Introduction
Gestational diabetes mellitus (GDM) can be defined as any degree of glucose
intolerance with an onset during pregnancy. Women diagnosed with GDM have a higher
risk of developing type 2 diabetes mellitus (T2DM) later in their life compared to
women with no GDM [1 ]. During pregnancy, the
body of the woman adapts according to the growing fetus and its glucose
requirements. Insulin secretion gets increased, which elevates maternal
storage of fat and glycogen for better sufficient maternal nutrition. At the
beginning of the mid- trimester, various placental hormones are produced that work
as insulin antagonists. These hormones increase insulin resistance and result in the
increase of maternal glucose and free fatty acids. Women with normal pregnancy
produce a surplus amount of insulin to bypass this insulin resistance and insulin
homeostasis falls back to non-pregnancy levels after delivery but on the contrary,
women with underlying metabolic disorders and genetic predisposition of relative
insulin secretion defect fail to increase their insulin secretion during this period
and develop GDM. Factors responsible for the development of GDM can be Ethnicity
(Asian women are more prone to developing GDM compared to white women), lack of
adequate glucose monitoring during pregnancy and follow up period, low level of
patient education regarding GDM, and unwilling patient attitude towards dietary and
lifestyle changes [2 ]. T2DM is spreading
across Asia as an epidemic and one aggravating factor is GDM for the female
population. Over and above GDM, other factors responsible for the development of
T2DM are hereditary T2DM, multiparity, older maternal age, weight gain during
pregnancy (BMI during pregnancy), and high blood sugar levels in the first
pregnancy. Chances of GDM progresses to T2DM sharply within the first 5 years after
delivery and then flattens after 10 years [3 ].
An increased risk of cardiovascular disease, T2DM, and obesity are the consequences
of GDM on the maternal side and the child has a risk of developing obesity, T2DM,
and cardiovascular diseases throughout their life. Furthermore, with an inherent
predisposition, birth complications like stillbirth, preterm birth, overweight baby,
polyhydramnios, breathing difficulty, jaundice, and hypoglycemia can result due to
GDM [4 ]. Women with GDM have a 7-fold risk
of developing T2DM post-pregnancy compared to normal women [5 ]. This review has been done to determine the
risk of developing T2DM after having GDM in Asian women and the exact
pathophysiology lying behind the conversion of GDM to T2DM and its associated
factors.
Data Search and Sources
Freely accessible, full-text articles, available in PubMed and Google Scholar,
and MEDLINE in the English language, till August 2022 pertaining to GDM were
reviewed. The references of these articles were also scrutinized for relevant
studies.
Study Selection
We included studies with a documented incidence of type 2 diabetes mellitus after
GDM with the precise follow-up record, carried out on humans and were published
in the English language. Studies with less than 100 patients and a low rate of
follow up after 6 months post-partum were excluded to reduce the downgrading
effect it can have on the study result; studies that did not fit in the criteria
were excluded. Any study with an overlapping population was checked for and the
one with the higher population was selected.
[Fig. 1 ] represents the data selection and
criteria on the basis of which a total of 53 articles were selected that
satisfied the aim and scope of the review; the data from these articles were
further used to calculate results.
Fig. 1 Data collection.
Pathophysiology
GDM is a type of diabetes that develops and is diagnosed during pregnancy, as the
name implies, it is a condition in which the body of a pregnant woman is unable
to utilize glucose (sugar) effectively. This causes a rise in blood glucose
(sugar) levels, which impacts both the mother and the fetus’ health and
development.
Insulin resistance and β-cell dysfunction are both important factors in
the pathogenesis of GDM. In the majority of cases, such abnormalities occur in
the body prior to conception and progress over time as one of the key risk
factors for the development of GDM and T2DM after delivery [6 ]. Apart from the pancreas, a variety of
other organs and organ systems, such as the placenta, heart, brain, liver,
kidney, eyes, skin, vascular system, neurological system, and adipose tissues
play a role in the development of GDM.
