**11. Programmes to control diabetes epidemic**

There are extensive work done and literature available regarding the diabetes epidemiology, healthy lifestyle, primary prevention of diabetes and effects of gestational diabetes and *in utero* malnutrition and hyperglycemia. Many of them have been cited in the various publications referred in this chapter [1–3, 7, 10, 25, 27, 29, 32, 39, 49, 56, 57, 67, 68]. In this section, the focus is on briefly highlighting the urgent priority public health programmes required to control the diabetes epidemic. The perspectives on controlling the diabetes epidemic in the population as a whole, not just primary prevention of diabetes in individuals, and the implementations of the required programmes are the dire needs today.

• the rapid transition in the nutritional status of population leading to dissociation in metabolic states of fetal life (associated with nutritional want) and adult life (with nutritional surfeit) of people (this factor of *in utero* undernutrition appears to limit the range of normal body mass index in adult life in such population and even in the individual person of any

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• maternal hyperglycemia during pregnancy affecting the *in utero* life of the offspring.

**11.2. Healthy diet and weight and regular physical activity and exercise** 

Whatever may be the differences of the initial rise in diabetes prevalence in the world and its pathogenesis, the fact remains that diabetes epidemic is now increasingly affecting the younger and younger population. There is, thus, the need to consider all possible factors to

Healthy diet with proportionate intake of nutrients, body weight as per the recommended body mass index for the population and regular physical activity and exercise are applicable to general population and people with impaired glucose intolerance, diabetes and

**Public health perspectives:** Campaigns and programmes are required to make the people, housewives and children well aware of the recommended bodyweight (as required for the respective population) and the recommendations regarding the daily intake of plain water, fruit, vegetables, salt, sugar, fat (with adequate proportion of mono- and poly-unsaturated and saturated fatty acid) and other nutrient avoiding the trans-fatty acid. Multisectoral population-based approaches, including trade and agricultural policies and the workplace-, schooland other setting-based interventions, for healthy diet and physical activity and exercise need to be considered

**Public health perspectives:** Pedestrians, cyclists and public transport passengers are the top three hierarchy groups recommended while developing transport and traffic strategies [61]. It is also essential to have campaigns and support system to develop various physical activity and exercise programmes at the community, school and various workplace levels like regular walking, games and sports, marathon running, aerobic dance and others

Taking a life-course perspective is essential for preventing type 2 diabetes, as it is for many health conditions [2]. Firstborn offspring in the resource poor settings may be at increased risk of glucose intolerance due to the likelihood of possible maternal malnutrition during the first pregnancy as compared to that in later pregnancy [56, 62]. Adequate nutrition and microand macronutrient supply before and during pregnancy are the steps to reduce the risk of *in utero* malnutrition and its ill effects [27]. Good nutrition during infancy and childhood and adequate physical activity among children are important for the development of a healthy

population group) and

**at the population level**

[2, 3, 10, 56].

[2, 3, 10, 56].

child and an adult [27].

CVDs [3, 10, 21, 25, 32, 39, 56].

control the epidemic of diabetes in all the populations.

**11.3. Prevention of maternal and childhood malnutrition**

#### **11.1. Factors fueling the diabetes epidemic**

The epidemic of glucose intolerance in the world is relatively a new phenomenon starting since the latter half of twentieth century and the initial rise in diabetes prevalence has occurred differently in various populations in the world [56, 57]. For example, gradual rise in diabetes prevalence has occurred in Europids in Europe, Canada and the USA since around 1940s with increasing sedentary life, obesity and aging with about a third of their population over 50 years of age. On the top of similar gradual rise, the migrant or urbanized Asian-Indian, Arab, African, Chinese and Hispanic people faced the rapid rise of diabetes prevalence since around 1970s mostly due to the rapid transition in the nutritional status of population leading to dissociation in metabolic states of fetal life (associated with nutritional want) and adult life (with nutritional surfeit) of people. The indigenous people of the USA, Canada, Australia and Pacific region also faced the rapid rise in diabetes prevalence (due to the rapid transition in their nutritional status) since around 1940s and subsequently further faced the accelerated rise mostly due to the addition of the factor of maternal hyperglycemia during pregnancy affecting the *in utero* life of the offspring [56].

