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Blood sugar level 165: High Blood Sugar (Glucose) Levels: Signs of Hyperglycemia

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Sir I have blood sugar fasting 165 and after food 230 now doctor advised for 3 times me.

..

88%

(29 ratings)

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Hello taper it slowly ones it comes to normel level and also take klaunji oil but organic one, onces a day put one tspoon in your meal .and also take jamun and krela juice.

General Physician

27yrs exp

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(3027 ratings)

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Dear Lybrateuser, – Depending on your blood sugar control with medication & the lifestyle changes the continuation or stoppage of medication will be done on the advise of your treating doctor
– a strict diet & exercise regime has to be followed to bring your blood sugar levels in the normal range
– avoid sweet, fried, processed & junk foods, have more of fruits & vegetables, whole grains, beans, legumes including pulses, lentils, peas, sprouts, nuts – do regular exercise like walking, jogging, swimming for 30-40 min, do mild weight lifting at least twice a week, also include yoga & deep breathing daily morning to reduce your blood sugar levels & keep it under control
– reduce weight by diet & exercise
– take diet & medication as advised, also monitor blood sugar before & after exercise, meals as advised
– chew your food well, do not skip meals, have meals on time.

1 person found this helpful

Endocrinologist

46yrs exp

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(11091 ratings)

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Hello, Thanks for the query.
If your blood glucose levels are FBG 165 mg & PP 230 mg, then taking oral antidiabetic medicine 3 times a day is rather too much.
Please check your HbA1c% also and come back. The present drug combination recommended Metformin + Glibenclamide 2.5 mg once may be ok. But it is better if more recent drugs like glimepiride, tenelgliptin etc are used rather than Glibenclamide. Please remember diabetes once diagnosed will remain with you for lifetime. There is no question of stopping the trratment once blood glucose level is normalised. Because if you stop the treatment again the levels will go up and there can be a number of long term serious complications. If you have any doubts please come back. Thanks.

The Pathophysiology of Cardiovascular Disease and Diabetes: Beyond Blood Pressure and Lipids

Abstract

In Brief

The pathophysiology of the link between diabetes and cardiovascular disease
(CVD) is complex and multifactorial. Understanding these profound mechanisms
of disease can help clinicians identify and treat CVD in patients with
diabetes, as well as help patients prevent these potentially devastating
complications. This article reviews the biological basis of the link between
diabetes and CVD, from defects in the vasculature to the cellular and
molecular mechanisms specific to insulin-resistant states and hyperglycemia.
It concludes with a discussion of heart failure in diabetes, a clinical entity
that demonstrates many of the mechanisms discussed.

Diabetes is a prime risk factor for cardiovascular disease (CVD). Vascular
disorders include retinopathy and nephropathy, peripheral vascular disease
(PVD), stroke, and coronary artery disease (CAD). Diabetes also affects the
heart muscle, causing both systolic and diastolic heart failure. The etiology
of this excess cardiovascular morbidity and mortality is not completely clear.
Evidence suggests that although hyperglycemia, the hallmark of diabetes,
contributes to myocardial damage after ischemic events, it is clearly not the
only factor, because both pre-diabetes and the presence of the metabolic
syndrome, even in normoglycemic patients, increase the risk of most types of
CVD.1–4

In 2002, a survey of people in the United States with diagnosed diabetes
found that, surprisingly, 68% of patients did not consider themselves at risk
for heart attack or
stroke.5 In
addition, only about half of patients surveyed reported that their health care
providers discussed the high risk of CVD in diabetes and what steps they could
take to reduce that
risk. 5 Fortunately,
we are now making the link. Health care providers are now focused on
decreasing cardiovascular risk in patients with diabetes by treating
dyslipidemia and hypertension and by improving glycemic
control.6 Moreover,
the American Diabetes Association/American College of Cardiology “Make
the Link” public awareness campaign has improved knowledge related to
CVD in patients with diabetes.

However, managing cardiovascular risk factors in patients with diabetes
does not eradicate these complications. We are only just beginning to
understand the complex and multifactorial etiology of CVD in diabetes. This
review will attempt to provide an explanation of the current scientific
knowledge in this field, from defects in the large blood vessels
(macrovasculature) and the small blood vessels (microvasculature) to the less
well-understood cellular and molecular mechanisms of CVD in patients with
diabetes.

Macrovasculature

Atherosclerosis is the major threat to the macrovasculature for patients
with and without diabetes. The general pathogenesis of atherosclerosis has
been reviewed
elsewhere,7 but
several factors specific to diabetes are worth mentioning here. Clinically,
dyslipidemia is highly correlated with atherosclerosis, and up to 97% of
patients with diabetes are
dyslipidemic.8 In
addition to the characteristic pattern of increased triglycerides and
decreased HDL cholesterol found in the plasma of patients with diabetes,
abnormalities are seen in the structure of the lipoprotein particles. In
diabetes, the predominant form of LDL cholesterol is the small, dense form.
Small LDL particles are more atherogenic than large LDL particles because they
can more easily penetrate and form stronger attachments to the arterial wall,
and they are more susceptible to oxidation. Because less cholesterol is
carried in the core of small LDL particles than in the core of large
particles, subjects with predominantly small LDL particles have higher numbers
of particles at comparable LDL cholesterol
levels. 9

Oxidized LDL is pro-atherogenic because once the particles become oxidized
they acquire new properties that are recognized by the immune system as
“foreign.” Thus, oxidized LDL produces several abnormal biological
responses, such as attracting leukocytes to the intima of the vessel,
improving the ability of the leukocytes to ingest lipids and differentiate
into foam cells, and stimulating the proliferation of leukocytes, endothelial
cells, and smooth muscle
cells,10 all of
which are steps in the formation of atherosclerotic plaque. In patients with
diabetes, LDL particles can also become glycated, in a process similar to the
glycation of the protein hemoglobin (measured in the hemoglobin A1c
[A1C] assay). Glycation of LDL lengthens its
half-life11 and
therefore increases the ability of the LDL to promote atherogenesis.
Paradoxically, however, glycation of HDL shortens its half-life and renders it
less protective against
atherosclerosis. 12

Moreover, diabetic blood is more likely to be high in triglycerides.
Hypertriglyceridemia in diabetes occurs, in part, because insulin action
regulates lipid flux. Insulin promotes the activity of the enzyme lipoprotein
lipase, which mediates free fatty acid uptake into adipose tissue (storage)
and also suppresses the activity of the enzyme hormone-sensitive lipase,
resulting in decreased release of free fatty acids into the
circulation.13
Hypertriglyceridemia can lead to increased production of the small, dense form
of LDL and to decreased HDL transport of cholesterol back to the
liver.14

Dyslipidemia is only one mechanism by which diabetes promotes
atherosclerosis; endothelial dysfunction often contributes. Healthy
endothelium regulates blood vessel tone, platelet activation, leukocyte
adhesion, thrombogenesis, and inflammation. The net effect of healthy
endothelium is vasodilatory, anti-atherogenic, and
anti-inflammatory.15

When these mechanisms are defective, the process of atherosclerosis is
accelerated. Therefore, both insulin deficiency and insulin resistance promote
dyslipidemia accompanied by increased oxidation, glycosylation, and
triglyceride enrichment of lipoproteins. In addition, endothelial dysfunction
is present, and all of these factors contribute to the increase in
atherogenicity, and thus macrovascular disease, found in patients with
diabetes.

Microvascular Disease

Typically, when we hear the term “microvascular disease”
associated with diabetes, we think of retinopathy, nephropathy, and
neuropathy. In addition, however, small vessels throughout the body are
affected by diabetes, including those in the brain, heart, and peripheral
vasculature. This small vessel damage is typically not related to
atherosclerosis and is not predicted by lipid levels. Whereas atherosclerosis
is the major threat to the macrovasculature, a variety of cellular and
molecular mechanisms contribute to microvascular disease in diabetes.

The microcirculation is regulated by central and local regulatory
mechanisms. The central regulation is via autonomic sympathetic and
parasympathetic nerves that reach the vascular smooth muscle. Local regulation
is carried out by substances produced by the endothelial cells and by local
products of metabolism. The endothelium produces both vasodilators and
vasoconstrictors. Normally, the vascular smooth muscle receives continuous
regulatory nerve signals and a continual supply of vasodilating nitric oxide
(NO) from the endothelium, as well as a continuous flow of metabolic products.
These regulatory mechanisms adjust microvascular flow instantaneously to meet
the metabolic needs of the
tissue.16

Diabetes contributes to defects in the autonomic nervous system, the
endothelium, and local metabolism, all of which can result in microvascular
disease. Diabetic autonomic neuropathy (DAN) is one factor associated with
impaired autoregulation of blood flow in a variety of vascular beds, including
the skin and the
heart.17,18
Patients with DAN have increased rates of sudden cardiac death as well as a
higher overall cardiovascular mortality rate. These patients have been found
to lack the normal cardiac flow reserve that is activated under conditions of
increased demand for myocardial
perfusion,19 which
may partially explain the high mortality rate in this population.

In addition to the dysregulation of vascular tone caused by DAN, subjects
with diabetes have been found to have decreased bioavailability of NO, a
potent vasodilator, as well as increased secretion of the vasoconstrictor
endothelin-1. This resulting state of vasoconstriction has been found in
subjects with the metabolic syndrome as well as those with
diabetes.20 In this
situation, the vasculature is in a hyper-constricted state. Not only do
hypertension and its concomitant complications result from vasoconstriction,
but blood flow is limited to respective tissues. Diabetes decreases NO
bioavailability because of either insulin deficiency or defective insulin
signaling (insulin resistance) in endothelial
cells.21
Hyperglycemia also acutely inhibits the production of NO in arterial
endothelial
cells. 22

In a sense, the ultimate outcome of blood flow to tissues is the transport
and exchange of substances between blood and tissue fluid. Thus, despite an
appropriate amount of blood flow, any process that inhibits product exchange
will impair the homeostasis of the tissue containing the vascular bed.
Capillary basement membrane thickening associated with prolonged hyperglycemia
is a structural hallmark of diabetic microvascular disease. Thickening of the
basement membrane impairs the amount and selectivity of transport of metabolic
products and nutrients between the circulation and the
tissue.23 In fact,
in skeletal muscle of patients with type 2 diabetes, exercise-stimulated
oxygen delivery from the capillaries is delayed, which may account in part for
the poor exercise tolerance found in people with type 2
diabetes.24

Transport of substances from the circulation, across the microvessel wall,
and into tissue interstitium is regulated by a variety of interdependent
mechanisms, including pressure, flow, and size and charge specificity.
Paradoxically, basement membrane thickening increases microvascular
permeability because of alterations in the physical dimensions of the meshwork
and changes in the normal electrical charge surrounding the pores between
endothelial cells. These abnormalities allow for the transport of large
molecules normally excluded from passage across the microvasculature. In
clinical terms, transcapillary leak of albumin in the kidney provides an
important indicator of microvascular
disease.25 The
urine microalbumin test, initially indicated for the detection of early
diabetic nephropathy, actually reflects the health of the entire
microvasculature. Thus, a patient with a microalbuminuria not only has
nephropathy, but also can be assumed to have widespread microvascular
disease.26

Inflammation

Inflammation is a normal response to tissue injury or pathogen exposure and
is a critical factor in the body’s ability to heal itself or to fight off
infection. The inflammatory response involves the activation of leukocytes
(white blood cells) and is mediated, in part, by a family of cytokines and
chemokines. Although inflammation is beneficial, if this response is
chronically activated it can have a detrimental effect. Diabetes has long been
considered a state of chronic, low-level
inflammation,27 and
there is some evidence to suggest that this immune activation may precede
insulin resistance in diabetic and pre-diabetic states and ultimately may be
the factor that initially increases cardiovascular risk in these disease
processes.28

Recent evidence suggests cross-talk between the molecular pathways involved
in both inflammation and insulin signaling, and this cross-talk may provide
clues to the strong relationship between insulin-resistant states (such as the
metabolic syndrome and type 2 diabetes), inflammation, and
CVD.29 As
previously discussed, researchers have found a reduced production of the
potent vasodilator NO and an increased secretion of the vasoconstrictor and
growth factor endothelin-1 in subjects with the metabolic syndrome, and these
abnormalities not only enhance vasoconstriction, but are associated with the
release of pro-inflammatory
cytokines. 30
Proinflammatory cytokines cause or exacerbate injury by a variety of
mechanisms including enhanced vascular permeability, programmed cell death
(apoptosis), recruitment of invasive leukocytes, and the promotion of reactive
oxygen species (ROS)
production.31

Recently, Pickup and
Mattock32 found
serum sialic acid, a marker of low-grade
inflammation,33 to
be strongly predictive of type 2 diabetes in 128 patients from the United
Kingdom who were followed for a mean of 12.8 years. In addition to predicting
type 2 diabetes, this marker also predicted cardiovascular mortality
independent of other known risk factors for CVD, including pre-existing
CVD.32 These
observations have led investigators to suspect a common, unknown
antecedent34 and to
consider chronic inflammation as one candidate for this precursor.