β-Cell Dysfunction
β-Cell dysfunction is a condition in which cells do not function
properly. The endocrine pancreas is made up of three different types of cells:
alpha, beta, and delta cells. Insulin is stored in pancreatic cells, which
release it in reaction to rising glucose levels in the body. β- Cell
dysfunction occurs when β-cells fail to detect glucose content in the
blood and are unable to produce enough insulin in response [7 ]. It occurs as a result of insufficient
glucose sensing to trigger insulin release, resulting in high blood glucose
levels. β-Cell dysfunction can be caused by a flaw in any phase of the
process. These steps include pro-insulin production, post-translational changes,
insulin storage, blood glucose monitoring, and the complicated mechanism
controlling granule exocytosis. GDM is linked to the majority of susceptibility
genes responsible for the β-cell function. KQT-like 1 (Kcnq1), a
potassium voltage-gated channel, and glucokinase are two of them (Gck) [8 ]. When β-cells are unable to
detect glucose levels in the blood, glucose uptake is reduced, resulting in
hyperglycemia. As a result, β-cells are forced to create more insulin.
Glucotoxicity is the word for the destruction of β-cells caused by
glucose [9 ]. This leads to further
β-cell breakdown and a cycle of consequences, including hyperglycemia
and insulin resistance.
Reduced β-cell mass and number as a result of pancreatectomy may also
contribute to the development of GDM, depending on the individual.
Chronic Insulin Resistance
Insulin resistance is the result of the inability of cells to respond to insulin
release. Glucose transporter 4 (GLUT4) is a glucose transport protein, which is
found primarily in adipose tissues, skeletal muscles, and cardiac muscles. It
facilitates the uptake of glucose molecules by the cells for its effective use
and plays an important role in regulating whole-body glucose homeostasis.
Inadequate translocation of glucose transporter 4 (GLUT4) to the plasma membrane
due to failure of insulin signaling contributes to insulin resistance. In
patients with GDM, the rate of glucose uptake due to insulin uptake is reduced
by 54% when compared with normal pregnancy. Generally, the abundance of
insulin receptors is unaffected but reduced tyrosine or increased
serine/threonine phosphorylation of the insulin receptor diminishes
insulin signaling [10 ]. Apart from this,
altered expression of downstream regulators of insulin signaling, including
insulin receptor substrate (IRS)-1, phosphatidylinositol 3- kinase (PI3K), and
GLUT4 have been associated in GDM. Most of the time these changes at the
molecular level remain persistent and can contribute to the development of T2DM
[11 ].
[Fig. 2 ]
[12 ] shows the relationship between
β-cell dysfunction, insulin resistance, and GDM. During the normal
gestational period, β-cells of the pancreas undergo hyperplasia and
hypertrophy in order to meet the requirements of metabolic processes occurring
during pregnancy and to compensate for increased blood glucose levels.
β-Cells, blood glucose levels, and insulin sensitivity return to normal
following pregnancy. However, in GDM, β-cells fail to compensate for
increased blood glucose levels and, when combined with reduced insulin
sensitivity, this results in hyperglycemia [8 ].
Fig. 2 Relationship between β-cell dysfunction, insulin
resistance, and GDM.
Adiponectin
Adiponectin is a protein hormone that is produced predominantly by adipocytes,
but also by muscle and the brain. The ADIPOQ gene encodes this hormone in
humans. It is involved in the regulation of glucose levels as well as the
breakdown of fatty acids in the body. Its concentration in plasma, on the other
hand, is inversely related to the mass of adipose tissue [13 ]. A reduction in adiponectin levels is
also linked to GDM. Adiponectin promotes fatty acid oxidation, insulin
sensitivity, and gluconeogenesis inhibition. This is accomplished via activating
the transcription factor peroxisome proliferator-activated receptor alpha
(PPARα) in the liver and the AMP-activated protein kinase (AMPK) within
insulin-sensitive cells, which facilitates IRS-1 function [14 ]. Insulin secretion is stimulated by
adiponectin, which increases insulin gene expression and exocytosis of insulin
granules from β-cells. Adiponectin is also produced in the
placenta’s syncytiotrophoblast, where it is controlled by cytokines such
as tumor necrosis factor alpha (TNF-α), interferon gamma
(IFN-γ), interleukin (IL)-6, and leptin at low concentrations [13 ].
