I'm currently involved in training as part of a Care Management team approach, which will help prepare me for the implementation of the Patient Centered Medical Home. This is the concept that...wait for it...wait for it....physicians actually ask the patient what we as clinicians can do to help them care for themselves better. Call me crazy but doctors are actually being taught they have to talk to their patients and then really, truly actually listen to what they have to say...A concept whose time, ummmmm, should've already come.
This weeks discussion was on diabetes and I had alot to say, but kept it short, for, uh, brevity's sake. First off, who is brevity and second off, it wasn't short....
Enjoy!
Remember, my blog posts are for informational purposes only and are not intended to diagnose, treat or cure any diseases. However, they are intended to hopefully eradicate the nutritional ignorance of the medical profession...
Diabetes
Forum;
As a family
physician with a profound concern for the diagnosis and correct treatment of
diabetes, and having been directly involved with the management and care of
thousands of diabetics over my 20 years of practice; I can state without reservation
that the current standards of care for diabetics is wrong. Unfortunately,
organizations like the American Diabetes Association, American Dietetic
Association, American Heart Association, American Cancer Society, the National
Institutes of Health, the National Heart Lung & Blood Institute, the
Surgeon General, TV personalities such as Dr. Oz and even the White House’s new
My Plate campaign, all have it wrong as far as the correct way to eat is
concerned.
My direct
clinical experience has taught me that in order to correctly treat diabetics,
carbohydrate (carb) restriction is
mandatory. The current ADA guidelines recommend that diabetics go no lower than
139 grams of carbs per day. This is wrong. Experience has shown me that when I
reduce the carb count to 20 to 40 grams of carbs a day, dramatic sugar control
becomes immediately apparent. Yes, you read that correctly; I did state that I
reduce my diabetic pt’s carb intake to 20 to 30 grams a day.
This
reduction is simple in a newly diagnosed Type 2 diabetic who is not on any
medications; but if I get a diabetic already diagnosed on meds, the clinical
approach needs to change. For instance, if I see a diabetic who is on insulin
(and this can be a type 1 or 2 ) and I get the impression that they are serious
about lowering their carbs to help lower their meds; I will immediately stop
any short acting insulin (e.g. Humulog) and cut in half the long acting insulin
they may be on. Also, meds like Byetta (a hormonal incretin analog which
increases GLP-1 secretion) and Januvia (a dipeptidyl peptidase type 4 inhibitor
which allows incretin analogs to stay in system longer) will be stopped as will
any sulfonylurea (e.g. glimeprimide and glipizide, which work by stimulating an
already fatigued pancreas to secrete more insulin hence facilitating B cell
burnout and the eventual need for insulin).
The insulin
can be stopped and adjusted and the meds can be d/c’ed because once a diabetic
reduces their carb amount these meds are no longer needed. I have a big issue
with any Type 2 being started on any sulfonylurea due to their mechanism of
action. As a side note, if anyone has seen the black box warnings on
sulfonylureas it includes ‘increased risk of cardiovascular mortality’ and that
it ‘should not be used for prolonged therapy,’ a fact that most clinicians have
either forgotten or had no idea about, because I still get diabetics in my
office on these meds; usually for many years.
Getting back
to adjustments and d/cing of meds, when one dramatically lowers their carb
intake there will not be a large increase in post prandial serum blood sugar;
therefore the short acting insulin (which is used to lower post prandial blood
glucose) will not be needed. Meds like Byetta & Januvia also work by
helping lower postprandial blood glucose and they will not be needed as there
will be no large increase in post prandial blood glucose because of the carb
lowering. The most dangerous of these meds are the sulfonylureas. These meds
need to be stopped immediately once a pt implements low carbs. This is because
the sulfonylureas will continue to force the pancreas to secrete insulin,
irrespective of the blood glucose readings and dangerous life-threatening
hypoglycemia can result. I have counseled many a pt who started a low carb
regimen on their own, without stopping the sulfonylurea, and subsequently woke
up in the hospital after their syncopal event. What’s even worse is that the ER
doctor or nutritionist who sees the patient tells the patient they should never
have lowered their carb intake; not understanding that is the wrong approach
and the pt should have stopped the medicine, not increased their carb intake. Why?
Because the pt was no longer consuming large amounts of carbs and does not need
the med any longer. This would also be true of Byetta, Januvia, and short
acting insulins.