In addition to diabetes, obesity is associated with increased levels of a
number of adipokines (cytokines released from adipose tissue), including tumor
necrosis factor-α, interleukin 1β, interleukin 6, and plasminogen
activator inhibitor 1 (PAI-1), all linked to the inflammatory
response. 35 The
levels of these pro-inflammatory cytokines typically increase as fat mass
increases; however, one exception is the adipokine adiponectin, which has
anti-inflammatory properties and is decreased in obese
subjects,36
exacerbating the chronic inflammatory nature of obesity. In addition to their
endocrine properties, these locally produced cytokines have been found to
possess autocrine and paracrine properties that can influence neighboring
tissues as well as the entire organism.

Oxidative Stress

As discussed earlier, pro-inflammatory cytokines can enhance the production
of ROS. The term ROS refers to a subset of molecules called “free
radicals.” This term refers to any molecule that contains an unpaired
electron in the outer orbital. This unpaired electron makes the molecule
highly reactive, seeking to either donate an electron to another compound or
take up protons from another compound to obtain a stable electron
pair.37 This high
reactivity leads to the formation of bonds between the ROS and other
compounds, altering the structure and function of the tissue. Because of the
reactive propensity of these molecules, ROS can directly damage a number of
cell components, such as plasma membranes and organelles.

ROS are produced by the immune system as a way to injure and destroy
pathogens, but they are also generated as a result of daily living. Normal
metabolism results in the production of ROS, which act as signaling molecules
for both physiological and pathophysiological properties. Oxidative stress
occurs when the cellular production of ROS exceeds the capacity of
anti-oxidant defenses within cells. Numerous studies have demonstrated chronic
oxidative stress in diabetic humans and animals, purportedly related to the
metabolism of excess substrates (glucose and fatty acids) present in the
hyperglycemic
state,38 as well as
to the mitochondrial dysfunction associated with insulin
resistance.39 For
example, plasma levels of hydroperoxides (one ROS) are higher in subjects with
type 2 diabetes compared to nondiabetic subjects, and these levels are
inversely correlated with the degree of metabolic
control. 38

The mitochondria are the major source of ROS. At the subcellular level, the
etiologies of insulin resistance and diabetes, as well as their complications,
are deeply related to defects in mitochondrial
function.40 The
mitochondria produce most of the body’s required adenosine triphosphate
through the process of oxidative phosphorylation (via the electron transport
chain). Oxidative phosphorylation is the major source of ROS under normal
physiological
conditions.41 There
are two sites in the mitochondrial electron transport chain that generate ROS,
and the increased flux of glucose in diabetes has been found to increase ROS
production.40

Oxidative stress is currently the unifying factor in the development of
diabetes complications. In 2004, the Banting Medal for Scientific Achievement,
the most prestigious award of the ADA, was given to Michael Brownlee, MD, for
his pivotal work in the etiology of diabetes complications. According to
Brownlee, there are four mechanisms by which chronic hyperglycemia causes
diabetes complications: activation of the polyol pathway; increased formation
of advanced glycosylation end products; activation of protein kinase C, an
enzyme involved in numerous molecular signaling pathways; and activation of
the hexsosamine pathway. Through decades of research, Brownlee and his
colleagues found that hyperglycemia-induced mitochondrial ROS production
activates each of the four major pathways of hyperglycemic damage. Moreover,
blocking ROS production or interfering with ROS signaling attenuated the
activity of all four
pathways.42 Thus,
oxidative stress is a crucially important concept in the pathophysiology of
the cardiovascular complications in diabetes.

Activated Leukocytes

As previously discussed, the inflammatory response appears to be
over-activated in insulin resistance and in diabetes. Leukocytes are major
mediators of inflammation. They also contribute to the oxidative stress
associated with diabetes. ROS are generated not only from the mitochondria,
but also from activated leukocytes. Hokama et al. found that the expression of
adhesion proteins on the surface of neutrophils, which suggests activation and
ROS production, was significantly increased in
diabetes.43
Freedman and Hatchell found that stimulated neutrophils from diabetic animals
generated superoxide radical (a type of ROS) at significantly higher rates
than did those from normal
animals. 44 Under
ischemic conditions, Hokama et al. found that leukocyte accumulation during
reperfusion was enhanced in the diabetic coronary microcirculation, suggesting
an increased ability of leukocyte-generated ROS to exacerbate tissue damage
after experimental myocardial infarction
(MI).43 The excess
chronic oxidative stress produced in the hyperglycemic state by the
mitochondria, as well as the additional acute stress mediated by accumulated
leukocytes, may largely explain the mechanism of increased oxidative injury
associated with ischemic heart disease in diabetes. This explanation, in turn,
aids our understanding of the excessive morbidity and mortality in patients
with diabetes after heart attacks when compared to patients without
diabetes.

Hypercoagulability

In addition to affecting the leukocytes in the blood, diabetes is also
related to a hypercoagulable state. The coagulability of the blood is
crucially important in ischemic cardiovascular events because the majority of
MI and stroke events are caused by the rupture of atherosclerotic plaque and
the resulting occlusion of a major artery by a blood clot (thrombus).

Up to 80% of patients with diabetes die a thrombotic death. Seventy-five
percent of these deaths are the result of an MI, and the remainder are the
result of cerebrovascular events and complications related to
PVD.45 The first
defense against a thrombotic event is the vascular endothelium. As previously
discussed, diabetes contributes to widespread endothelial dysfunction. The
endothelium and the components of the blood are intricately linked, such that
clotting signals initiated in the endothelial cell can activate platelets and
other blood components, and vice
versa.46 Patients
with diabetes exhibit enhanced activation of platelets and clotting factors in
the blood. Increased circulating platelet aggregates, increased platelet
aggregation in response to platelet agonists, and the presence of higher
plasma levels of platelet coagulation products, such as beta-thromboglobulin,
platelet factor 4, and thromboxane B2, demonstrate platelet
hyperactivity in diabetes. Coagulation activation markers, such as prothrombin
activation fragment 1+2 and thrombin–anti-thrombin complexes, are also
elevated in diabetes. In addition, patients with diabetes have elevated levels
of many clotting factors including fibrinogen, factor VII, factor VIII, factor
XI, factor XII, kallikrein, and von Willebrand factor. Conversely,
anticoagulant mechanisms are diminished in diabetes. The fibrinolytic system,
the primary means of removing clots, is relatively inhibited in diabetes
because of abnormal clot structures that are more resistant to degradation,
and also because of an increase in
PAI-1.47

Clinicians attempt to reverse this hypercoagulable state with aspirin
therapy, widely recommended for use as primary prevention against thrombotic
events in patients with diabetes. However, numerous studies have suggested
that aspirin in recommended doses does not adequately inhibit platelet
activity in patients with diabetes. This concept of “aspirin
resistance” is controversial and has not been found consistently in all
diabetic patient populations, but it may provide insight into the high rates
of thrombotic events in diabetes even among those appropriately
treated. 48

In summary, the increase in cardiovascular morbidity and mortality is
complex and multifactorial and is usually related to a combination of both
macrovascular and microvascular dysfunction. Perhaps no clinical entity
demonstrates all of the components of diabetes-related CVD better than the
diabetes patient also diagnosed with chronic heart failure.

Heart Failure

Chronic heart failure is a complex clinical syndrome that can result from
any structural or functional cardiac disorder that impairs the ability of the
ventricle to fill with or eject
blood.49 Systolic
heart failure arises from a compromise in the contractility of the heart and
is defined as a left ventricular ejection fraction of < 45%. Diastolic
dysfunction interferes with the heart’s ability to relax and fill with
blood.50 Heart
failure in a patient with diabetes may arise from myocardial damage resulting
from an ischemic, thrombotic event. In this case, endothelial dysfunction,
oxidation and glycation of atherogenic lipids, and the hypercoagulability of
the blood are major contributors to the patient’s resulting heart failure. In
many cases, however, heart failure in patients with diabetes may have a
non-thrombotic etiology and other pathophysiological factors are at play, as
in the case of diabetic cardiomyopathy.

Diabetic cardiomyopathy can be defined as myocardial disease in patients
with diabetes that cannot be attributed to any other known CVD, such as
hypertension or
CAD.51 Because of
the structural and functional changes that occur in diabetic cardiomyopathy,
patients with diabetes are vulnerable to heart failure even early in the
course of their disease. At least two different epidemiological studies using
sensitive diagnostic methods found the prevalence of asymptomatic diastolic
dysfunction in patients with type 2 diabetes to be between 52 and 60%, despite
meeting clinical criteria for acceptable glycemic
control.52,53
Left ventricular diastolic dysfunction, characterized by impaired early
diastolic filling, prolonged isovolumetric relaxation, and increased atrial
filling has even been demonstrated in young patients with type 1
diabetes. 54

Myocardial damage in the absence of CAD (macrovascular) is most likely
related to microvascular dysfunction. Microvascular damage in the diabetic
heart may lead to the myocardial injury, fibrosis, and hypertrophy found in
diabetic
cardiomyopathy.55
In type 1 diabetic patients without CAD, impaired coronary flow reserve
(dependent on the microvasculature) predicts diastolic dysfunction and may be
related to autonomic
neuropathy.56 A
similar relationship between the magnitude of coronary flow reserve reduction
and the degree of myocardial diastolic dysfunction was found in uncomplicated
hypertension,57
another condition characterized by impaired coronary microcirculation. This
association is not surprising because coronary flow occurs predominantly
during diastole,58
so that normal coronary flow and diastolic dysfunction are interdependent.

