then
eat the next meal because its meal time. Its a good idea not to wait
until one is revenously
Protein and oils -- I am including protein and
fats/oils in the same section as they are so frequently found together
in our foods. And they both have developed a bad reputation (abet for
different reasons) in the last few decades.
I have read in many popular publications that we
Americans get too much protein. The idea has been promoted that we
really don’t need to do anything special, protein wise, as virtually
all foods have some small percentage of protein. We have been encouraged
to eliminate any concern about eating a specific quanity of protein
itself. The possible exception to this advise was for vegatarians, who
have been urged to combine grains (rice and beans for instnace) in oder
to get all 8 essential amino acids in the same meal. Perhaps this innate
sufficiently of protein in the diet is true for some or even many folks.
However, i know of several people who only appreciated how protein
deficient their diet had been after trying this different approach.
This eating plan is designed to meet normal
nutritional needs (no food group is eliminated) without unduly
stimulating insulin production (ie keeping blood glucose levels nearly
or at normal levels) and over time, diminishing insulin resistence.
Blood glucose lower is an immediate effect. However it requires a
extended time of normalized blood glucose levels to positively impact on
insulin resistance. Over-stuffed carbohydrate storage mechanisms must be
unloaded by gradually utilizing those stored calories while not adding
any more. So some effects are immediate while others are cumulative.
This is not accomplished counting calories but rather
by focusing at each meal on
a more balanced intake of all three major food types -- protein,
carbohydrates (with a strong showing of non-starchy vegatables) and fats
or oils in the whole form (olive oil, butter, cream, cheese). Rather
than giving a specific number of grams for each food type, i suggest
that people simply think in terms of reducing complex carbo and simple
sugars, consider non-starchy carbo as a “free” food (free of
damaging side effects of starch carbos), and increasing the level of
proteins and good fats/oils until people find themselves to be
appropriately satiated most of the time. This means (perhaps for the
first time), that you aren’t hungry again until the next meal time and
you aren’t thinking of food (or nibbling) between times, except for a
planned snack if the time between meals is unduly long.
Substances to restrict to small or occasional use:
Caffeine, tobacco, alcohol (eliminate if pregnant), aspertame,
partially hydrinated oils (used by fast food resturants to deep fry
foods such as french fries).
These very different ideas on diet produces a very
different relationship with carbohydrate, especially those with no
nurtitional content (vitamins, minerals, etc). A useful way to think
about such things as candy and soft drinks are to see them in the same
light a second-hand cigarette smoke -- extremely toxic and totally
without socially redeaming value. This is not to say that we do not as
individuals have an occassional bite or two (even three!) of candy, cake
or a glass of wine on a special occassions. But it does balance off
the innate attractiveness of non-nutrient foods with the sobering
reality of their biological cost.
coke/pepsi 41 grams carbohydrate
Good fats/oils as precursors to healthy hormone
Most people know that the role of dietary protein is
to repair and maintain body structures. That means rebuilding cells (for
example muscle mass). It also is a crucial link in the production of
neurotransmitters such as seratonin and other substances that help us
feel healthy and happy.
Fats in particular are precuror nutrient for the
production of the hormones that regulate every aspect of body function,
from sexuality to mental function.
Inadaquate calories puts the body in a starvation
mode. That includes a rise in blood sugars due to glycogen release by
the liver. It also initially stimulates seratonin release which
unfortunately is followed by a “crash” -- a high or rush followed by
an intense dificiency.