Let’s take
some time to discuss insulin and its role in the treatment of diabetics. There
are four types of diabetics; Type 1 DM whose pancreas’s no longer can make
insulin so they need to take it exogenously; the Type 2 DM whose pancreas is
actually hyper-secreting insulin and represents the most common type. This
hyper-secretion can go on for years which is why eventually the B cells can
burn out (a process facilitated by sulfonylureas and assuaged somewhat by the
use of exogenous insulin). This hyper-secretion is also the reason the cellular
insulin receptors become resistant due to receptor down regulation as one of
the contributors; and this is also the main reason we should never, ever use a
sulfonylurea to treat a type 2 diabetic, as their pancreas is already
overworking and these meds facilitate its demise. There is also a less
recognized type of diabetes known as type 1 and a half or type 3 diabetes. This
type of diabetic is one who is insulin requiring, but now has developed
resistance to exogenous insulin, a situation we are seeing more of as more
clinicians are using insulin in the initial treatment of even type 2 diabetics
(a treatment I do agree with but with some caveats). The fourth type is
gestational diabetes and these pts do very well with carb restriction which is
safe in pregnancy, so long the pt is eating more fat, cholesterol and protein.
Some authors have argued there are at least two more types (drug induced
diabetes as one sees with steroid use and Juvenile onset type 2 diabetes, which
is self-explanatory) but for brevity’s sake we’ll limit our discussion to the 4
types above.
Now let’s get
back to insulin. We all learned in nursing or medical school that insulin helps
to lower serum blood sugar. This is done via a second messenger system
specifically the Inositol 1-4-5 triphosphate, e.g. IP3 and the diacylglycerol
or DAG molecules. This fact was learned when we took biochemistry but
unfortunately was quickly forgotten. Analyzing this second messenger system
further and looking specifically at the DAG molecule, we need to note that one
of the ‘acyl’ groups is arachidonic acid which when metabolized releases
pro-inflammatory mediators (Click Here for more on Arachidonic Acid). It is these mediators that can and
do cause a cellular apoptosis. What’s even more of a concern is that some of
these mediators have been shown to be oncogenic. The possible end result of
allowing our cells to see too much insulin is the eventual death of the cell. Said
another way, not only does the elevated blood sugar cause cellular damage, but
so too insulin can cause cellular damage or death (culminating in organ damage)
and this is a point missed by most clinicians. Therefore I disagree with the
intensive insulin therapy and do agree with lowering the carb intake in our 60
yo female pt.
While some
may be thinking it difficult to lower the carb intake so strictly, I must state
that the majority of my patients are very happy to have this option to treat,
an option too few doctors even know about. As far as motivational interviewing
is concerned it really is a treatment that sells itself. Most pts do not want
to take meds and they especially do not want to take insulin as this requires a
needle. I have successfully treated thousands of diabetics with a low carb
approach with success nothing short of miraculous. The only problem is that
most clinicians, dieticians, nutritionists, and politicians do not even
understand the correct way to eat.
I want to
get back to insulin a little while longer because it is such an important
hormone to understand. When a healthcare professional is asked to describe the
effects of insulin secretion, all will correctly state that it helps lower
serum blood sugar; but insulin has many more effects biochemically which I want
to discuss further, as it directly affects diabetes care. Insulin also
increases the activity of HMG Coenzyme reductase as well as acetyl Coenzyme A
carboxylase. The first enzyme catalyzes the rate limiting step in cholesterol
biosynthesis; the second enzyme catalyzes the start of the biosynthesis of
fatty acids. Therefore, any increase in the secretion of insulin which occurs
via the consumption of carbs, will also increase the biosynthetic rate of both
cholesterol and fatty acid synthesis. The end result is progression of
atherosclerosis, elevation of triglycerides, lowering of HDL, and increases in
weight all of which contribute to the manifestation of ‘the metabolic syndrome’
which culminates in development of overt type 2 diabetes. In fact, the
treatment and reversal of not only type 2 diabetes but of the entire metabolic
syndrome is so easy; it should be an embarrassment to the medical community
that we haven’t been able to do this yet on a widespread scale. As a side note,
there is a website that lists doctors who understand the importance of low
carbs in the treatment of disease, just go to LowCarbDoctors.com
Now it is
easy to say we need to dramatically lower our carb intake to experience better
and ultimate sugar control, but we aslo have to analyze further what exactly
carbs are and this is where it can become controversial. Everyone knows that
cakes and candies are bad for us as well as the white starchy foods; but what
about whole grains, muti-grains, whole wheat pasta, brown rice, yogurt, oatmeal
and fruit? Are these foods safe for a diabetic to eat? Well, let’s analyze
those foods further. Diabetics are often told that they can eat whole grains
and the like, and that fruit is fine to eat too. This is false. Whole grains
are complex carbs and as such contain many sugar molecules (one grain contains
6 x 10 exponent 1017 molecules which is a 6 times 10 to the 1017 power!) and
one slice of whole grain bread may contain even more carbs (even after
subtracting the fiber) than its white counterpart. The body will break down
these complex carbs into simple sugars and that’s where the trouble starts. One
may not see an immediate rise in blood sugar for an hour or so after consuming
complex carbs, but it will happen if one keeps checking blood glucose levels.