It is unclear what role placental adiponectin plays in normal and GDM pregnancy.
However, new research suggests that it interferes with insulin signaling and
amino acid transport through the placenta, limiting fetal growth. As a result,
maternal glucose intolerance and fetal macrosomia are linked to adiponectin gene
methylation in the placenta [15 ].
Placental Movement
The placenta, through its production of hormones and cytokines, contributes to
insulin resistance throughout pregnancy. During GDM, the placenta, which serves
as a barrier between the maternal and fetal surroundings, is also subjected to
hyperglycemia and its effects. This can affect glucose, amino acids, and lipid
transport across the placenta [16 ].
Protein: Amino acid transport across the placenta is also a key factor in fetal
growth. GDM is linked to an increase in System A and L activity.
Pro-inflammatory cytokines like TNF-α and IL-6 can also influence them.
Excess protein consumption may potentially lead to GDM through altered amino
acid transport [17 ].
Lipids: Finally, while GDM has traditionally been thought of as a hyperglycemic
condition, the growth in obesity-related GDM has forced a greater focus on the
involvement of hyperlipidemia in the disease. When compared to glucose pathways
(9%), lipid pathways (67%) account for the majority of changes
in placental gene expression in GDM [18 ].
When compared to T1DM, GDM is related to preferential activation of placental
lipid genes. GDM has been linked to various abnormalities in the placenta in
addition to these changes in placental transport. GDM has been linked to global
DNA hypermethylation in the placenta in recent investigations [19 ].
Epidemiology
Gestational diabetes mellitus (GDM) is one of the most common endocrinopathies in
pregnancy that can be characterized as hyperglycemia at any time in pregnancy
based on defined thresholds [20 ].
Placental production of diabetogenic hormones in late pregnancy such as human
placental lactogen, leads to progressive insulin resistance; when β-cell
hyperfunctionality adaptation during pregnancy fails to compensate maternal
insulin resistance, it may lead to gestational diabetes [21 ]. It is well documented that GDM is
linked with adverse maternal and neonatal outcomes along with lifelong risk of
obesity and diabetes in both mother and child later in life.
It is estimated that GDM affects around 7–10% of all pregnancies
worldwide; however, it is difficult to estimate the prevalence as rates differ
between studies due to prevalence of different risk factors in the population,
such as maternal age, BMI, ethnicity, lifestyle, comorbidities, socioeconomic
status, substance abuse, etc. Moreover, testing methods, screening strategies,
and even glycemic thresholds for GDM remain the subject of concern and thus
prevalence of gestational diabetes mellitus widely varies depending on the
population studied and the diagnostic criteria used. The data source used also
leads to substantive divergence in the reporting of preponderance of GDM.
Accurate estimate of GDM prevalence is essential for planning, evaluation,
policy development, and research. We aimed to determine the prevalence of GDM
using a variety of data sources and to evaluate the correspondence between
different data sources, to generate common end points for the same, the
information was gathered using standard sources of references, which included
IDF, WHO, CDC, ADA, and national health surveys.
[Fig. 3 ] indicates the %
prevalence of GDM in the global division of 7 regions out of the total
pregnancies, compiled from various authenticated, time tested sources with the
numerical percentage prevalence data.
Fig. 3 Prevalence of gestational diabetes mellitus (GDM).
[Fig. 4 ] indicates the total number of
live births, which are directly affected by GDM, in the global division of 7
regions out of the total pregnancies, compiled from various authenticated, time
tested sources with the numerical values.
