::IMVA :: Internacional Medical Veritas Association ::
Diabetes is disabling, deadly and
on the rise and in certain places has reached fifty
percent of local populations.
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Magnesium and Diabetes
Magnesium affects
carbohydrate metabolism by influencing the release and
activity of insulin, the hormone that controls blood sugar
levels, by influencing the resistance and sensitivity to
insulin. Magnesium for diabetics is critical.At least
twenty five percent of diabetics have hypomagnesemia[i]
and this is likely an underestimate. One group has
recently suggested that the effects of reduced glutathione
on glucose metabolism may be mediated, at least in part,
by intracellular magnesium levels.[ii]
Dr. Carolyn Dean
indicates that magnesium deficiency may be an independent
predictor of diabetes and that diabetics both need more
magnesium and lose more magnesium than most people.
Magnesium is necessary for the production, function &
transport of insulin.
Magnesium deficiency is associated with insulin resistance
and increased platelet reactivity. According to Dr. Jerry
L. Nadler, “The link between diabetes mellitus and
magnesium deficiency is well known. A growing body of
evidence suggests that magnesium plays a pivotal role in
reducing cardiovascular risks and may be involved in the
pathogenesis of diabetes itself. While the benefits of
oral magnesium supplementation on glycemic control have
yet to be demonstrated in patients, magnesium
supplementation has been shown to improve insulin
sensitivity. Based on current knowledge, clinicians have
good reason to believe that magnesium repletion may play a
role in delaying type 2 diabetes onset and potentially in
warding off its devastating complications --
cardiovascular disease, retinopathy, and nephropathy.”
A separate Gallup
survey (in 1995) of 500 adults with diabetes reported that
83 percent of those with diabetes are consuming
insufficient magnesium from food, with many by significant
margins.[iii]
One group has recently suggested that the effects of
reduced glutathione on glucose metabolism may be mediated,
at least in part, by intracellular magnesium levels.[iv]
The mechanism of
hypomagnesemia in diabetic patients still remains unsolved
but there is enough evidence to suggest that Mg levels
drop in the course of recovery from ketoacidosis, during
insulin therapy[v]
or with severe retinopathy[vi]
or proteinuria.[vii]
Diabetic patients, especially those with poor glucose
control, develop hypomagnesemia from a glucose-induced
osmotic diuresis.
Insulin resistance
and magnesium depletion may result in a vicious cycle of
worsening insulin resistance and decrease in intracellular
Mg(2+) which may limit the role of magnesium in vital
cellular processes. Diabetic ketoacidosis (DKA)[viii]
is a state of inadequate insulin levels resulting in high
blood sugar and accumulation of organic acids and ketones
in the blood. Increased blood acids (ketoacidosis) can be
an acute complication of diabetes. It occurs when your
muscle cells become so starved for energy that your body
takes emergency measures and breaks down fat, a process
that forms acids known as ketones.[ix]
Hyperglycemia
initially causes the movement of water out of cells, with
subsequent intracellular dehydration, extracellular fluid
expansion and hyponatremia (sodium loss). It also leads
to a diuresis in which water losses exceed sodium chloride
losses. It is believed that magnesium is also lost by
osmotic action. Urinary losses then lead to progressive
dehydration and volume depletion, which causes diminished
urine flow and greater retention of glucose in plasma. The
net result of these alterations is hyperglycemia with
metabolic acidosis.[x]
Proteinuria is
protein in the urine, caused by damaged kidneys and a
declining ability of the kidneys to protect the body from
protein loss. This is frequently seen in longstanding
diabetes, hypertension, as well as other chronic renal
conditions. In the United States, diabetes is the leading
cause of end-stage renal disease (ESRD), the result of
chronic kidney disease. In both type 1 and type 2
diabetes, the first sign of deteriorating kidney function
is the presence of small amounts of albumin in the urine,
a condition called microalbuminuria. As kidney function
declines, the amount of albumin in the urine increases,
and microalbuminuria becomes full-fledged proteinuria.