In addition to microvascular disease, hyperglycemia is clearly another
factor that increases the risk for the development of heart failure in
patients with diabetes. In the U.K. Prospective Diabetes Study, every 1%
increase in A1C was associated with a 12% increase in heart
failure.59 In the
Strong Heart Study, the presence of type 2 diabetes was associated with left
ventricular enlargement and decreased myocardial function in both men and
women. In addition, the extent and frequency of diastolic dysfunction was
directly proportional to A1C
level.60 There are
a number of mechanisms by which hyperglycemia can contribute to the
development and progression of diabetic heart failure. Diastolic dysfunction
in diabetic cardiomyopathy is thought to be the result of myocellular
hypertrophy and myocardial
fibrosis.61 In the
laboratory, there is evidence that cardiac efficiency is decreased in diabetes
because of increased fatty acid utilization, which leads to an increased
production of
ROS.62 The increase
in oxidative stress in diabetic hearts has been found to decrease NO levels,
worsen endothelial function, and induce myocardial injury through stimulation
of inflammatory
mediators. 63

Moreover, a strong correlation was found between left ventricular
hypertrophy and markers of chronic inflammation in patients with type 2
diabetes. In the Strong Heart Study, which included 1,299 adults with type 2
diabetes, those with left ventricular hypertrophy had higher levels of
fibrinogen and C-reactive protein (both markers of chronic inflammation) and
urinary albumin independent of traditional cardiovascular risk
factors.64 In
addition, fibrinogen and C-reactive protein levels were independently and
significantly higher in subjects with left ventricular hypertrophy among those
without pathological albuminuria, suggesting that the association between
cardiac hypertrophy and low-grade inflammation may precede development of the
vascular
dysfunction.64

In summary, diabetic cardiomyopathy demonstrates multiple mechanisms by
which diabetes affects the cardiovascular system. Microvascular disease,
including endothelial dysfunction caused by DAN and decreased NO
bioavailability is of crucial importance. In addition, the underlying defects
of inflammation and oxidative stress contribute to diastolic dysfunction,
especially in the presence of poor metabolic control.

CVD accounts for the majority of the morbidity and mortality associated
with diabetes. As we continue to learn more about the complex pathophysiology
underlying this crucial health problem, more effective therapies for
prevention and treatment will emerge.

Footnotes

  • Betsy B. Dokken, PhD, NP, CDE, is an assistant professor of medicine in
    the Section of Endocrinology, Diabetes, and Hypertension at the University of
    Arizona, in Tucson. She is an associate editor of
    Diabetes Spectrum.

  • American Diabetes Association

References

  1. Muhlestein JB,
    Anderson JL, Horne BD, Lavasani F, Allen-Maycock CA, Bair TL, Pearson RR,
    Carlquist JF: Effect of fasting glucose levels on mortality rate in patients
    with and without diabetes mellitus and coronary artery disease undergoing
    percutaneous coronary intervention. Am Heart J146
    : 351–358,2003

  2. Thrainsdottir IS,
    Aspelund T, Thorgeirsson G, Gudnason V, Hardarson T, Malmberg K, Sigurdsson G,
    Rydén L: The association between glucose abnormalities and heart
    failure in the population-based Reykjavík Study. Diabetes
    Care 28:612
    –616, 2005

  3. Nielson C, Lange
    T: Blood glucose and heart failure in nondiabetic patients.
    Diabetes Care 28:607
    –611, 2005

  4. The DECODE Study Group.: Glucose
    tolerance and mortality: comparison of WHO and American Diabetic Association
    diagnostic criteria. Lancet354
    : 617–621,1999

  5. Merz CN, Buse JB,
    Tuncer D, Twillman GB: Physician attitudes and practices and patient awareness
    of the cardiovascular complications of diabetes. J Am Coll
    Cardiol 40:1877
    –1881, 2002

  6. Garber AJ:
    Attenuating cardiovascular risk factors in patients with type 2 diabetes.
    Am Fam Phys 62:2633
    –2642, 2645–2646,2002

  7. Libby P, Theroux
    P: Pathophysiology of coronary artery disease.
    Circulation 111:3481
    –3488, 2005

  8. Fagot-Campagna A,
    Rolka DB, Beckles GL, Gregg EW, Narayan KM: Prevalence of lipid ablormalities,
    awareness, and treatment in US adults with diabetes [Abstract].
    Diabetes 49 (Suppl.
    1): A78, 2000

  9. Rosenson RS:
    Clinical role of LDL and HDL subclasses and apolipoprotein measurement.
    ACC Curr J Rev May, 2004,
    p. 33–37

  10. Chan AC: Vitamin E
    and atherosclerosis. J Nutr128
    : 1593–1596,1998

  11. Napoli C,
    Triggiani M, Palumbo G, Condorelli M, Chiariello M, Ambrosio G: Glycosylation
    enhances oxygen radical-induced modifications and decreases acetylhydrolase
    activity of human low density lipoprotein. Basic Res
    Cardiol 92:96
    –105, 1997

  12. Bucala R, Makita
    Z, Koschinski T, Cerami A: Lipid advanced glycosylated pathway for lipid
    oxidation in vivo. Proc Natl Acad Sci USA91
    : 9441–9445,1993

  13. Shen GX: Lipid
    disorders in diabetes mellitus and current management. Curr Pharm
    Analysi
    s 3:17
    –24, 2007

  14. Duell PB, Oram JF,
    Bierman EL: Nonenzymatic glycosylation of HDL and impaired
    HDL-receptor-mediated cholesterol efflux. Diabetes40
    : 377–384,1991

  15. Celermejer D:
    Endothelial dysfunction: does it matter? J Am Coll
    Cardiol 30:325
    –333, 1997

  16. Lewis DH: The
    effect of trauma on the regulation of the microcirculation [Abstract].
    Pathophysiol 5 (Suppl.
    1): 191, 1998

  17. Smith SE, Smith
    SA, Brown PM: Cardiac autonomic dysfunction in patients with diabetic
    retinopathy. Diabetologia 21:525
    –528, 1981

  18. Ewing DJ, Campbell
    D, Clarke BF: The natural history of diabetic autonomic neuropathy.
    Q J Med 49:95
    –108, 1980

  19. Taskiran M,
    Fritz-Hansen T, Rasmussen V, Larsson HBW Hilsted J: Decreased myocardial
    perfusion reserve in diabetic autonomic neuropathy.
    Diabetes 51:3306
    –3310, 2002

  20. Koh KK, Han SH,
    Quon MJ: Inflammatory markers and the metabolic syndrome [Abstract].
    J Am Coll Cardiol 46:1978
    –1985, 2005

  21. Brownlee M:
    Biochemistry and molecular cell biology of diabetic complications.
    Nature 414:813
    –820, 2001

  22. Williams SB,
    Goldfine AB, Timimi FK, Ting HH, Roddy MA, Simonson DC, and Creager MA: Acute
    hyperglycemia attenuates endothelium-dependent vasodilation in humans in vivo.
    Circulation 97:1695
    –1701, 1998

  23. Hayden MR, Sowers
    JR, Tyagi SC: The central role of vascular extracellular matrix and basement
    membrane remodeling in metabolic syndrome and type 2 diabetes: the matrix
    preloaded. Cardiovasc Diabetol4
    : 9–29,2005

  24. Bauer TA, Reusch
    JEB, Levi M, Regensteiner JG: Skeletal muscle deoxygenation after the onset of
    moderate exercise suggests slowed microvascular blood flow kinetics in type 2
    diabetes. Diabetes Care 30:2880
    –2885, 2007

  25. Tooke JE:
    Microcirculation and diabetes. British Med Bull45
    : 206–223,1989

  26. Weir M:
    Microalbuminuria and cardiovascular disease. Clin J Am Soc
    Nephrol 2:581
    –590, 2007

  27. Pickup JC, Mattock
    MB, Chusney GD, Burt D: NIDDM as a disease of the innate immune system:
    association of acute-phase reactants and interleukin-6 with metabolic syndrome
    X. Diabetologia 40:1286
    –1292, 1997

  28. Festa A,
    D’Agostino Jr R, Howard G, Mykkänen L, Tracy RP, Haffner SM: Chronic
    subclinical inflammation as part of the insulin resistance syndrome.
    Circulation 102:42
    –47, 2000

  29. Kim J, Koh KK,
    Quon MJ: The union of vascular and metabolic actions of insulin in sickness
    and in health. Arterioscler Thromb Vasc Biol46
    : 1978–1985,2005

  30. Woods M, Mitchell
    JA, Wood EG, Barker S, Walcot NR, Rees GM, Warner TD: Endothelin-1 is induced
    by cytokines in human vascular smooth muscle cells: evidence for intracellular
    endothelin-converting enzyme. Mol Pharmacol55
    : 902–909,1999

  31. Chung KF, Barnes
    PJ: Cytokines in asthma. Thorax54
    : 825–857,1999

  32. Pickup JC, Mattock
    MB: Activation of the innate immune system as a predictor of cardiovascular
    mortality in type 2 diabetes mellitus. Diabet Med20
    : 723–726,2003

  33. Pickup JC, Mattock
    MB, Chusney GD, Burt D:. NIDDM as a disease of the innate immune system:
    association of acute-phase reactants and interleukin-6 with metabolic syndrome
    X. Diabetologia 40:1286
    –1292, 1997

  34. Jarrett RJ,
    Shipley MJ: Type 2 (non-insulin-dependent) diabetes mellitus and
    cardiovascular disease: putative association via common antecedents; further
    evidence from the Whitehall Study. Diabetalogia31
    : 737–740,1988

  35. Trayhurn P, Wood
    IS: Signalling role of adipose tissue: adipokines and inflammation in obesity.
    Biochem Soc Trans 33:1078
    –1081, 2005

  36. Arita Y, Kihara S,
    Ouchi N, Takahashi M, Maeda K, Miyagawa J, Hotta K, Shimomura I, Nakamura T,
    Miyaoka K, Kuriyama H, Nishida M, Yamashita S, Okubo K, Matsubara K, Muraguchi
    M, Ohmoto Y, Funahashi T, Matsuzawa Y: Paradoxical decrease of an
    adipose-specific protein, adiponectin, in obesity. Biochem Biophys
    Res Comm 257:79
    –83, 1999

  37. Testa CM.
    Mitochondria in movement disorders. In Movement
    Disorders, 2nd ed. Watts RL, Koller WC, Eds. McGraw Hill, New
    York. 2004, p. 61–86

  38. Nourooz-Zadeh J,
    Rahimi A, Tajaddini-Sarmadi J, Tritschler H, Rosen P, Halliwell B, Betteridge
    DJ: Relationships between plasma measures of oxidative stress and metabolic
    control in NIDDM. Diabetologia40
    : 647–653,1997

  39. Petersen KF,
    Dufour S, Befroy D, Garcia R, Shulman GI: Impaired mitochondrial activity in
    the insulin-resistant offspring of patients with type 2 diabetes. N
    Engl J Med 350:664
    –671, 2004

  40. Nishikawa T, Araki
    E: Impact of mitochondrial ROS production in the pathogenesis of diabetes
    mellitus and its complications. Antiox Redox Sig9
    : 343–353,2007

  41. Sohal RS, Sohal
    BH: Hydrogen peroxide release by mitochondria increases during aging.
    Mech Aging Dev 57:187
    –202, 1991

  42. Brownlee M: The
    pathobiology of diabetic complications: a unifying mechanism.
    Diabetes 54:1615
    –1625, 2005

  43. Hokama J, Ritter
    LS, Davis-Gorman G, Cimetta AD, Copeland JG, McDonagh PF: Diabetes enhances
    leukocyte accumulation in the coronary microcirculation early in reperfusion
    following ischemia [Abstract]. J Diabetes Comp14
    : 96–107,2000

  44. Freedman SF,
    Hatchell DL: Enhanced superoxide radical production by stimulated
    polymorphonuclear leukocytes in a cat model of diabetes [Abstract].
    Exp Eye Res 55:767
    –773, 1992