Fig. 4 Live births affected by GDM.
Risk Factors
On reviewing various critically acclaimed articles, the well-documented risk
factors for GDM were identified and they are discussed below to help identify
women at risk of gestational diabetes at an early stage, which could provide a
window for preventive measures. GDM itself being a risk factor for T2DM, they
share the majority of the risks involved. The risk factors stated below have
differing relative risks on the development of gestational diabetes. The
well-documented factors for GDM are advanced maternal age,
BMI≥25 kg/m2 , family history of T2DM, macrosomia,
cigarette smoking, and non-Caucasian ethnicity. Advanced maternal age and
obesity are well-known predictors of GDM, according to a study a pre- pregnancy
BMI of>30 kg/m2 in women aged from 30–35
years has a stronger effect on GDM, furthermore, gain in BMI from pre-pregnancy
to 15–20 weeks of gestation and advanced maternal age are strongly
associated with the risk of developing GDM [22 ]. Heredity as a risk factor for GDM holds a strong pursuit, even
though an established genetic background for diabetes mellitus remains unclear,
a history of diabetes on the maternal side is quite prominent a risk factor than
on the paternal side. The role of genetics on the future risk of diabetes is
quite notable pertaining to the fact that phenotypes responsible for glucose
homeostasis are heritable [23 ]. In a
heritability estimate study on UK families, it was found that fasting glucose
concentration and homeostasis model of pancreatic cell dysfunction has the
highest heritability estimate of 0.72 and 0.78, respectively [24 ]. In all the findings, it is suggested
that genetic as well as environmental factors play an important role in
gestational diabetes. Macrosomia termed by Spellacy et al. [25 ], is a new-born with a birth weight of
4–4.5 kg, and a woman giving birth to a macrosomic baby has a
higher chance of developing diabetes in the future compared to women giving
birth to an infant that does not exceed the 90th percentile of normal
gestational weight. Fetuses with higher maternal glucose receive excess glucose
via the placenta and hence they develop a unique pattern of overgrowth resulting
in deposition of subcutaneous fat in the abdominal and interscapular region.
Among these factors, diet and physical activity also play an indispensable role,
the obvious consumption of high fat and sugary food leads to increased blood
glucose. Smoking and the drinking status of the parents before and during
pregnancy could result in a higher risk of GDM [26 ]. Polycystic ovary syndrome is an endocrine disorder in females,
and insulin resistance has been observed in 50% of women with PCOS, they
have a four-fold risk of T2DM than normoglycemic women and are at a higher risk
of GDM. In 2012, Marshall [27 ] associated
PCOS with hyperinsulinemia, and it has become clear hyperandrogenism and
impaired glucose tolerance are correlated. GDM and T2DM are both increasing on a
large scale in the Asian and Middle Eastern and African countries, resonating an
endemic even. According to a combined study by WHO (World Health Organisation)
and IADPSG (The International Association of Diabetes and Pregnancy Study
Groups) [28 ], the percentage of GDM
prevalence in East Asian, South Asian, and African countries is remarkably
higher than European and North American region. In a study by Savitz et al.
[29 ] conducted in New York City where
ethnic diversity is increasing on the go, birth reports and hospital data
collected from 1995 to 2015 show that non-Caucasian population born in their
native country and then migrating to the U.S. had an elevated risk at developing
GDM compared to the ones born in the U.S.