Such variations in the rise in diabetes prevalence in different populations can just be ascribed to the effect of ethnic variations leading to a sense of fatalism. The concept of ethnicity does provide self-identification with cultural traditions and social identity and boundaries between groups, but it has dynamic nature [58]. Ethnicity is a sort of surrogate marker for multiple environmental and genetic factors (though genetics playing a relatively small part), in disease causation and for public health policy [56, 59, 60]. In terms of the scientific approach and public health policy, ethnic variations in the prevalence of any disease or condition should lead the humankind to search for such environmental or genetic factors [59]. The different pattern of initial rise in diabetes prevalence in various populations in the world, thus, appears to be related to the various proportions of three groups of risk factors present in different populations. Thus, the three groups of such possible factors to consider are [56]:

• obesity, sedentary life and aging;


Whatever may be the differences of the initial rise in diabetes prevalence in the world and its pathogenesis, the fact remains that diabetes epidemic is now increasingly affecting the younger and younger population. There is, thus, the need to consider all possible factors to control the epidemic of diabetes in all the populations.

#### **11.2. Healthy diet and weight and regular physical activity and exercise at the population level**

**11. Programmes to control diabetes epidemic**

**11.1. Factors fueling the diabetes epidemic**

affecting the *in utero* life of the offspring [56].

sible factors to consider are [56]:

• obesity, sedentary life and aging;

today.

190 Diabetes and Its Complications

There are extensive work done and literature available regarding the diabetes epidemiology, healthy lifestyle, primary prevention of diabetes and effects of gestational diabetes and *in utero* malnutrition and hyperglycemia. Many of them have been cited in the various publications referred in this chapter [1–3, 7, 10, 25, 27, 29, 32, 39, 49, 56, 57, 67, 68]. In this section, the focus is on briefly highlighting the urgent priority public health programmes required to control the diabetes epidemic. The perspectives on controlling the diabetes epidemic in the population as a whole, not just primary prevention of diabetes in individuals, and the implementations of the required programmes are the dire needs

The epidemic of glucose intolerance in the world is relatively a new phenomenon starting since the latter half of twentieth century and the initial rise in diabetes prevalence has occurred differently in various populations in the world [56, 57]. For example, gradual rise in diabetes prevalence has occurred in Europids in Europe, Canada and the USA since around 1940s with increasing sedentary life, obesity and aging with about a third of their population over 50 years of age. On the top of similar gradual rise, the migrant or urbanized Asian-Indian, Arab, African, Chinese and Hispanic people faced the rapid rise of diabetes prevalence since around 1970s mostly due to the rapid transition in the nutritional status of population leading to dissociation in metabolic states of fetal life (associated with nutritional want) and adult life (with nutritional surfeit) of people. The indigenous people of the USA, Canada, Australia and Pacific region also faced the rapid rise in diabetes prevalence (due to the rapid transition in their nutritional status) since around 1940s and subsequently further faced the accelerated rise mostly due to the addition of the factor of maternal hyperglycemia during pregnancy

Such variations in the rise in diabetes prevalence in different populations can just be ascribed to the effect of ethnic variations leading to a sense of fatalism. The concept of ethnicity does provide self-identification with cultural traditions and social identity and boundaries between groups, but it has dynamic nature [58]. Ethnicity is a sort of surrogate marker for multiple environmental and genetic factors (though genetics playing a relatively small part), in disease causation and for public health policy [56, 59, 60]. In terms of the scientific approach and public health policy, ethnic variations in the prevalence of any disease or condition should lead the humankind to search for such environmental or genetic factors [59]. The different pattern of initial rise in diabetes prevalence in various populations in the world, thus, appears to be related to the various proportions of three groups of risk factors present in different populations. Thus, the three groups of such posHealthy diet with proportionate intake of nutrients, body weight as per the recommended body mass index for the population and regular physical activity and exercise are applicable to general population and people with impaired glucose intolerance, diabetes and CVDs [3, 10, 21, 25, 32, 39, 56].