Lower serum magnesium levels are associated with more
rapid decline of renal function. During insulin
treatment, neither magnesium nor potassium can be
metabolized properly, so these essential minerals must be
replaced.
Severe symptomatic
hypermagnesemia is relatively rare. But high levels
of magnesium can develop in people, most commonly
those with renal insufficiency or renal failure.[xi]
(diabetes, chronic renal insufficiency). Kidney disease,
rather than diet, is the usual cause of magnesium
overload, because the kidneys lose the ability to
remove excess magnesium.
Magnesium is
regulated and excreted primarily by the kidneys where
various ATPase enzymes are responsible for maintaining
homeostasis.[xii]
However hypermagnesemia can also occur in people with
hypothyroidism, those using magnesium containing
medications such as antacids, laxatives, cathartics, and
in those with certain types of gastrointestinal disorders,
such as colitis, gastroenteritis and gastric dilation,
which may cause an increased absorption of magnesium.
[i]Department of
Internal Medicine, Overlook Hospital, Summit, NJ, USA.
Hypomagnesemia has long been known to be associated
with diabetes mellitus. Mather et al confirmed the
presence of hypomagnesemia in nearly 25% of their
diabetic out-patients. Low serum magnesium level has
been reported in children with insulin-dependent
diabetes and through the entire spectrum of adult type
I and type II diabetics regardless of the type of
therapy. Hypomagnesemia has been correlated with both
poor diabetic control and insulin resistance in
nondiabetic elderly patients.
Hypomagnesemia and diabetes mellitus. A review of
clinical implications. Tosiello L; Arch Intern Med.
1996 Jun 10;156(11):1143-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=
[ii]
Barbagallo, Mario et al. Effects of
Vitamin E and Glutathione on Glucose Metabolism: Role
of Magnesium; (Hypertension. 1999;34:1002-1006.)
American Heart Association
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&l
[iii]
v57, Better Nutrition for Today's Living, March '95,
p34.
http://www.mgwater.com/articles.shtml
[iv]
Barbagallo, Mario et al. Effects of
Vitamin E and Glutathione on Glucose Metabolism: Role
of Magnesium; (Hypertension. 1999;34:1002-1006.)
American Heart Association
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=
[v]Hua H. et al: Magnesium transport induced ex vivo by a
pharmacological dose of insulin is impaired in
non-insulin-dependent diabetes mellitus.Magnes Res.
1995, Dec; Magnes Res. 1995 Dec;8(4):359-66. PMID:
8861135 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display&DB=pubmed
[vi]A tendency for magnesium deficiency in patients with
diabetes mellitus is well-established. Glucosuria-related
hypermagnesiuria, nutritional factors and
hyperinsulinaemia-related hypermagnesiuria all can
contribute. The plasma magnesium level has been shown
to be inversely related to insulin sensitivity.
Magnesium supplementation improves insulin sensitivity
as well as insulin secretion in patients with type 2
diabetes. Nevertheless, no beneficial effects of oral
magnesium supplementation has been demonstrated on
glycaemic control either in patients with diabetes
type 1 or 2. Oral magnesium supplementation reduced
the development of type 2 diabetes in predisposed
rats. There are some indications that magnesium
decreases blood pressure, but negative results have
been observed in trials that were, however, not
designed to test effect on blood pressure as primary
parameter. Patients with (severe) retinopathy have a
lower plasma magnesium level compared to patients
without retinopathy and a prospective study has shown
the plasma magnesium level to be inversely related to
occurrence or progression of retinopathy. Further
study on magnesium (supplementation) is warranted in
the prevention of type 2 and of (progression of)
retinopathy as well as a means to reduce high blood
pressure. Magnesium in Diabetes Mellitus;
de Valk HW.
Neth J Med. 1999 Apr;54(4):139-46.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstr
[vii]Lower serum magnesium levels are associated with more
rapid decline of renal function in patients with
diabetes mellitus type 2.Clin Nephrol.