Another side note is that blood sugar should always be normal, it should never
be elevated. This sounds like a tautology but let me explain further. I use a
normal range of 80-100 and I warn my diabetics they should always be in that
range. That any increase in blood sugar will create cell damage and is dangerous
to their organs. I am confused as to why the ADA allows a post-prandial
increase in blood sugar and considers this to be ‘normal.’ It is not and any
rise above 100 should be evaluated. In fact, I tell my patients who are going
to get their labs drawn to not fast, as fasting is cheating and changes the
blood chemistry into what it truly isn’t and we want to see what the blood
normally looks like. Another fact is that a simple 6 hour fast (and a lot of
clinicians tell their pts to fast 12-14 hours) can normalize blood sugars and
triglycerides, and the clinician will not know a pt is over consuming carbs and
cannot counsel the pt effectively. Another reason blood sugar should always
remain normal is that the attachment of glucose molecules to cells in our organs
occurs via a nonenzymatic pathway, referred to as nonenzymatic glycosylation.
What this means is that glucose attaches to the cells in a concentration
dependent manner and no intermediaries are needed for this to happen. This
glycosylation process is what leads eventually to end organ damage and the only
way to prevent this is by having normal blood sugars all the time.
Getting back
to the whole grains (and this goes for any grain, oatmeal etc.) once they are
metabolized to simple sugars, insulin will be secreted form the pancreas and
this will facilitate persistent insulin resistance as well as increase the
biosynthesis of cholesterol, free fatty acids, help to lower HDL, encourage
weight gain, & create pro-inflammatory mediators via the second messenger
system. This cascade of events will occur with any glucose molecule. The
glucose released from complex carbs is not ‘special’ in any sense. To think
that at the level of the cell a cell can ‘recognize’ a glucose molecule as
being from whole grains, oatmeal, white starchy food or a chocolate bar is wrong.
Cells are not cognizant of where a glucose molecule comes from, they just do
biochemically what they’re programmed to do when glucose enters them; make us
fatter, create plaque forming deadly cholesterol and of course elevate blood
glucose serum levels.
And now a
word about fruit. I tell my diabetics that fruit is a poison and they should
stay away from it. Any diabetic who actually checks their blood sugar level
after eating fruit knows this. I am utterly confused as to why the
organizations as delineated above refuse to understand this. Another
biochemical fact is our cells use both glucose and fructose to make cholesterol
and fat and that fructose is actually transformed into cholesterol & fat faster than glucose. This means that
when one eats a piece of candy and piece of fruit, the fructose in the fruit
will be converted more quickly into fat & cholesterol, than the glucose in
the piece of candy will be. This is a biochemical fact. Why? Quite simply
because fructose enters the glycolytic pathway about a third of the way in and
needs to be modified less than glucose. So, no, diabetics should not be eating
fruits as allowed by the ADA guidelines.
I want to
take time out now to dispel a few myths about glucose. Glucose is not the
primary energy source of the body. I know this is a controversial statement but
let me explain further. The fact is that
our skeletal muscles, renal cortex and myocardium all prefer free fatty acids for fuel, not glucose.
Also, when given the choice the brain prefers ketone bodies for fuel over
glucose. Interestingly enough, the breakdown products of fatty acid metabolism
(in a process referred to as beta-oxidation) are ketone bodies. Another
interesting point is that some will claim that the only way glycogen can be
stored (in the liver and muscles) is by the consumption of carbs, which allows
glucose to be stored as glycogen. This is not true. We can also make glucose
from the glucogenic amino acids as well as the glycerol backbone chain found in
triglycerides. The utilization of free fatty acids for energy comes from
shuttling 2 carbon acetyl fragments into the Kreb’s cycle then onto the
oxidative phosphorylation pathway, not by creating glucose (this is the beta
oxidative pathway).