Diagnostic Criteria
Usually, any woman with a family history of diabetes or hyperglycemia will be
screened for an IGT (impaired glucose tolerance) during 24–36 weeks of
pregnancy period because hormonal changes during pregnancy can lead to impaired
insulin production in the body, which is tolerated well by some women but could
result into gestational diabetes in others. Glycosuria, polyuria, frequent
thirst, obesity are the early signs of gestational diabetes, and any women
showing these symptoms should be checked for hyperglycemia. In 2014, the USA
Preventive Service Task Force recommended screening every woman post 24 weeks of
pregnancy for GDM as only screening women with a symptom and history of
hyperglycemia failed to identify half of the women with GDM [30 ]. The GDM screening guidelines of the
USA and Canada agree on a two-step approach, including an initial test with
50 g 1-hour plasma glucose test (positive test
if>140 g/dl). Women with a positive result are f ollowed
up on the 100 g OGTT, the women having 2 or more than 2 abnormal values
of plasma glucose are diagnosed with GDM. The guidelines followed by the UK and
Australia include an initial test with 75 g 2-hour OGTT and a fasting
blood glucose≥126 mg/dl and a 2-
hour≥140 g/dl is taken as a diagnosis for GDM. The WHO
recommends a 75 g OGTT irrespective of the last meal with a threshold
value of 2-hour PG>140 mg/dl for GDM [31 ]. The ADA has recommended the use of
either the one or two-step approach at 24–28 weeks of gestation in
pregnant women without the diagnosis of diabetes.
The 75 g 2-hour test is a widely accepted standard because of
convenience, it has also shown more sensitive results in predicting pregnancy
complications like gestational hypertension, preeclampsia, and macrosomia
compared to the 100 g 3-hour test [32 ]. The fact behind its increased sensitivity is that it requires
only one elevated glucose value to diagnose GDM but the 100 g 3-hour
test requires two abnormal glucose values. In this group of gravida at
24–28 weeks’ gestation, the one-step strategy entails doing a
75 g OGTT with plasma glucose measurement when the patient is fasting
and at 1 and 2 hours. After an overnight fast of at least
8 hours, perform the OGTT in the morning. When any of the following
criteria are met or surpassed, GDM is diagnosed, 92 mg/dl
(5.1 mmol/l) fasting, 180 mg/dl
(10.0 mmol/l) after 1 hour, 153 mg/dl
(8.5 mmol/l) after 2 hours. A 1-hour (nonfasting) plasma
glucose measurement following a 50 g oral glucose load is used in women
between 24–28 weeks of pregnancy who have never been diagnosed with
diabetes, then perform a fasting 100 g OGTT if the plasma glucose level
after 1 hour is 130 mg/dl, 135 mg/dl, or
140 mg/dl (7.2 mmol/l, mmol/l, or
7.8 mmol/l, respectively). If at least two of the following four
plasma glucose values are attained or exceeded, GDM is diagnosed:
95 mg/dl (5.3 mmol/l) while fasting
180 mg/dl (10.0 mmol/l) after 1 hour,
155 mg/dl (8.6 mmol/l) after 2 hours,
140 mg/dl (7.8 mmol/l) after 3 hours
[33 ].
The different criteria used for GDM screening bring out individual outcomes.
O’Sullivan and Mahan were the first ones to identify a need for
diagnostic criteria for GDM and create one, based on their study on 752 women by
performing a 3-hour 100 g OGTT on them. Further, O’Sullivan
suggested a 50 g 1-hour OGTT for GDM. O’Sullivan and
Mahan’s test used whole blood instead of plasma for measuring glucose
concentration [34 ]. NDDG (National
Diabetes Data Group) identified this drawback and suggested using plasma instead
of whole blood pertaining to the fact that plasma has 11% more glucose
concentrations than whole blood [35 ].
Following this, Carpenter and Coustan replaced the calorimetric assays with
enzyme assays which further brought down the NDDG cut-offs and if any two or
more values exceeded the cut-off, it would result in the diagnosis of GDM [36 ]. In 1999, WHO suggested that the
diagnosis of GDM was made on a single cut-off value of 140 gm/dl
after a 2-hour 75 g post glucose concentrations were measured after
overnight fasting. This test became inconvenient as it required antenatal women
to fast on the day of testing and it was against the belief system at that time.