  45. Gu K, Cowie CC,
    Harris ML: Mortality in adults with and without diabetes in a national cohort
    of the US population, 1971–1993. Diabetes Care21
    : 1138–1145,1998

  46. Weyrich AS,
    Prescott SM, Zimmerman GA: Platelets, endothelial cells, inflammatory
    chemokines, and restenosis: signaling in the vascular play book.
    Circulation106:1433
    –1435, 2002

  47. Carr ME: Diabetes:
    a hypercoagulable state. J Diabetes Comp15
    : 44–54,2001

  48. Evangelista V,
    Totani L, Rotondo S, Lorenzet R, Tognoni G, De Berardis G, Nicolucci A:
    Prevention of cardiovascular disease in type 2 diabetes: how to improve the
    clinical efficacy of aspirin. Thromb Haemost93
    : 8–16,2005

  49. Hunt SA, Baker DW,
    Chin MH, Cinquegrani MP, Feldmanmd AM, Francis GS, Ganiats TG, Goldstein S,
    Gregoratos G, Jessup ML, Noble RJ, Packer M, Silver MA, Stevenson LW: ACC/AHA
    Guidelines for the evaluation and management of chronic heart failure in the
    adult: executive summary. Circulation104
    : 2996–3007,2001

  50. Gutierrez C,
    Blanchard DG: Diastolic heart failure: challenges of diagnosis and treatment.
    Am Fam Phys 69:2609
    –2616, 2004

  51. Marwick TH:
    Diabetic heart disease. Heart92
    : 296–300,2006

  52. Poirier P, Bogaty
    P, Garneau C, Marois L, Dumesnil JG: Diastolic dysfunction in normotensive men
    with well-controlled type 2 diabetes: importance of maneuvers in
    echocardiographic screening for preclinical diabetic cardiomyopathy.
    Diabetes Care 24:5
    –10, 2001

  53. Redfield MM,
    Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR, & Rodeheffer RJ: Burden of
    systolic and diastolic ventricular dysfunction in the community.
    JAMA 289:194
    –202, 2003

  54. Schannwell CM,
    Schneppenheim M, Perings S, Plehn G, Strauer BE: Left ventricular diastolic
    dysfunction as an early manifestation of diabetic cardiomyopathy.
    Cardiol 98:33
    –39, 2002

  55. Kawaguchi M,
    Techigawara M, Ishihata T, Asakura T, Saito F, Maehara K, Maruyama Y: A
    comparison of ultrastructural changes on endomyocardial biopsy specimens
    obtained from patients with diabetes mellitus with and without hypertension.
    Heart Ves 12:267
    –274, 1997

  56. Pop-Busui R,
    Kirkwood I, Schmid H, Marinescu V, Schroeder J, Larkin D, Yamada E, Raffel DM,
    Stevens MJ: Sympathetic dysfunction in type 1 diabetes: association with
    impaired myocardial blood flow reserve and diastolic dysfunction. J
    Am Coll Cardiol 44:2368
    –2374, 2004

  57. Galderisi M,
    Cicala S, Caso P, De Simone L, D’Errico A, Petrocelli A, de Divitiis O:
    Coronary flow reserve and myocardial diastolic dysfunction in arterial
    hypertension. Am J Cardiol 90:860
    –864, 2002

  58. Galderisi M:
    Diastolic dysfunction and diabetic cardiomyopathy: evaluation by Doppler.
    J Am Coll Cardiol 48:1548
    –1551, 2006

  59. Stratton IM, Adler
    AI, Neil HAW, Matthews DR, Manley SE, Cull CA, Hadden D, Turner RC, Holman RR:
    Association of glycaemia with macrovascular and microvascular complications of
    type 2 diabetes (UKPDS 35): prospective observational study.
    BMJ 321:405
    –412, 2000

  60. Devereux RB, Roman
    MJ, Paranicas M, O’Grady MJ, Lee ET, Welty TK, Fabsitz RR, Robbins D, Rhoades
    ER, Howard BV: Impact of diabetes on cardiac structure and function: the
    Strong Heart Study. Circulation101
    : 2271–2276,2000

  61. Bell DS: Diabetic
    cardiomyopathy: a unique entity or a complication of coronary artery disease?
    Diabetes Care 18:5708
    –5714, 2003

  62. Boudina S, Abel
    ED: Mitochondrial uncoupling: a key contributor to reduced cardiac efficiency
    in diabetes. Physiol 21:250
    –258, 2005

  63. Szabo C: PARP as a
    drug target for the therapy of diabetic cardiovascular dysfunction.
    Drug News Persp 15:197
    –205, 2002

  64. Palmiere V, Tracy
    RP, Roman MJ, Liu JE, Best LG, Bella JN, Robbins DC, Howard BV, Devereux RB:
    Relation of left ventricular hypertrophy to inflammation and albuminuria in
    adults with type 2 diabetes. Diabetes Care26
    : 2764–2769,2003

Proven Tips & Strategies To Bring High Blood Sugar Down (Quickly)

Untreated, high blood sugar can cause many problems and future complications.

Recognizing signs of high blood sugar levels and knowing how to lower them can help you prevent these complications and increase the quality and length of your life.

Topics covered (click to jump to specific section)

  1. How can you lower your blood sugar level quickly?
  2. What is a dangerous blood sugar level?
  3. When should I call for medical help?
  4. General tips on how to keep you blood sugar levels in control
  5. High blood sugar level symptoms and signs
  6. What causes the blood sugar levels go to high?
  7. What impacts on your health does high blood sugar have?
  8. How can I prevent high blood sugar from happening?
  9. Which foods increase blood sugar levels?
  10. Which foods keep your sugar levels in control?
  11. How do I lower my blood sugar level if I have gestational pregnancy?

High blood sugar level symptoms and signs

Symptoms of high blood sugar include:

  • Increased thirst
  • Tired all the time
  • Irritability
  • Increased hunger
  • Urinating a lot
  • Dry mouth
  • Blurred vision
  • Severe high blood sugar can lead to nausea and fruity smelling breath

The signs and symptoms for high blood sugar are the same for both type 1 and type 2. Signs usually show up quicker in those who have type 1 because of the nature of their diabetes. Type 1 is an autoimmune disease that causes the body to stop making insulin altogether. Type 2 is caused by lifestyle factors when the body eventually stops responding to insulin, which causes the sugar to increase slowly. People with type 2 can live longer without any symptoms creeping because their body is still making enough insulin to help control it a little bit.

What causes the blood sugar levels go to high?

Our bodies need sugar to make energy for the cells. Without it, we cannot do basic functions. When we eat foods with glucose, insulin pairs with it to allow it to enter into the cell wall. If the insulin is not there, then the glucose molecule can’t get through the wall and cannot be used. The extra glucose hangs out in the bloodstream which is literally high blood sugar.

The lack of insulin can be caused by two different things.

  • First, you can have decreased insulin resistance which means that your insulin doesn’t react the way that it is supposed to. It doesn’t partner with glucose to be used as fuel.
  • Secondly, you can have no insulin, which is the case with type 1 diabetes.

Regardless of how it is caused, it is imperative to control blood sugars to help prevent problems.

What impacts on your health does high blood sugar have?

Having extra sugar in your bloodstream can be very harmful to the vessels in your body, as well as some major organs. Complications of diabetes include and are not limited to:

  • Decreased kidney function which could eventually lead to dialysis
  • Problems with your eyes which could lead to loss of vision
  • Neuropathy (loss of feeling or pain in your legs)
  • Poor wound healing which could lead to an amputation
  • Increased risk of heart disease and stroke

These complications are not caused by a spike in the blood sugar. They are caused by an increased number of high blood sugar events over a period of time. Do not think that one or two high blood sugars are going to cause you to go blind. However, it is important to know what caused those high sugars so that you can prevent it from happening again. Hemoglobin A1C levels are checked to see what the average blood sugar has been over the past 120 days. Your doctor will check this to see if how your blood sugar levels have been trending.

I suggest the following articles:

How can I prevent high blood sugar from happening?

There are only a few things that can prevent hyperglycemia.

They are:

  • Medications
  • Exercise
  • A good diet
  • Decreased stress
  • Adequate sleep

The rest of this article explains these in further detail.

Always talk to your doctor before making any changes to your diet or exercise regimen.

Check your blood sugar levels!

It is important that you check your blood sugar levels on a regular basis. It is the one way that you are able to check and see if what you are doing is working, or if any changes are needed to be made in your lifestyle. Don’t think of checking your sugar as some type of pass or fail test. It’s just like any other numerical value that you get, such as your weight. You may not like what you see, but you can always do your best to improve it.

There are critical times that you should check your blood sugar.

They include:

  • Anytime you try something new, such as food, exercise class, or a medication. This will let you know if there is any type of problem that is caused by it.
  • Always check before and after you exercise. Your blood sugar drops while you exercise. If you start at a level that is too low, it can lead to hypoglycemia, which is dangerous.
  • Be sure you check your blood sugar before you go to bed. You may need a bedtime snack to keep your number at a healthy range.
  • Before and while you are drinking alcohol. Your sugar can either increase or decrease, so be sure to know which way it is going.

Keeping a log of your blood sugars is a great way to be knowledgeable about your body and how it is reacting to foods and events. To start, check before and after every meal, along with one in-between meal check. It is important that you keep a log of these blood sugars, along with all of the foods that you are eating, activities you are performing and any insulin or medications that you are taking. Do this for a week, and see if you can identify any patterns. Take this log to your doctor and talk to them about your findings.

There are times when our health is well out of our control. Checking your blood sugar is one way that you can stay in control. Take this control and use it to better your health and your life.

According to the NIDDK, when checking your blood sugar levels, consider the following tips:

  • Why is it important to check your blood sugar numbers
  • How to check for them
  • What your target levels are
  • What to do in the even that your blood sugar levels are too high or too low

How can you lower your blood sugar level quickly?

You need to be very careful if you are trying to lower your blood sugar level quickly. It can cause you to drop too fast or too low, which is dangerous. There are a few things that you can do to decrease it quickly.

Here are 4 ways to lower your blood sugar fast (includes natural solution as well):

  • Chugging water. Drinking a lot of water quickly will dilute your blood sugar and cause you to urinate a lot of it out. Do not drink a lot of water if you have any type of kidney problems or heart problems.
  • Increasing your heart rate for 15 minutes can maximize your insulin response and drop your blood sugar down. Be sure to check your blood sugar when you are finished.
  • Eat a snack that is high in protein. Protein stabilizes blood sugar. Make sure that the food doesn’t have a lot of sugar in it. Good choices are cheese or almonds.
  • Administer a quick-acting insulin if your doctor has prescribed it, such as Novolog. Insulin is a very rapid way to lower your sugar. Be sure to check your level about 30 minutes after you administer the insulin to see if it prevented the hypoglycemia.

With any of these quick remedies, it is imperative to have a snack handy in case your blood sugar drops too low. Always discuss any plans that you have with your physician.

How can you reduce your blood sugar levels naturally without medications?

Like I mentioned above, diet and exercise are the two ways that you can to lower blood sugar. Did you know that losing just 5 pounds can reduce your need for medications or insulin?

Foods that you should consume should include lots of lean meats, fruits, and vegetables. Read on for more details about how exercise and a healthy diet can lower your sugar.

How can exercise lower my blood sugar?

Exercise can help lower your blood sugar in two ways:

  • A quick “right now” drop. When you exercise, your insulin sensitivity increases and the glucose is able to pair up with the insulin easier and be used by the cells. You are also burning fuel off by exercising, so your sugar will drop.
  • A long term drop. Exercise is great for improving your overall health and helping you shed some extra pounds. Just dropping a few pounds can help you tremendously and can decrease or eliminate your need for diabetes medications or insulin.