Another
misconception I wish to clear up is the whole ‘burning of fat’ or ‘burning of
calories’ notion. When we catabolize or breakdown macronutrients (fat,
carbohydrates or protein) this is not a combustion process, it is a digestive
process. For example, the breakdown of carbohydrates begins when a carb is
ingested. If it is a complex carb, it will be acted upon by different enzymes
(mono & disaccharidases) to release a glucose molecule(s). This glucose
molecule will then enter the cell and be shuttled into the glycolytic pathway.
The end result of this pathway is the creation of a molecule (actually 2) of
pyruvate which then will be transformed to Acetyl CoA. I often refer to Acetyl
CoA as a pivotal biomolecule because its fate depends upon how much
carbohydrate one has consumed. If there is an overabundance of carbs ingested,
the Acetyl CoA will be shuttled into the cholesterol and fatty acid
biosynthetic pathway. If there is not an overabundance of carbs consumed it
(Acetyl CoA) will then move into the Kreb’s cycle and then finally into the
oxidative phosphorylation pathway (the final step in the oxidation of glucose.)
It is important to stress that nothing is burned because it creates a
misunderstanding of what really is happening biochemically. Glucose is
metabolized to create either ATP (the energy currency of our bodies) or is used
to make cholesterol or fat, there is no actual burning. The same is true of fat
and protein digestion, they are not combustion processes. This is so germane to
a diabetic (and anyone) because we are told to count calories. This is wrong.
We often hear the phrase ‘I need to burn up my calories,’ and this, too, is
wrong. We are not burning any calories or fat. We metabolize fat, protein
and/or carbs to either create biomolecules and/or to create ATP. Again, there
is no combustion going on here.
Now the
process to determine how many calories are in an item of food is indeed a
combustion process. We’ve all come across the calorimeter; a cylindrical metal
device containing water, a thermometer, a lid and a heat source. To determine
the amount of calories we simply place an item of food inside, heat it to
reduce it to carbon, and record the temperature rise of the thermometer. The
temperature rise is how we actually measure calories. In fact, the definition
of a calorie takes all this into account; i.e. a calorie is the amount of heat
needed to raise the temperature of 1 gram of water by 1 degree Celsius. All
this is very important to understand when caring for a diabetic. Only by
realizing that the calorie is irrelevant in human nutrition, that the burning
of anything from a nutritional standpoint is a fallacy, can we better care for
our diabetics. The bottom line is that we need to be counting grams of carbs,
not calories. Also, by focusing on calories and suggesting they be lowered,
will often deprive the pt of important sources of fat & cholesterol in the
diet.
With this
introduction I will now move onto the questions for this week’s forum;
1)
What might you assume is causing the
patient’s blood sugar variability?
We have here
a 60 yo female suffering from diabetes for 8 years, stated as non-compliant,
with concomitant diagnoses of CVA, HTN and depression; she’s also stated to be
‘maxed’ out on oral meds. My first encounter with this pt would consist of an
in depth discussion with the pt about her diabetes, determine exactly why pt is
experiencing difficulty with blood sugar control and ascertain how much her
depression contributes to her ‘non-compliance.’ I put non-compliance in quotes
because I have seen many a pt whose sole reason for non-compliance was a lack
of understanding about their disease and not a voluntary attempt to disregard
the advice of the physician or nurse.
I would also
address the 2 other medical conditions (HTN & CVA) and discuss with pt that
many people experience depression with having only one medical condition e.g.
diabetes, but she is dealing with 2 more, greatly increasing her risk for
depression. I would then add that many pts can get depressed from the simple
act of taking meds on a daily basis; this increased risk of depression (&
frustration) increases the more meds one has to take. It also needs to be
ascertained exactly what type of CVA pt suffered and if (depending on area of
brain involved) the location of CVA is contributing to depression e.g. deep
limbic system, pre-fontal cortex, anterior cingulate gyrus, basal ganglia &/or
temporal lobes. It should be noted that evidence based studies have shown
antidepressants to be ‘modestly beneficial’ with ‘adverse events significantly
more common.’ (Hackett,
Anderson, House; Cochrane Database Syst Review 2008.) Also, psychotherapy was shown to have ‘no
evidence of benefit.’ (Ibid). Another trial revealed ‘that a care management
program, which included depression education, antidepressant treatment guided
by algorithm, and monitoring of therapy was more effective than usual care’
i.e. discretionary use of antidepressants. (Stroke. 2007;38(3):998) Further
studies go on to state an ‘eight-week psychosocial-behavioral intervention plus
antidepressant therapy was superior to antidepressant treatment alone.’