2005 Jun;63(6):429-36. PMID: 15960144
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&li
[viii]
Diabetic ketoacidosis (DKA) is a dangerous condition
that can cause you to lose consciousness. If
untreated, it can be fatal. This is a diabetic crisis
state, and can quickly lead to fatality, including
cerebral edema, most often seen in children. It is
also common in DKA to have severe dehydration
and significant alterations of the body’s blood
chemistry. Diabetic ketoacidosis is a triad of
hyperglycemia, ketonemia and acidemia. (ketones and
acid in the bloodstream) Major components of the
pathogenesis of diabetic ketoacidosis are reductions
in effective concentrations of circulating insulin and
concomitant elevations of counterregulatory hormones (catecholamines,
glucagon, growth hormone and cortisol). These hormonal
alterations bring about three major metabolic events:
(1) hyperglycemia resulting from accelerated
gluconeogenesis and decreased glucose utilization, (2)
increased proteolysis and decreased protein synthesis
and (3) increased lipolysis and ketone production.
[ix] Diabetic ketoacidosis: Check your
ketones; From
MayoClinic.comSpecial
to CNN.com
http://www.cnn.com/HEALTH/library/DA/00064.html
[x]
This article exemplifies the AAFP 1999 Annual Clinical
Focus on management and prevention of the
complications of diabetes. Diabetic ketoacidosis is an
emergency medical condition that can be
life-threatening if not treated properly. The
incidence of this condition may be increasing, and a 1
to 2 percent mortality rate has stubbornly persisted
since the 1970s. Diabetic ketoacidosis occurs most
often in patients with type 1 diabetes (formerly
called insulin-dependent diabetes mellitus); however,
its occurrence in patients with type 2 diabetes
(formerly called noninsulin-dependent diabetes
mellitus), particularly obese black patients, is not
as rare as was once thought. The management of
patients with diabetic ketoacidosis includes obtaining
a thorough but rapid history and performing a physical
examination in an attempt to identify possible
precipitating factors. The major treatment of this
condition is initial rehydration (using isotonic
saline) with subsequent potassium replacement and
low-dose insulin therapy. The use of bicarbonate is
not recommended in most patients. Cerebral edema, one
of the most dire complications of diabetic
ketoacidosis, occurs more commonly in children and
adolescents than in adults. Continuous follow-up of
patients using treatment algorithms and flow sheets
can help to minimize adverse outcomes. Preventive
measures include patient education and instructions
for the patient to contact the physician early during
an illness. (Am Fam Physician 1999;60:455-64.)ABBAS E.
KITABCHI, PH.D., M.D., and BARRY M. WALL, M.D.
University of Tennessee, Memphis, College of Medicine
Memphis, Tennessee
http://www.aafp.org/afp/990800ap/455.html
[xi]Chronic
Renal Failure (Chronic Renal Insufficiency, Kidney
Failure, Renal Insufficiency)
(CRF) Irreversible, progressive impaired kidney
function. The early stage, when the kidneys no longer
function properly but do not yet require dialysis, is
known as Chronic Renal Insufficiency (CRI). CRI
can be difficult to diagnose, as symptoms are not
usually apparent until kidney disease has progressed
significantly. Common symptoms include a
frequent need to urinate and swelling, as well as
possible anemia, fatigue, weakness, headaches and loss
of appetite. As the disease progresses, other symptoms
such as nausea, vomiting, bad breath and itchy skin
may develop as toxic metabolites, normally filtered
out of the blood by the kidneys, build up to harmful
levels. Over time (up to 10 or 20 years), CRF
generally progresses from CRI to End-Stage Renal
Disease (ESRD, also known as Kidney Failure).
Patients with ESRD no longer have kidney function
adequate to sustain life and require dialysis or
kidney transplantation. Without proper treatment, ESRD
is fatal.
[xii] Sloan Kettering
Health Care Information for Professionals:
http://www.mskcc.org/mskcc/html/11571.cfm?RecordID=481&tab=HC
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