It is very important that you are aware of your sugar levels during exercise. Since your sugar can drop, always be sure to have a snack available. Exercise not only improves your diabetes but it also has a great impact on other aspects of your life such as:

When you are choosing types of exercise, pick activities which are going to be enjoyable for you. When you perform activities that you enjoy, you have a better chance of sticking with them. You can occasionally change up the exercises that you do to prevent yourself from getting tired of following the same routine. Great examples of fun exercises are swimming, walking with a friend, or a dance class.

There is one exception to exercising with diabetes. If your blood sugar is too high (such as over 240) and you are spilling ketones into your urine, then exercise is only going to increase your blood sugar. You can buy a dipstick urine test to check for ketones, but the best thing to do would be to talk to your doctor about what is safe for you to do.

How can you lower your blood sugar levels through diet?

Diet is key when trying to lower blood sugar. Foods that you eat are the direct sources of glucose that cause your blood sugar to increase. Choosing the right foods can be the best way to keep your blood sugar levels consistent and within a healthy range. Please consider the following important tips:

  • Stay hydrated! Drinking lots of water helps in flushing out the excess fluids from your bloodstream. Make sure that you are drinking water and not drinks that are full of sugar.
  • Eat a lot of fiber. Fiber slows down digestion of carbohydrates and sugar. This can help lower your levels. Examples of high fiber foods include:
    • Nuts
    • Berries
    • Cucumbers
    • Beans
  • Indulge on leafy greens. They do not increase your blood sugar and they can actually decrease your risk of type 2 diabetes if you are have pre-diabetes.
  • Increasing your protein is beneficial. Lean proteins such as chicken and fish do not raise your blood sugar, but they do fill you up so that you are not hungry.
  • Drink apple cider vinegar. Having 2 tablespoons mixed in water can help lower your sugar.
  • Add Cinnamon to foods to add flavor. This can help lower your sugar as well as add a great taste.

What foods can lower blood sugar levels quickly?

There are no magic foods that will lower your blood sugar quickly. Drinking lots of water and eating protein can help you lower it, however it will not be as quick as administering insulin. Please check your blood sugar frequently if you are trying to lower it quickly. It can be dangerous and bad for your health.

Which foods increase blood sugar levels?

Carbohydrates ultimately break down into glucose. Many people believe that carbs are bad for people with diabetes. This is not true. Carbs are fuel for the body, so they have to be eaten. You just need to be smart about which ones you eat and how much you eat of them. Picking foods that are high in carbs but have no other nutrition is not smart. Examples of these foods are:

  • Pastas
  • Desserts or anything sugary
  • Sodas or juices
  • Breads or grains
  • Snacks such as crackers or chips
  • Fried or breaded items
  • Full fat yogurt or milk

Which foods keep your sugar levels in control?

Carbohydrates need to be consistent. You don’t want to eat all of your daily carb count in one meal. That will cause your blood sugar to spike, and then drop during the other meals. Giving your body a steady amount of carbohydrates will provide a stable amount of energy. It will also help your body make enough insulin to keep your blood sugar at a healthy number.

The easiest way to make sure that your carb intake is appropriate is to count carbohydrates. It is a simplified way to evaluate foods based on their nutritional value. The best place to start when counting is to aim for 45 to 60 grams of carbohydrates per meal and roughly 15 to 30 grams for each snack in between meals. You may have to adjust this based on your individual needs and your blood sugar readings. It is a lot easier to calculate the carbohydrates when you have a food with a label, but many foods do not. Check the serving size on the label to be sure that you are counting correctly. The US Department of Agriculture has a website that allows you to type in any food and it will give you the nutritional values. Check it out at https://ndb.nal.usda.gov/ndb/. A few examples of 15 grams of carbs include:

  • 1 slice of bread
  • 6 chicken nuggets
  • ½ cup of oatmeal
  • 1 small piece of fresh fruit

It is important that you pay attention to nutrients other than the carbs too. Be sure to have adequate protein and fiber, while keeping lots of fat to a minimum.

I could go on for days about how a good diet can keep your blood sugar in control. To receive the most efficient information, set up a meeting with a dietician to look at your specific needs and you recent sugar readings. They can provide you with recipes and tools which make it easier for you to know exactly what you are putting into your body. 40 states in the United States require insurance companies to cover a meeting with a dietician for those with diabetes. Check with your insurance to see if this benefit is available for you.

A great educational sheet about carbohydrates and counting them is listed here: http://professional.diabetes.org/pel/all-about-carbohydrate-counting-english. It’s a fantastic reference that you can learn a lot of information from.

How do I lower my blood sugar level if I have gestational pregnancy?

A little more than 9.2% of pregnant women have gestational diabetes. It is very common that all women are tested during their pregnancy. If you haven’t yet, bring it up to your physician’s attention. The cause is really unknown, but doctors believe that it is because the extra hormones that are released during pregnancy hinder the insulin sensitivity and increase the need for more insulin. It is very important to keep blood sugar levels under control because high blood sugars can lead to complications such as:

  • Premature labor
  • Caesarean section
  • Large baby with hypoglycemia
  • Pre-eclampsia which can lead to seizures
  • Increased risk of the mother to develop type 2 diabetes later in life

Lowering blood sugar with gestational diabetes is a lot like the other ways mentioned above.

They include:

  • Staying hydrated with water. Stay away from sugary drinks such as juice or sodas. Water can help in flushing out some of the extra sugar in the blood.
  • The key with diabetes is always consistency. A steady intake of the right amount of carbohydrates helps in keeping things under better control and prevents blood sugar spikes. Although many people believe that low-carb is best, that is not true during pregnancy. You need the carbohydrates for the growth of the fetus and to keep your energy level up. Talk to your doctor and nutritionist about what is best for you.
  • It is a great idea to meet with a dietician about what foods you should eat. There are certain vitamins such as Folic Acid and Iron that are very important for your growing baby. Eating those foods and trying to watch your carbohydrates can be difficult.
  • Do low impact exercises such as swimming or walking. Not only do they help to lower blood sugar levels, but they also help your body get into shape for labor and decrease your risk for developing type 2 diabetes later in life.
  • Be sure to get enough sleep. Many women are unable to sleep while they are pregnant. Try to take naps or go to bed early if you are able to. Not getting enough sleep can cause your sugar to increase.
  • Try to decrease your stress level as much as you can. If you have other children or a demanding job, this may not be possible. Stress releases hormones that raise your blood sugar. Yoga is a great way to destress. (Plus it is also a great exercise!)
  • Medications may be prescribed by your doctor if diet and exercise do not work. Metformin and insulin have both been tested and are safe to take during pregnancy.

Breastfeeding after the baby is born is a great way to lower your risk of developing type 2 diabetes later in life as well as providing many benefits for the baby. Read this article https://www.thediabetescouncil.com/can-you-breastfeed-if-you-have-diabetes/ that I wrote about all of the benefits of breastfeeding.

According to the National Institutes of Health, a mother’s high normal blood sugar levels can put their baby at risk for birth problems. If the mother’s blood sugar levels were high, it is more likely that the baby will have high insulin levels as well at birth. Therefore it is important that during your pregnancy, you are following under the directions of your physician any guidelines which will help you balance your blood sugar levels.

What is a dangerous blood sugar level?

A normal blood sugar level is between 70 and 130 after you have been fasting for a few hours. Blood sugar levels can be dangerous if they are too high or too low.

Low blood sugars can be caused by not eating enough, or by trying to lower your sugar too quickly. A blood sugar under 60 is considered dangerous. It can lead to confusion or loss of consciousness, which can be deadly. It is important to have a snack with you at all times in case this happens to you. If it does happen, think about what you did or didn’t do that lead to the low number. If it happens often, start writing things down to help you track what the cause is so that you can avoid it.

High blood sugars over 300 are pretty concerning.  A lot depends on what your sugar typically runs. If you are normally in the 200s, then a sugar of 320 wouldn’t affect you the way that it would for someone whose typically runs 150.

If your blood sugar gets too high, then you may have Ketoacidosis. What happens is that the body does not have enough insulin to use the glucose cells, so it starts to break down fat and muscle for fuel. This causes ketones to enter the bloodstream and causes a pretty bad chemical imbalance. Ketones can also be found in your urine, which is an easy way to test. Signs of Diabetic Ketoacidosis are:

  • Fruity smelling breath
  • Rapid breathing
  • Thirsty and urinating a lot
  • Confusion or blurred vision
  • Vomiting or stomach pain
  • Dry, flushed, and hot skin

You need to seek medical attention right away if you experience any of these symptoms.

Another complication of hyperglycemia is Hyperosmolar Hyperglycemia Non-ketonic Syndrome. This is just a fancy term meaning that the body tries to flush out any excess sugar and dehydrates itself in the process. This is more common for those with type 2 diabetes when they have an illness and their sugar increases. Signs and symptoms include:

  • Fever
  • Tiredness
  • Dehydration
  • Loss of vision
  • An abnormal increase in blood sugar

You should also seek medical attention for this as well to rehydrate your body before any complications happen.

At the University of Leicester, scientists have showing that the level of sugar in your blood can affect blood vessels which in turn can have potentially dangerous effects on your heart and blood pressure. Glucose has an important role to play in the normal functions of the cardiovascular system.  Untreated high sugar levels can lead to life threatening illnesses.

Why are my blood sugar levels really high in the morning?

There are two reasons that you can wake up with a high blood sugar.

The Dawn Phenomenon happens because your body is trying to make sugar to prepare your body for the next day. A hormone that decreases insulin sensitivity is also released, which only helps the blood sugar increase.

The Somogyi Effect occurs when your sugar drops too low during the night and your body kicks into overdrive to increase it.

It is important to check your blood sugar before you go to bed and when you wake up to see what your next action should be.

When should I call for medical help?

It is great to have regular medical care for your diabetes. There are some instances that you should call your doctor right away.

They include:

  • If you experience an abnormally high blood sugar for more than 24 hours (such as greater than 250)
  • If you have fruity smelling breath or test positive for ketones in your urine
  • If you become severely dehydrated
  • If you are unable to eat or take your medications without vomiting

If someone ever loses consciousness, call 911 right away. This could be caused by blood sugar levels that are too high or too low.

General tips on how to keep you blood sugar levels in control

You should eat foods that are high in protein, fiber, and lower in carbohydrates. You should aim at having around 45 to 60 carbs for each meal. Consistency throughout the day is key to keeping blood sugar levels in control. Foods low in fat and high in nutrients should be picked to maximize your nutrition.

Vegetables and fruits are great as well as eggs, fish, beans, and oatmeal. There is also research that shows cinnamon and apple cider vinegar can help lower your sugar.

Avoiding foods like soda, juice, pasta, candy, and other desserts can help keep your sugar from climbing too high. These foods are high in sugars and fat but low in other nutrients.

Avoiding excess alcohol is also better for you. Read the following article that I wrote about drinking alcohol when you have diabetes to learn more about this topic: https://www.thediabetescouncil.com/effects-of-alcohol-on-diabetes/

Signs of high blood sugar include: increased thirst and hunger, blurred vision, irritability, dry mouth, tired, and urinating a lot.

Patterns can be great because they help you figure out what is causing undesirable blood sugar values. A good way to track of it is to keep a journal of all of the food you eat, activities you do and your blood sugar levels for 1 week. During this week, check your sugar before and after you eat, as well as in between meals. Also document any insulin that you give yourself.