Therefore, in 2016 DIPSI (Diabetes in Pregnancy Study Group in India) came out
with an upgraded version of WHO, which included a 75 g 2-hour OGTT
plasma glucose that was measured in a non-fasting state during the 24–28
weeks of pregnancy irrespective of the last meal [37 ]. The WHO also claimed it as an
efficacious test similar to the fasting test. This was followed by the HAPO
(Hyperglycemia and Adverse Pregnancy Outcomes) study in 2008, which explained
that varying degrees of maternal hyperglycemia can result in adverse outcomes
from the pregnancy but they were not as severe as in overt diabetes [1 ]. Soon, in 2010, IADPSG (International
Association of Diabetes and Pregnancy Study Group) after reviewing the HAPO
study, formed international guidelines to unify the diagnostic criteria for GDM
globally, but soon it was criticized as the HAPO study was based mainly on the
Caucasian population and left out other ethnicities, especially Asian [38 ].
[Table 1 ]
[39 ] shows comparison of different
diagnostic criteria for GDM (NDDG: National diabetes data group, ADA: American
diabetic association, WHO: World Health Organisation, ADIPS: Australian Diabetes
in Pregnancy).
Table 1 Comparison of different diagnostic criteria for
GDM.
Criteria
NDDG
Carpenter and Coustan
ADA
WHO
ADIPS
Glucose
100
100
75
75
75
FPG (mg/dl)
105
95
95
126
99
OGTT (mg/dl)
1 h level
190
180
180
–
–
2 h level
165
155
155
140
144
3 h level
145
140
–
–
–
Diagnostic criteria
2 of 4
2 of 4
2 of 3
1 of 2
1 of 2
Risk of Subsequent T2DM after GDM
GDM occurs in women with a genetic or historical predisposition of glucose
intolerance, it leads to the fact that the affected women have the inability to
maintain the required plasma glucose concentration in the body, so this leads to
future diabetes mellitus with increasing age, glucose intolerance also advances.
With advancing maternal age and a sedentary lifestyle, GDM has become more
common. Studies have found out that GDM prevalence is 7% worldwide and
it has increased up to 30% in recent decades, becoming one of the most
common complications of pregnancy. Women with GDM have a 7-fold risk of
developing T2DM later in life which institutes the fact that increasing
prevalence of GDM can fuel the T2DM epidemic [40 ]. In a study by Ornoy, Asher et. al. [41 ], the probability of development of
diabetes was 3.7% at 9 months, 4.9% at 15 months, and
13.1% at 5.2 years, women with GDM had a higher rate of developing overt
diabetes in the early 9 months compared to after years. This led to the fact
that most of these women had undiagnosed T2DM, which was identified during
pregnancy. Women with diagnosed diabetes before pregnancy suffer from lower
birth complications than women with undiagnosed diabetes. GDM has been
associated with various short and long-term health complications, both fetal and
maternal. It increases the short-term maternal risk of polyhydroamnios,
pre-eclampsia, prolonged labor, obstructed labor, caesarean section, uterine
prolapse, postpartum hemorrhage, and infections [31 ]. Even though serum glucose levels return to normal after delivery
it can also lead to the fetal risk of spontaneous abortion, intrauterine death,
stillbirth, congenital malformation, shoulder dystocia, birth injuries, neonatal
hypoglycemia, infant respiratory distress syndrome, and macrosomia [42 ]. On top of T2DM, it can further lead to
long-term health complications for both mother and offspring. These long-term
complications include metabolic syndrome, malignancies, cardiovascular
disorders, renal diseases, and gestational diabetes in the subsequent pregnancy.
The long-term complications on the offspring can be T2DM, obesity, and
neuropsychiatric disorders like sleep apnea, autistic spectrum disorders,
cerebral palsy, and infantile spasms [43 ].
Prevention of GDM
Prevention of GDM can simultaneously prevent the complications for both mother
and the fetus and helps them lead a healthy life.