**Public health perspectives:** Campaigns and programmes are required to make the people, housewives and children well aware of the recommended bodyweight (as required for the respective population) and the recommendations regarding the daily intake of plain water, fruit, vegetables, salt, sugar, fat (with adequate proportion of mono- and poly-unsaturated and saturated fatty acid) and other nutrient avoiding the trans-fatty acid. Multisectoral population-based approaches, including trade and agricultural policies and the workplace-, schooland other setting-based interventions, for healthy diet and physical activity and exercise need to be considered [2, 3, 10, 56].

**Public health perspectives:** Pedestrians, cyclists and public transport passengers are the top three hierarchy groups recommended while developing transport and traffic strategies [61]. It is also essential to have campaigns and support system to develop various physical activity and exercise programmes at the community, school and various workplace levels like regular walking, games and sports, marathon running, aerobic dance and others [2, 3, 10, 56].

#### **11.3. Prevention of maternal and childhood malnutrition**

Taking a life-course perspective is essential for preventing type 2 diabetes, as it is for many health conditions [2]. Firstborn offspring in the resource poor settings may be at increased risk of glucose intolerance due to the likelihood of possible maternal malnutrition during the first pregnancy as compared to that in later pregnancy [56, 62]. Adequate nutrition and microand macronutrient supply before and during pregnancy are the steps to reduce the risk of *in utero* malnutrition and its ill effects [27]. Good nutrition during infancy and childhood and adequate physical activity among children are important for the development of a healthy child and an adult [27].

#### **11.4. Maintenance of optimal pre-pregnancy bodyweight: the key programme required**

even below 75 mg/dL (4.2 mmol/L) [67, 68]. Macrosomia is to a great extent measurable but the fetal programming due to relative maternal hyperglycemia is difficult to assess and is obviously likely to be affected earlier than the overt macrosomia. Weeks 3–8 encompass organogenesis and major malformations in infants of diabetic mother occur during these periods [69]. So to protect the fetus from any possible effect of maternal hyperglycemia, blood glucose during the whole duration, including the early stage, of pregnancy has to be within the safe normal level [56, 57]. As discussed earlier that even in non-pregnant state, the risk of insulin resistance and diabetes in adult increases progressively upwards

middle-income countries and nearly two thirds of diabetes globally are attributable to

and increasing age of mother, the pre-pregnancy bodyweight should preferably around or below the middle of the recommended BMI for the population [56]. In Finland with predominant Europid population, the mean pre-pregnancy BMI of women were 21.9 and

other populations, the risk of glucose intolerance during pregnancy may also increase. Women who had a child gains extra weight than women who remained nulliparous [71] and the second and subsequent offspring were anticipated about a decade earlier to have increased risk of *in utero* exposure to the maternal clinical or sub-clinical hyperglycemia due to the increased weight of mothers [56]. A recent study indeed reported increased risk of GDM with increasing weight gain from first to second pregnancy [72]. In summary, campaign and programmes for maintenance of optimal pre-pregnancy body weight as per the recommended body mass index of the respective populations along with regular physical activity and exercise during pregnancy are the essential measures available at hand to prevent the possibility of maternal hyperglycemia right from the early pregnancy