  • Test sugar levels regularly

Knowing your blood sugar level is the number one way to take control of your diabetes. You should check your blood sugar every morning and night, as well as before you eat. You can also check it 2 hours after you eat to make sure that you didn’t have a spike.

  • Make small incremental changes to your lifestyle

Making small changes in your life are better than trying to make big ones. If you try to make changes that are impossible, you won’t stick with them and you will end up right back where you started. Find things that you can change that will fit into your lifestyle. Some good examples are:

  • Walking three nights a week after dinner
  • Eating one apple a day instead of an unhealthy snack
  • Replacing juice with water flavored lemon or cucumber

Don’t think that making small changes won’t make a big difference in your life. It definitely will.

  • Manage your stress and get enough sleep

Stress does many bad things to your body. Not only does it raise your blood sugar, but it also increases your blood pressure and heart rate. Try to avoid stress if possible or find coping mechanisms such as exercise, meditation, or talking with a friend.

Getting enough sleep is almost as important for managing your blood sugar level. One study showed that not sleeping enough can decrease your insulin sensitivity up to 25%. Talk to your doctor if you are having problems sleeping. You may have sleep apnea or another problem that they can help with.

  • Consider speaking to your doctor if all fails

You should always be in touch with your doctor about your disease and any changes you make or problems that you notice. Having that line of open communication is key to gaining knowledge and insight into what can make your life and your health better. Try the things mentioned in this article, but if they don’t help, then talk to your physician about what else is available for you. If you have any comments post them down below.

TheDiabetesCouncil Article | Reviewed by Dr. Christine Traxler MD on May 20, 2020

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Sugar levels of diabetics rose by 20% during COVID-19 lockdown: Report

Worldwide, numerous studies show how stress increases the chances of developing various ailments, particularly chronic ones. Similarly, stressed persons suffering from diabetes run a greater risk of poor blood glucose levels. A major reason for the higher sugar levels is because of stress hormones such as cortisol. As the COVID-19 outbreak began spreading across the nation in March this year, blood glucose levels of diabetics began rising simultaneously, suggested a new report.

Pan-India, it was clear that anxiety about COVID-19 and the stress arising from lockdown restrictions as well as the lack of prompt medical attention had caused an overall increase of 20 per cent in blood sugar levels. The results were derived from 8,200 diabetic patients across India, as per the analysis conducted by Beato – a full-stack digital ecosystem for diabetes care and management.

While the average pre-pandemic fasting sugar levels in January till mid-February was 138 mg/dl, in March 2020, the blood glucose level of diabetics began rising. Average fasting sugar levels in March till mid-April was 165 mg/dl. As per Beato, key factors for the rise were stress, anxiety, overall disruption of lives, restrictive regimens and confinement at home.

Among those showing a greater spike in blood sugar levels were regions in the North, West and North-east India with major states like Rajasthan, Ladakh, Andhra Pradesh and Uttarakhand being affected. The analysis linked the rise to how these states were typically rice and carbohydrate-consuming states. Overall, the highest rise in blood glucose levels was seen in Daman and Diu (49 per cent), Tripura (38 per cent), Nagaland (30 per cent), Manipur (28 per cent), Uttarakhand (25 per cent), Jannu and Kashmir (23 per cent), Ladakh (23 per cent), Jharkhand (22 per cent), Rajasthan (21 per cent), Andhra Pradesh (20 per cent) and Bihar (20 per cent).

The report underlined that since stress and anxiety were “active triggers in raising blood sugar levels”, daily diabetes management is imperative in tracking and managing the chronic disorder. This is particularly important due to the threat of grave consequences if the ailment is not managed proactively.

Management of Gestational Diabetes Mellitus

1. Xiong X,
Saunders LD,
Wang FL,
Demianczuk NN.
Gestational diabetes mellitus: prevalence, risk factors, maternal and infant outcomes. Int J Gynaecol Obstet.
2001;75:221–8….

2. Periodic health examination, 1992 update: 1. Screening for gestational diabetes mellitus. CMAJ.
1992;147:435–43.

3. Screening for gestational diabetes mellitus: recommendation and rationale. Am Fam Physician.
2003;68:331–5.

4. Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care.
2003;26suppl 1:S5–20.

5. Sermer M,
Naylor CD,
Gare DJ,
Kenshole AB,
Ritchie JW,
Farine D,

et al.
Impact of increasing carbohydrate intolerance on maternal-fetal outcomes in 3637 women without gestational diabetes. The Toronto Tri-Hospital Gestational Diabetes Project. Am J Obstet Gynecol.
1995;173:146–56.

6. Casey BM,
Lucas MJ,
Mcintire DD,
Leveno KJ.
Pregnancy outcomes in women with gestational diabetes compared with the general obstetric population. Obstet Gynecol.
1997;90:869–73.

7. Dang K,
Homko C,
Reece EA.
Factors associated with fetal macrosomia in offspring of gestational diabetic women. J Matern Fetal Med.
2000;9:114–7.

8. Langer O,
Levy J,
Brustman L,
Anyaegbunam A,
Merkatz R,
Divon M.
Glycemic control in gestational diabetes mellitus—how tight is tight enough: small for gestational age versus large for gestational age?. Am J Obstet Gynecol.
1989;161:646–53.

9. O–Sullivan JB,
Charles D,
Mahan CM,
Dandrow RV.
Gestational diabetes and perinatal mortality rate. Am J Obstet Gynecol.
1973;116:901–4.

10. Beischer NA,
Wein P,
Sheedy MT,
Steffen B.
Identification and treatment of women with hyperglycaemia diagnosed during pregnancy can significantly reduce perinatal mortality rates. Aust N Z J Obstet Gynaecol.
1996;36:239–47.

11. Wood SL,
Sauve R,
Ross S,
Brant R,
Love EJ.
Prediabetes and perinatal mortality. Diabetes Care.
2000;23:1752–4.

12. Gabbe SG,
Mestman JG,
Freeman RK,
Anderson GV,
Lowensohn RI.
Management and outcome of class A diabetes mellitus. Am J Obstet Gynecol.
1977;127:465–9.

13. Cundy T,
Gamble G,
Townend K,
Henley PG,
MacPherson P,
Roberts AB.
Perinatal mortality in Type 2 diabetes mellitus. Diabet Med.
2000;17:33–9.

14. Gestational diabetes mellitus. .
Diabetes Care.
2003;26suppl 1:S103–5.

15. ACOG Practice Bulletin.
Gestational diabetes. Number 30, September 2001 (replaces Technical Bulletin Number 200, December 1994). Obstet Gynecol.
2001;98:525–38.

16. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes.
1979;28:1039–57.

17. Carpenter MW,
Coustan DR.
Criteria for screening tests for gestational diabetes. Am J Obstet Gynecol.
1982;144:768–73.

18. Schwartz ML,
Ray WN,
Lubarsky SL.
The diagnosis and classification of gestational diabetes mellitus: is it time to change our tune?. Am J Obstet Gynecol.
1999;1806 pt 1:1560–71.

19. De Veciana M,
Major CA,
Morgan MA,
Asrat T,
Toohey JS,
Lien JM,

et al.
Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy. N Engl J Med.
1995;333:1237–41.

20. Walkinshaw SA.
Dietary regulation for “gestational diabetes.“. Cochrane Database Syst Rev.
2003;(2):CD000070.

21. Rizzo T,
Metzger BE,
Burns WJ,
Burns K.
Correlations between antepartum maternal metabolism and child intelligence. N Engl J Med.
1991;325:911–6.

22. Rizzo TA,
Dooley SL,
Metzger BE,
Cho NH,
Ogata ES,
Silverman BL.
Prenatal and perinatal influences on long-term psychomotor development in offspring of diabetic mothers. Am J Obstet Gynecol.
1995;173:1753–8.

23. Avery MD,
Leon AS,
Kopher RA.
Effects of a partially home-based exercise program for women with gestational diabetes. Obstet Gynecol.
1997;89:10–5.

24. O’Sullivan JB,
Gellis SS,
Dandrow RV,
Tenney BO.
The potential diabetic and her treatment in pregnancy. Obstet Gynecol.
1966;27:683–9.

25. Coustan DR,
Lewis SB.
Insulin therapy for gestational diabetes. Obstet Gynecol.
1978;51:306–10.

26. Thompson DJ,
Porter KB,
Gunnells DJ,
Wagner PC,
Spinnato JA.
Prophylactic insulin in the management of gestational diabetes. Obstet Gynecol.
1990;75:960–4.

27. Persson B,
Stangenberg M,
Hansson U,
Nordlander E.
Gestational diabetes mellitus (GDM). Comparative evaluation of two treatment regimens, diet versus insulin and diet. Diabetes.
1985;34suppl 2:101–5.

28. Garner P,
Okun N,
Keely E,
Wells G,
Perkins S,
Sylvain J,

et al.
A randomized controlled trial of strict glycemic control and tertiary level obstetric care versus routine obstetric care in the management of gestational diabetes: a pilot study. Am J Obstet Gynecol.
1997;177:190–5.

29. Langer O,
Berkus M,
Brustman L,
Anyaegbunam A,
Mazze R.
Rationale for insulin management in gestational diabetes mellitus. Diabetes.
1991;40suppl 2:186–90.

30. Coustan DR,
Imarah J.
Prophylactic insulin treatment of gestational diabetes reduces the incidence of macrosomia, operative delivery, and birth trauma. Am J Obstet Gynecol.
1984;150:836–42.

31. Jovanovic L,
Ilic S,
Pettitt DJ,
Hugo K,
Gutierrez M,
Bowsher RR,

et al.
Metabolic and immunologic effects of insulin lispro in gestational diabetes. Diabetes Care.
1999;22:1422–7.

32. Ziegler MH,
Grafton TF,
Hansen DK.
The effect of tolbutamide on rat embryonic development in vitro. Teratology.
1993;48:45–51.

33. Elliott BD,
Schenker S,
Langer O,
Johnson R,
Prihoda T.
Comparative placental transport of oral hypoglycemic agents in humans: a model of human placental drug transfer. Am J Obstet Gynecol.
1994;171:653–60.

34. Langer O,
Conway DL,
Berkus MD,
Xenakis EM,
Gonzales O.
A comparison of glyburide and insulin in women with gestational diabetes mellitus. N Engl J Med.
2000;343:1134–8.

35. Glueck CJ,
Wang P,
Goldenberg N,
Sieve-Smith L.
Pregnancy outcomes among women with polycystic ovarian syndrome treated with metformin. Hum Reprod.
2002;17:2858–64.

36. Acker DB,
Sachs BP,
Friedman EA.
Risk factors for shoulder dystocia. Obstet Gynecol.
1985;66:762–8.

37. Nahum GG,
Stanislaw H.
Ultrasonographic prediction of term birth weight: how accurate is it?. Am J Obstet Gynecol.
2003;188:566–74.

38. Rouse DJ,
Owen J,
Goldenberg RL,
Cliver SP.
The effectiveness and costs of elective cesarean delivery for fetal macrosomia diagnosed by ultrasound. JAMA.
1996;276:1480–6.

39. Caplan RH,
Pagliara AS,
Beguin EA,
Smiley CA,
Bina-Frymark M,
Goettl KA,

et al.
Constant intravenous insulin infusion during labor and delivery in diabetes mellitus. Diabetes Care.
1982;5:6–10.

40. Kim C,
Newton KM,
Knopp RH.
Gestational diabetes and the incidence of type 2 diabetes: a systematic review. Diabetes Care.
2002;25:1862–8.