Diet
Just like any other pregnancy complications, GDM can also be prevented by leading
a healthy life and leading a healthy life starts with a healthy diet. A healthy
diet comprises of different varieties of food like proteins, carbohydrates, fats
and vitamins in a specific quantity, also termed as balanced diet. Higher intake
of fruits/fruit fiber pre-pregnancy is associated with decreased risk of
GDM. Higher intake of potato is associated with increased risk of GDM due to its
high glycemic index. Replacing two potato servings per week with other vegetable
types, legumes or wholegrain foods resulted in a 9%, 10% and
17% of reduction in GDM risk respectively. Higher consumption of sugar
sweetened beverage (SSB) was associated with risk of GDM. Intake of protein from
animal origin increased the risk of GDM by 50% when compared to intake
of protein sourced from vegetables which was protective by 30%.
Replacing 5% energy of animal protein for protein of plant origin
reduced the risk of GDM by 51% [44 ]. Increased instances of fast food intake pre pregnancy was
associated with a significant increased risk or incidence of developing GDM.
Luoto et al. [45 ], explained in their
article the protective role of probiotics in pregnancy by modifying intestinal
microbiota, altering the fermentation of dietary polysaccharides, improving the
function of intestinal barrier and their capability to regulate the inflammatory
pathways resulted in a reduced risk of maternal and fetal heperglycemia, the gut
microbiota is recently associated with setting the tone of inflammation in the
body, which modulated the host’s sensitivity towards insulin.
Mediterranean diet was the most consistently reported protective diet for
protection against GDM [46 ]. Complying
with a diet with higher AHEI 2010 score was associated with a decreased risk of
GDM by 19% or 46% [47 ]. A
greater adherence to Dietary Approaches to Stop Hypertension (DASH diet) was
linked with a 34% reduction in GDM risk. A randomized control trial
compared the pregnancy outcomes of normal diet and DASH diet mothers, DASH diet
mothers not only required low insulin therapy post-delivery, but also resulted
in normal birth weight infants, lower caesarean sections and lower HbA1c levels
pre and postgestation in mothers. Lowering the intake of foods rich in high heme
iron, sugar sweetened cola, potatoes, fatty foods, and sweets can reduce the
risk of GDM, especially among the high-risk population and before getting
pregnant [48 ].
Maintaining a Healthy Lifestyle
Lifestyle adjustment, in addition to diet, is an equally essential element in
reducing the incidence of GDM. Exercising or engaging in a physical activity is
a vital part of maintaining a healthy body weight. Exercise helps the body to
become more sensitive to the insulin and helps regulate blood sugar levels
effectively. At least 30 minutes of moderate-intensity exercise
4–5 days a week reduces the risk of developing GDM [49 ]. Moderate-intensity exercise is an
exercise that causes sweating. For a person living sedentary lifestyle, try
starting with brisk-walking, climbing stairs, active leisure activities like
hiking, gardening, or playing with children outdoors and swimming. Cardio
exercises can also be involved. A study by Badon and colleagues [47 ] stated that engaging in Leisure Time
Physical Activity (LTPA) pre and during pregnancy was associated with
46% reduction in GDM risk. Indulging in healthy diet, physical activity,
not smoking, and maintaining a low stress level were associated with a lower
risk of GDM. The study also stated that women without any of the four healthy
lifestyle outcomes were at 4.43 times higher risk of GDM. Women with all 4
healthy lifestyle outcomes were 35% less likely to develop GDM compared
to women with 3 or less components. Out of all the four components, non-smoking
was the most significant factor associated with development of GDM. Education
and counselling of the mother regarding lifestyle changes, fetal health
evaluation, diet, exercise and diabetes screening plays a crucial role in its
prevention, although there are no standard guidelines for the same.
Post-Delivery Care
Post-delivery care is as important as care taken before and during pregnancy.
Some of the same risk factors that put you in risk of getting GDM can also
increase your chances of develop T2DM later in life. And if you have GDM, the
risk of developing T2DM after your pregnancy rises. Following the same healthy
diet and exercise plan post pregnancy and getting back to a healthy weight will
lower your risk of developing T2DM in future.