**Research perspective:** Long-term follow-up study of offspring with exposure to different levels of maternal plasma glucose correlating with other risk factors can be conducted. Possible risk of obesity and early glucose intolerance in both female and male offspring due to the *in utero* hyperglycemia could also be due to the involvement of mitochondrial DNA. Exposure of mitochondrial DNA to reactive oxygen species (ROS) can lead to mitochondrial mutation [73]. Glucose excursions can lead to the formation of ROS, such as superoxide, which leads to oxidative stress in the body [74] and acute hyperglycemia can lead to oxidative stress with increase in the markers of oxidative damage [75–77]. Such oxidative stress due to high glucose level for the fetus during pregnancy can thus be postulated to lead to oxidative damage to fetal mitochondrial DNA and the offspring in this way may later be at increased risk of obesity and glucose intolerance. Superoxide anions, markers of oxidative damage and mediators of subclinical inflammation can be analyzed in the fetal, amniotic and/or maternal samples. If it is such mitochondrial inheritance as postulated, the affected female offspring would transmit the disease to all their children, and affected male offspring, however, would not transmit the disease to their children. The possibility of such pattern can be studied in the populations with high prevalence of type 2 diabetes

**Public health perspectives:** Examples of prevention and control programmes in the communicable diseases as a model for similar strategies required at individual and population levels for diabetes epidemic are summarized [78] in **Table 3**. Control programme to protect the other susceptible populations (**Table 3**) is the dire need today to

and are the urgent priority to control diabetes epidemic.

in 1960s and 2000, respectively [70]. If it increases to higher level, as in many

and more than 80% of the people with diabetes live in low- and

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[10]. Considering the inherent insulin resistance during pregnancy

of a BMI of 20–22 kg/m<sup>2</sup>

BMI above 21 kg/m<sup>2</sup>

23.7 kg/m2

in young age.

control diabetes epidemic.

The diagnosis of gestational diabetes mellitus (GDM) usually made at 24–28 weeks is applicable for the clinical management of the women and their children during and after pregnancy and it may also be useful for the mothers for primary prevention of later development of diabetes. From further public health perspectives to avoid any possible longterm *in utero* effect, prevention of subclinical maternal hyperglycemia right from the time of conception needs to be considered [56]. The sedentary lifestyle, obesity and glucose intolerance affecting relatively younger population are increasing in the community. The risk of maternal hyperglycemia during pregnancy has thus increased (**Figure 5**) [56]. The relative risk of developing overt GDM over the age of 35 years is 2.57 [63]. However, significant increase in the risk of overt GDM is reported even at age >25 years as compared to that in lower age [64].

The exact 'safe' normal level of maternal plasma glucose to prevent relative hyperglycemia *in utero* for fetus appears difficult to define. To find out such level, long period of follow-up is required after birth of offspring with exposure to different levels of maternal plasma glucose correlating with other risk factors [56, 57]. The normal value of neonatal plasma glucose may give some insight. However, the limits of normal plasma glucose defining neonatal hypoglycemia in infants are arbitrary. Neonatal glucose concentrations may decrease after birth, to as low as 30 mg/dL during the first 1–2 hours after birth, and then increase to higher and relatively more stable concentrations, generally above 45 mg/dL by 12 hours after birth [65, 66]. Later, it will gradually rise to adult levels.

Considering the risks of the macrosomia development, the safe normal level of fasting plasma glucose during pregnancy appears to be below 80 mg/dL (4.4 mmol/L), perhaps

**Figure 5.** A vicious circle of glucose intolerance in younger population and maternal hyperglycemia during pregnancy. \* The two preventable factors from the public health and clinical management perspectives. (Figure published with minor modification with kind permission from *JNMA*2009;48;173 [56]).