41. Kjos SL,
Henry O,
Lee RM,
Buchanan TA,
Mishell DR Jr.
The effect of lactation on glucose and lipid metabolism in women with recent gestational diabetes. Obstet Gynecol.
1993;82:451–5.

Triglycerides and Lowering Triglyceride Levels

Good and bad cholesterol. Saturated and unsaturated fat. Sometimes it seems like you need a program to keep track of all the fat players in the story of heart disease.

Triglycerides may be the easiest to understand.

Simply put, they are fat in the blood. They are used to give energy to your body. If you have extras, they are stored in different places in case they are needed later.

A high level of triglycerides has been linked to a greater chance for heart disease. But just what your own level means and how much it helps to lower it is sometimes less clear.

You and your doctor have ways to lower your level if it is running high.

What Are Triglycerides?

They are important to life and are the main form of fat — they are sometimes called “lipids” — in the body. When you think of fat developing and being stored in your hips or belly, you’re thinking of triglycerides.

They are the end product of digesting and breaking down fats in food. Some are made in the body from other energy sources, such as carbohydrates. When you’re between meals and need more energy, your body’s hormones release them so you tap those unused calories.

How Are Triglycerides Measured?

Your doctor may give you a common test called a lipid panel. It checks for different types of cholesterol, including the levels of the “good” kind and the “bad” kind. The American Heart Association recommends that everyone 21 and older get a lipid panel at least every 5 years.

The levels are checked after an overnight fast. Fat from a recent meal can muddy the picture.

These tests are important because you rarely have any symptoms when your triglycerides are high, unlike with many other conditions.

What Are Normal and High Triglyceride Levels?

The National Cholesterol Education Program sets guidelines for triglyceride levels:

  • Normal levels: Less than 150 milligrams per deciliter
  • Borderline high:150 to 199
  • High: 200 to 499
  • Very high: 500 or more

Elevated levels may lead to heart disease, especially in people with low levels of “good” cholesterol and high levels of “bad” cholesterol. The same is true if you have type 2 diabetes.

Experts once debated how important triglycerides are, but it now seems clear that higher levels are linked to problems such as heart disease.

One thing is clear, though: A good diet and exercise plan can lower triglyceride levels, improve cholesterol, and decrease the chance of heart disease.

What Can You Do at Home to Treat High Triglycerides?

The main way to deal with high triglycerides is to eat better and get more exercise. Here are some guidelines to help you manage your level:

Moderate exercise: Try to exercise 5 or more days each week. Lack of movement makes it hard for your body to process blood sugar and triglycerides as it normally does. So it’s important for you to get up and get moving more each day. Skip the escalator or elevator and climb stairs. Get off the bus or subway one stop early and walk. Find activities you enjoy: Walk, swim, or ride a bike. Join a gym. Talk to your doctor before you begin any exercise plan.

Watch your weight: If you’re carrying extra pounds, losing 5% to 10% of your weight can lower triglycerides. People with a healthy weight are more likely to have normal levels. Belly fat is associated with higher numbers.

Eat less bad fat and carbs: Try to lower the saturated fat, trans fat, and cholesterol in your diet. Cutting back on carbohydrates will help, too. Foods high in saturated fat, such as red meat, boost levels. Butter and cheese contain these same triglyceride-boosting fats. Choose lean meats or protein alternatives, such as chicken and unprocessed turkey, that are lower in saturated fat.

Another healthy option: Make meatless meals. Vegetarian pastas, chilis, and stir-fries are a delicious alternative to meat dishes. Avoid dishes loaded with cream or cheese in favor of recipes that use vegetable or olive oil and feature plenty of vegetables.

Carbs that are “white foods” — like pasta or bread made with white flour or semolina — can raise triglyceride levels. So can starchy foods like white rice and potatoes.

Whole-grain pasta is a great alternative, especially for bold sauces. Look for a tasty whole-grain bread for sandwiches. And eat brown rice instead of white rice. It has a rich flavor that’s perfect for making stir-fry. Instead of white potatoes, try grains like quinoa and barley.

Drink less alcohol: Beer, wine, and liquor can raise levels. Some studies show that more than 1 drink a day for women or 2 for men can increase levels by a lot. If you’ve cut back and your triglyceride levels aren’t going down enough, your doctor may recommend skipping alcohol altogether.

Eat fish: Mackerel, lake trout, herring, sardines, albacore tuna, and salmon are high in omega-3s, a fat that’s good for you. It may be hard to get enough omega-3s from food. Your doctor may recommend a supplement or prescription.

Make sure your fish is prepared in a healthful way. Frying fish uses a lot of added oil — the unhealthy type, with saturated fat. That fat overpowers the healthier fat found in fish, omega-3 fatty acids, which helps keep triglycerides down. 

Instead, choose fatty fish such as salmon, freshwater trout, or tuna, which are especially rich in omega-3s, then grill or broil them. Look for recipes with flavors you like. If you’re still having trouble tempting your taste buds (not everybody likes fish, after all), take heart. Walnuts, flaxseed, soy products, and dark greens are good sources of triglyceride-lowering omega-3s.

Drink more water: Sugar and fructose — which are used as sweeteners in soda, sweet tea, or fruit juices — can raise triglycerides. The extra calories in sugary drinks can also make you gain weight, which puts added strain on your heart and contributes to cholesterol and triglyceride levels.

Water is the most convenient and inexpensive thirst quencher around. To add some zing, squeeze lemon or lime in sparkling water. Leave the sugar out of your tea and try one flavored with herbs, spices, or flowers.

Don’t overeat: Very large meals can send your triglyceride level into the danger zone. Spikes are dangerous because they can increase your risk of a heart attack.

Divide your usual serving in half. At home, cook the usual amount but serve only half. At restaurants, divide your meal into smaller portions. Eat slowly to give your body time to figure out that you’re full. Get another helping only if you’re still hungry. If you feel satisfied, pack away what’s left to enjoy later.

Don’t skip meals: Maybe you’re too busy to eat. Maybe you think you’ll lose weight if you skip a meal. The problem: you’re likely to get so hungry later that you’ll grab anything, healthy or not. Or you overeat at the next meal, which causes triglyceride levels to jump.

It’s better to eat sensible-sized meals a few times a day. Enjoy breakfast, lunch, and dinner and stick to recommended serving sizes. Have healthy snacks like nuts, fruit, or carrot and celery sticks around when hunger strikes.

Quit smoking:  When you have high triglycerides, heart disease is a major concern. If you smoke, your risk of heart disease dramatically increases.

Make up your mind to quit. If you need help, talk to your doctor. When you’re ready, take action. Choose a date to give up your habit. Get support from friends and family. Buy sugar-free gum and low-calorie snacks to reach for instead of cigarettes. Talk to your doctor about medications that may help you quit. Find a local support group. Stay committed — you’ll kick cigarettes to the curb and add years to your life.

Which Medicines Can Lower Triglycerides?

For some people, good habits may not be enough. Medication might be needed. The decision for you and your doctor can be complicated because other health conditions are usually involved. Several types of medicine can improve levels. They include:

  • Fibrates (Fibricor, Lopid, and Tricor)
  • Nicotinic acid (Niaspan)
  • High doses of omega-3s are needed to lower triglycerides and should be taken only under a doctor’s care. Epanova, Lovaza, and Vascepa are prescription forms of omega-3s.

Your doctor may also prescribe a class of drugs called “statins” that lower cholesterol. Examples include: atorvastatin (Lipitor), rosuvastatin (Crestor), and simvastatin (Zocor).

You may feel side effects from these drugs. Be sure to talk it over with your doctor or pharmacist.

90,000 The norm of blood sugar in men by age – table, deviations and therapy

Today we will study blood sugar, the norm in men by age is presented, the table is slightly

below

… This is due to the fact that the prognosis of diabetes mellitus, when it is detected at an early stage and a competent approach to therapy, is considered conditionally favorable. Because its late detection can lead to serious life-threatening conditions. Among them: diabetic ketoacidosis, coma and severe pathologies of the organs of vision, kidneys, nervous system or musculoskeletal system.

Contents

Regulation of glucose in the human body

Sugar, like all other carbohydrates, for full assimilation by the human body must be decomposed to simple monosaccharides (

glucose

, fructose). For this, special enzymes are synthesized, united by the general term sucrase or glucosyl hydrolases.

The process of glucose utilization by tissues is under the control of the glands of the endocrine system.The content of simple sugars in cells and tissues is influenced by hormones: insulin, thyrotropin, cortisol, adrenaline, triiodothyronine and thyroxine.

The norm of blood sugar in men and women is largely supported by the hormone insulin secreted by the cells of the pancreas. The mechanism of its activity is based on increasing the rate of glucose utilization by cells. The triggering of insulin receptors activates reactions within the cell that control the functioning of membrane proteins that transport glucose into cells.

Glucose is necessary for living organisms to carry out vital processes, since it serves as a source of energy for many metabolic reactions. The tissues of the brain, as well as the nervous and cardiovascular systems, are most sensitive to changes in the level of glucose in the blood.

Table of blood sugar norms in men by age

Reference (normal) blood sugar values ​​depend on the laboratory method used and the place of collection of the biomaterial (from the finger or vein), as well as the age of the patient.The table shows the rate of sugar in the analysis of blood in men from a finger and vein on an empty stomach, taking into account age.

Age of male Norm from a vein, mmol / l Norm from finger, mmol / l
Up to 14 years old 2.5 – 4.5 2.3 – 3.9
From 14 to 20 years 3 – 5.5 2.5 – 4
From 20 to 50 years 3.5 – 6.5 3 – 5.5
After 50 years 4 – 6.9 3.5 – 6.5

The norm of blood sugar in men after 40 years should not exceed 6.5 mmol / l, while small deviations directly correlate with dietary habits and alcohol or tobacco abuse.

Particular attention should be paid to the indicator after 50 years. So, the permissible norm of blood sugar in men after 50 years should be regularly maintained, and with a stable deviation, you should consult a specialist (even in the absence of clinical signs of the disease).

The norm of blood glucose in women is similar to the data presented for male patients.

When should you get tested?

Determination of blood sugar in men and women can be prescribed by a general practitioner, gynecologist, endocrinologist or gastroenterologist if a deviation from the norm is suspected.

The norm of blood sugar in men and women is measured at:

  • standard prophylactic examination of patients;
  • 90,085 the patient has symptoms of diabetes mellitus;

    90,085 suspicion of hyper- (excess) and hypoglycemia (deficiency). Biomaterial for research can be collected before or after meals, in critical conditions – spontaneously at any time;

  • differential diagnosis of diabetes mellitus in combination with glucose tolerance test.To make the final diagnosis, the study is repeated twice at different times of the day;
  • 90,085 daily monitoring for people with proven diabetes mellitus. This is necessary to adjust the dosage of drugs and insulin injections;

  • the need to exclude gestational diabetes – a temporary increase in blood sugar levels in pregnant women. In the absence of timely treatment, gestational diabetes can lead to the fading of pregnancy, damage to the nervous tissues and internal organs of the fetus, miscarriage, severe gestosis in a pregnant woman, hypoglycemia in a newborn, etc.d.

Symptoms of an increase in the level of simple sugars in the blood: frequent urge to urinate, intense thirst, decreased visual acuity, fatigue, drowsiness, low performance, frequent relapses of infectious diseases, dry and itchy skin, dry mucous membranes, etc.

Signs of sugar reduction include:

  1. excessive sweating,
  2. excessive appetite,
  3. obscurity of consciousness,
  4. mental disorders,
  5. increased nervousness,
  6. feeling anxious and blurred vision,
  7. disorientation in space,
  8. fainting, etc.d.