(Stroke. 2009;40(9):3073) With all this conflicting data it is easy to see why
the treatment of depression of this pt that’s post-CVA can be a challenge. That
said, a care management approach, which is exactly what these tutorial sessions
are teaching us, appears to be the best approach.
After
discussing with pt her individual med conditions and assessing where her
knowledge base is at, I would then go over her medications with her, again
asking what she takes and how she takes it. For my own edification, I also
review the med list from a pharmacodynamic and pharmacokinetic perspective.
The med list
appears to only list the diabetic meds and it immediately became apparent to me
that meds the pt may be taking for her HTN or CVA could be contributing to her
depression; for brevity’s sake I will only focus on the diabetic meds. The
first med listed is metformin. This is a safer med for diabetics to take as its
mechanism of action is to help increase a cell’s sensitivity to insulin and
also decreases gluconeogenesis in the liver; this has the effect of more
effective utilization of circulating insulin and diminished ‘dumping’ of blood
sugar into the serum. This is a medication that does not (usually) cause a
precipitous drop in blood glucose, so I can safely allow my pts to continue
this drug when starting a low carb regimen. Both glimeprimide & glipizide
are sulfonyl ureas and stimulate an already overworked pancreas to secrete even
more insulin. As mentioned above, but it bears reiterating, this will have the
effect of increasing insulin
resistance (despite the package insert’s contradictory comments), increasing the likelihood of beta-cell
burnout, increasing the intracellular
production of both cholesterol & triglycerides (which directly increased
cardiovascular morbidity & mortality), increasing
cellular apoptosis via the use of the second messenger system, and slowing down and/or preventing weight
loss by its inhibitory action on hormone sensitive lipase; this is not an
exhaustive list but I will stop here.
Now the next
2 meds, Byetta and Januvia are an interesting combination and it appears the
prior physician was using them for their complimentary actions. Januvia was the
dipeptidyl peptidase type 4 inhibitor which interestingly enough, would prevent the Byetta from being
metabolized, allowing Byetta to exert its physiological effects longer
(increasing glucose dependent insulin secretion, decreasing glucagon secretion,
slowing gastric emptying…) As a side noted, studies have shown Byetta to reduce
the HgA1c by 0.5-1%,( immediate release) to 1.5-1.9% (sustained release), which
would reduce our pt’s HgA1c to 12.0 (sustained release), which is a negligible
lowering of average blood sugar. In addition, post-marketing studies have shown
increased risk of pancreatitis with Byetta use.
After review
of her med list. I would immediately begin counseling on carb counting and
would gauge pt’s motivation for starting. If I sensed she would seriously
consider starting to lower her carbs, I would stop the glimepiride, glipizide, Byetta
and Januvia.
I agree with
the start of Insulin therapy, but I would need clarification of what ‘intensive
insulin therapy’ means. The orders do not reveal if we are adding Insulin in addition to or are we eliminating any
meds once starting insulin? These orders immediately reminded me of a study I
read a few years back which suggested that tight HgA1c control (<6 .5="" 3="" about="" all="" am="" amp="" and="" answer="" as="" associated="" be="" better="" blood="" bolt="" came="" certainly="" death="" disease="" end-organ="" equates="" finally="" greater="" i="" in="" into="" less="" me="" morbidity="" morning="" mortality.="" of="" one="" over="" read="" regulation="" researchers="" sat="" seeing="" so.="" so="" study.="" study="" style="mso-bidi-font-style: normal;" sugar="" sure="" t="" taught="" that="" the="" this="" tissue="" to="" upright="" was="" wasn="" we="" were="" weren="" why="" with="" would="">the increased morbidity & mortality was
not due to the tight control of the HgA1c
,
it was due to all the meds the pts were on to get the HgA1c lower.