Laboratory diagnostic methods

Glucometer – a device for measuring sugar levels. Its advantage is that a person can use it independently. A small amount of capillary blood is placed on a special disposable test strip in the meter. Then the indicator is measured. It is important to remember that the accuracy of a device depends on its quality and service life. It is recommended that you periodically check the accuracy of the readings from your home-use meter.

The hexokinase technique is used in routine laboratory practice. Its essence lies in the implementation of two consecutive reactions:

  • cleavage of glucose molecules to equimolar concentrations of glucose-6-phosphate;
  • Enzymatic conversion of the resulting molecules into 6-phosphogluconate.

Reactions release NADH, the rate of formation of which is a measurable feature at 340 nm. It is this indicator that makes it possible to determine the level of the criterion in question in the studied biomaterial.

According to modern diagnostic rules and standards, it is the hexokinase test that is recognized as a universal and reliable method.

What can cause an increase in blood sugar in a man?

The most common cause is diabetes mellitus. It occurs as a result of abnormal changes in the tissues of the pancreas and, as a result, insufficient insulin secretion or the formation of tolerance of the cells of the human body to the effects of the hormone.

Diseases of the pancreas, such as pancreatitis or cancer, also lead to hyperglycemia. In this, damage to the cells of the pancreas that secrete insulin is observed.

It is possible that you receive a false positive result while taking medications. So, some groups of psychotropic and hormonal drugs, as well as diuretics, activate the process of glucose deposition in human tissues and organs.

An overestimation of the sugar norm in a blood test from a vein or finger in the results of laboratory diagnostics is detected if the rules for preparing a man for the collection of biomaterial are not followed.A pronounced emotional reaction to various traumatic situations, the presence of concomitant pathologies (a recent stroke or heart attack), physical fatigue lead to a short-term increase in glucose levels.

Also, the glucose level can increase with cystic fibrosis, adrenal tumors, mumps with pancreatic lesions, thyrotoxicosis, acromegaly, etc.

In case of obtaining results that significantly exceed the reference values, a second analysis is carried out.Two-fold obtaining of consistently high data is a reason for conducting an extended examination for diabetes mellitus: determining the content of insulin, glycated hemoglobin and binding peptide in the blood.

Causes of hypoglycemia when the glucose concentration drops sharply:

  • development of a benign neoplasm of the pancreas, uncontrollably secreting insulin in excess amounts;
  • significant overdose of insulin injections;
  • 90,085 exhaustion and prolonged starvation;

    90,085 Addison’s disease;

  • liver cirrhosis;
  • 90,085 fibrosarcomas;

  • taking anabolic steroid drugs and acetaminophen.

Recommendations for keeping the parameter normal

Minor discrepancies with standard values ​​are restored by correcting the male diet. It is recommended to cut back on meals high in carbohydrates. Lean fish or meat and vegetable proteins should be preferred. Completely excluded from the diet:

90,084

  • alcohol;
  • sauces;
  • 90,085 pasta and bakery products;

    90,085 sweets;

    90,085 carbonated drinks.

    Patients with an established fact of diabetes mellitus are selected a special diet, taking into account the type and severity of the disease. It is recommended to replace sugar with special sweeteners: sucrasite or saccharin, however, the permitted dosage is determined exclusively by the attending physician.

    It is important not only what a person eats, but also a diet and adequate physical activity. It is not enough just to adjust the diet, you should pay special attention to sports, during which there is an excess consumption of glucose.

    Revealing secondary diabetes mellitus in a man against the background of pathological changes in organs requires the selection of therapy, taking into account all concomitant diseases. If it is necessary to remove the pancreas, the patient is assigned a lifelong intake of drugs containing insulin.

    Important findings

    To summarize, there are important points to be emphasized:

    • the value of the criterion in question in the blood of a man depends on the age, the drugs taken and the presence of combined pathologies;
    • control over the value of the laboratory parameter will reveal early signs of hyperglycemia or diabetes mellitus, which significantly reduces the risks of adverse consequences and complications;
    • blood test for one parameter is not enough for a final diagnosis.Additional laboratory tests are carried out to identify the level of hormones and proteins;
    • the return of the parameter to the normal range is possible by making adjustments to the nutrition and physical activity of the patient, however, when diabetes is detected, the need to use insulin injections is not excluded;
    • Repeated tests carried out at different times in the same laboratory acquire undeniable value for accurate diagnosis.

    Material provided

    medseen.ru

    Take a blood sugar test, the price of a blood glucose test in Pervouralsk in the Invitro laboratory

    Method of determination
    Hexokinase.

    Study material
    See description

    Serum or blood plasma. If it is not possible to centrifuge the sample 30 minutes after collection to separate the serum / plasma from the cells, the sample is taken into a special tube containing a glycolysis inhibitor (sodium fluoride).

    Synonyms: Blood glucose test; Plasma or serum glucose; Blood sugar; Blood glucose; Fasting blood glucose test; Blood sugar analysis. Glucose, Plasma or Serum; Fasting blood glucose; FBG; Fasting plasma glucose; Blood glucose; Blood sugar; Fasting blood sugar; FBS.

    Brief characteristics of the analyte Glucose

    Sources of glucose for the body are carbohydrates (fast and slow), supplied with food in the form of sucrose, fructose, maltose, lactose, starch, etc.In the body, glucose accumulates in the form of glycogen in the liver and, if necessary, can be synthesized from non-carbohydrate substrates (amino acids, glycerol, lactate).

    Maintaining blood glucose at a certain level is an example of one of the most perfect mechanisms for regulating homeostasis, in the functioning of which the liver, extrahepatic tissues and some hormones are involved. Insulin transports glucose into cells and is the only hormone that lowers blood glucose levels.Other hormones such as glucagon, cortisol, adrenaline, thyroid hormones, growth hormone cause an increase in its level in the blood, exhibiting a counterinsular effect. As a result of the action of regulatory mechanisms, the blood glucose level normally fluctuates within a narrow range of values.

    The main laboratory test for assessing carbohydrate metabolism is the determination of fasting blood glucose. Its increased content is called hyperglycemia and can be a symptom of diabetes mellitus.

    Diagnostic criteria for diabetes mellitus

    Laboratory criteria in the diagnosis of diabetes mellitus based on blood glucose levels are currently considered:

    1. fasting glucose level 7.0 mmol / l and above;
    2. combination of clinical symptoms of diabetes and an accidental (independent of the time of the previous meal) increase in blood plasma glucose to 11.1 mmol / L and higher;
    3. glucose level two hours after taking glucose (75 g) when performing an oral glucose tolerance test of 11.1 mmol / l and higher.

    Since changes in blood glucose concentration can be detected much earlier than clinical manifestations of diabetes mellitus, it is recommended that all people over 45 years of age (even without symptoms of diabetes mellitus) have an annual fasting blood glucose control test. At an earlier age, screening is done in people at increased risk of diabetes (including children over ten years of age). Also, the determination of fasting blood glucose is included in the mandatory examination of pregnant women.Hormonal changes during pregnancy cause a physiological increase in insulin resistance in a woman’s body. The relative lack of insulin during this period in some women can lead to an increase in blood glucose and the development of diabetes during pregnancy (gestational diabetes).

    What is the purpose of determining the level of glucose in serum or plasma

    Determination of the level of glucose in plasma or serum is used for the diagnosis and control of diabetes mellitus and other diseases associated with impaired carbohydrate metabolism.

    What can affect the test result Glucose

    In vitro, glucose can be determined in whole blood, serum or plasma (the latter is preferred). When interpreting the results of glucose studies, it is useful to take into account the following data: glucose freely penetrates into erythrocytes, but its concentration in blood plasma is about 11-14% higher than in whole blood due to different water content in plasma and blood cells. Thus, the glucose content in the plasma of venous blood taken on an empty stomach may be higher than in the whole blood sample taken from a fingertip at the same time.Heparinized plasma glucose is 5% lower than serum glucose. Whole venous blood contains less glucose than finger capillary blood due to the utilization of glucose in tissues. This difference is insignificant when taking blood on an empty stomach (the difference is about 0.1 mmol / L), but it increases markedly after eating (the difference is about 15%) or when an oral glucose tolerance test is performed (the difference is 20-25%) – the effect of insulin release.

    90,000 Lawyer Tsirit announced a political trace in the Barabanshchikov case / 15 November 2021 | Northwest, News of the day 15.11.21

    The court session in the Barabanshchikov case did not take into account the arguments of the defense about the transfer of the suspect to house arrest. The official’s defense intends to file a petition for the interrogation of high-ranking officials of the executive authorities of St. Petersburg. The political nature of the case is also not excluded. This was stated by the lawyer of the ex-head of the Department of Social Catering of St. Petersburg Alexei Barabanshchikov Anton Tsirit.

    On Monday, November 15, the ex-official, accused of causing property damage under Article 165 of the Criminal Code of the Russian Federation, was placed in a pre-trial detention center for a period of two months.Barabanshchikov is accused of allegedly conspiring with third parties to lobby for the victory of KSP Krasnoselsky in the 2020 tender for the supply of social food. The defense side notes that the court’s decision was made without presenting evidence of the defendant’s guilt. The arguments on the basis of which it would have been possible to mitigate the measure of restraint for Barabanshchikov were also not taken into account, placing him under house arrest.

    Tsirit noted that his client was following the instructions of the Governor of St. Petersburg Alexander Beglov, including on the enlargement of lots so that the State Order Committee would be responsible for their distribution.The new system caused discontent among food factories, as it made it impossible for them to receive tenders in collusion with other market players and regional administrations.

    “During the court session, the question arose about the execution of the instructions of the Governor of St. Petersburg, and Alexey Barabanshchikov carried out these instructions, and this is in the materials of the criminal case. In general, some players in the social catering market were dissatisfied with the appointment of Barabanshchikov, they were dissatisfied with the principled and open policy that he pursued as head of the department, ” – the lawyer of the accused said.

    Tsirit also added that his client was repeatedly hinted at the idea of ​​leaving his post, but he did not follow the recommendations.

    “The only way to remove him was a criminal case”, – explained the representative of Barabanshchikov’s interests in court.

    The situation is rather complicated, and therefore Tsirit does not exclude that high-ranking officials of St. Petersburg will be involved in the investigation.

    “I fully admit that in this criminal case, the defense will file petitions for interrogating officials of the executive authorities of St. Petersburg, and we will not look at what high positions these persons occupy,” – the lawyer shared.

    The media reported earlier that the initiative to enlarge lots and centralize public procurement in the field of social nutrition came directly from the mayor of St. Petersburg. The information was confirmed by the head of the committee on state orders, Alexander Zhemyakin, who was summoned last Sunday for interrogation in the Barabanshchikov case. He confirmed that the ex-head of the USP was engaged only in food quality control issues. And this may indicate that the claims against the official are inappropriate.

    Tsirit does not exclude that the pressure on Barabanshchikov is of a political nature.

    “I believe that there is, of course, a political component, and who is afraid, it’s difficult for me to say now, but in my opinion it’s absolutely certain that there is not only law, but politics as well,” the lawyer expressed his opinion.

    Many experts also agree that the persecution of the ex-head of the USP caused his reform activities and his readiness to speak openly about existing problems. It is possible that the devastating interview of Barabanshchikov, published about a month ago, in which he spoke about the corruption of the city authorities and the cartelization of the social food market, became the main reason for initiating a criminal case against him.

    St. Petersburg, Ekaterina Popova

    St.