The pt’s blood sugars were not being controlled through the correct way to eat,
but through the use of these medications and the pts were suffering because of
this.
Getting back
to my pt, I would stop the meds as described and start solely on long acting
insulin (assuming pt allows), and yes, using the pens makes it much easier
(some insurances wont allow), discuss the importance of low carbs, and have the
pt call my office on a daily basis with blood sugar results. Now some may
immediately become concerned at me stopping 4 PO meds and starting on just
long-acting insulin stating (correctly) that the pt’s blood glucose will almost
certainly rise. That is correct, but it is OK. Hypoglycemia is more dangerous
in the short term than hyperglycemia, so I’m ok allowing my pt to run a little
higher as we figure out the correct dose of insulin. Another couple points
about insulin. Once we take more than 20 units at once (some authors say 10
units), there can be erratic absorption so it is best to ‘split’ the dose
above, say, 30 units; i.e. give 20 units SQ in one area and 10 units SQ in
another. Also, we run the risk of creating more insulin resistance by using
increasing doses of insulin; thus the pt runs the risk of developing type 3
diabetes. This is where metformin is helpful because it helps maintain insulin
sensitivity.
In 1 week pt
will return with both a sugar and food diary (remember she was in contact with
me daily all week) and we will discuss the results.
As far as
what’s causing the blood reading variability, it is because pt most likely
received inadequate diabetic teaching (or more importantly, the incorrect
diabetic training) and may possibly be ‘afraid’ to use the insulin; this is why
it’s important to have pt come back with not only a sugar diary, but a food diary
as well and we would want to ask exactly
how she is taking insulin.
Looking at
pt’s labs reveals a diabetic nephropathy as microalbuminuria is elevated with
an elevated Cr. I would like to stress that the correct approach is to not restrict protein intake, but
encourage increased consumption of protein, fat and cholesterol and to lower
the carb intake. What is happening in diabetic nephropathy (as well as all the
other end-organ damaging effects) is that the aforementioned non-enzymatic
glycosylation is occurring at the glomerular level and this impairs the
filtration mechanism of the nephron. This impaired filtering mechanism, with
the subsequent increased proteinuria, is not
from the consumption of protein, but from the overconsumption of sugar. Eating more protein will not
create more kidney damage as is commonly thought. In fact it’s beneficial. I
have seen microalbuminurias in the 100 range (highest 800) revert to normal
upon eating the correct way. This is a reversal of the nephropathy. In addition,
other end organ damage (eye and nerve) can also reverse when a pt begins to eat
the correct way. A quick note about the lipid profile; the triglycerides are
elevated. These will also lower once the pt lowers their carbs and begins to
eat more fat, cholesterol & protein.
2)
What would your next steps include in
care-managing this pt?
A full
discussion of diabetes including the correct way to eat; recommended reading:
my favorite is Dr. Bernstein’s Diabetes
Solution by Richard K. Bernstein (2007).; I would have anyone on my care
management team read this book and keep it as a handy reference; training of my
support staff as to the correct way to eat for counseling our pts….
I have so
much more to say, but I think this is a good primer for continued study J
My question was about feeding a 3 year old child a low carb paleo diet. My girlfriend and I follow a low carb paleo diet, not for weight loss purposes but rather for overall health and wellness. Our diet consists mainly of meat (chicken, beef, pork, turkey, fish), non-starchy vegetables (broccoli, cauliflower, carrots, cabbage and so forth), eggs, nuts (raw mixed nuts), cheese (usually aged cheddar), low sugar fruits (mostly berries), and the occasional dessert (dark chocolate, ice cream). Naturally, my girlfriend's child eats the same food that we do.
Based on the research I have done this type of diet is ideal not only for adults but children as well. However, the child's biological grandmother is alleging that the diet we feed the child is a form of child abuse because it restricts, among other things, whole grains. She has stated an intention to make it an issue in family court and has already contacted CPS. Accordingly, I am feeling a pressing need to contact a low carb pediatric expert and get advice on the diet that we follow.
I understand that without seeing the child in person you couldn't make any pronouncement about the child's health but I was hoping to get a statement on the safety of the diet for a child in general. Again, it isn't for weight loss purposes, but only overall health. It is our desire to instill healthy eating habits into the child while he is young and to ensure that he develops into a healthy adult who will avoid things like diabetes, obesity and other problems associated with the standard American diet in the long run.
Thank you very much for your time sir.