even below 75 mg/dL (4.2 mmol/L) [67, 68]. Macrosomia is to a great extent measurable but the fetal programming due to relative maternal hyperglycemia is difficult to assess and is obviously likely to be affected earlier than the overt macrosomia. Weeks 3–8 encompass organogenesis and major malformations in infants of diabetic mother occur during these periods [69]. So to protect the fetus from any possible effect of maternal hyperglycemia, blood glucose during the whole duration, including the early stage, of pregnancy has to be within the safe normal level [56, 57]. As discussed earlier that even in non-pregnant state, the risk of insulin resistance and diabetes in adult increases progressively upwards of a BMI of 20–22 kg/m<sup>2</sup> and more than 80% of the people with diabetes live in low- and middle-income countries and nearly two thirds of diabetes globally are attributable to BMI above 21 kg/m<sup>2</sup> [10]. Considering the inherent insulin resistance during pregnancy and increasing age of mother, the pre-pregnancy bodyweight should preferably around or below the middle of the recommended BMI for the population [56]. In Finland with predominant Europid population, the mean pre-pregnancy BMI of women were 21.9 and 23.7 kg/m2 in 1960s and 2000, respectively [70]. If it increases to higher level, as in many other populations, the risk of glucose intolerance during pregnancy may also increase. Women who had a child gains extra weight than women who remained nulliparous [71] and the second and subsequent offspring were anticipated about a decade earlier to have increased risk of *in utero* exposure to the maternal clinical or sub-clinical hyperglycemia due to the increased weight of mothers [56]. A recent study indeed reported increased risk of GDM with increasing weight gain from first to second pregnancy [72]. In summary, campaign and programmes for maintenance of optimal pre-pregnancy body weight as per the recommended body mass index of the respective populations along with regular physical activity and exercise during pregnancy are the essential measures available at hand to prevent the possibility of maternal hyperglycemia right from the early pregnancy and are the urgent priority to control diabetes epidemic.

**11.4. Maintenance of optimal pre-pregnancy bodyweight: the key programme required**

lower age [64].

192 Diabetes and Its Complications

[65, 66]. Later, it will gradually rise to adult levels.

modification with kind permission from *JNMA*2009;48;173 [56]).

The diagnosis of gestational diabetes mellitus (GDM) usually made at 24–28 weeks is applicable for the clinical management of the women and their children during and after pregnancy and it may also be useful for the mothers for primary prevention of later development of diabetes. From further public health perspectives to avoid any possible longterm *in utero* effect, prevention of subclinical maternal hyperglycemia right from the time of conception needs to be considered [56]. The sedentary lifestyle, obesity and glucose intolerance affecting relatively younger population are increasing in the community. The risk of maternal hyperglycemia during pregnancy has thus increased (**Figure 5**) [56]. The relative risk of developing overt GDM over the age of 35 years is 2.57 [63]. However, significant increase in the risk of overt GDM is reported even at age >25 years as compared to that in

The exact 'safe' normal level of maternal plasma glucose to prevent relative hyperglycemia *in utero* for fetus appears difficult to define. To find out such level, long period of follow-up is required after birth of offspring with exposure to different levels of maternal plasma glucose correlating with other risk factors [56, 57]. The normal value of neonatal plasma glucose may give some insight. However, the limits of normal plasma glucose defining neonatal hypoglycemia in infants are arbitrary. Neonatal glucose concentrations may decrease after birth, to as low as 30 mg/dL during the first 1–2 hours after birth, and then increase to higher and relatively more stable concentrations, generally above 45 mg/dL by 12 hours after birth

Considering the risks of the macrosomia development, the safe normal level of fasting plasma glucose during pregnancy appears to be below 80 mg/dL (4.4 mmol/L), perhaps

**Figure 5.** A vicious circle of glucose intolerance in younger population and maternal hyperglycemia during pregnancy. \* The two preventable factors from the public health and clinical management perspectives. (Figure published with minor **Research perspective:** Long-term follow-up study of offspring with exposure to different levels of maternal plasma glucose correlating with other risk factors can be conducted. Possible risk of obesity and early glucose intolerance in both female and male offspring due to the *in utero* hyperglycemia could also be due to the involvement of mitochondrial DNA. Exposure of mitochondrial DNA to reactive oxygen species (ROS) can lead to mitochondrial mutation [73]. Glucose excursions can lead to the formation of ROS, such as superoxide, which leads to oxidative stress in the body [74] and acute hyperglycemia can lead to oxidative stress with increase in the markers of oxidative damage [75–77]. Such oxidative stress due to high glucose level for the fetus during pregnancy can thus be postulated to lead to oxidative damage to fetal mitochondrial DNA and the offspring in this way may later be at increased risk of obesity and glucose intolerance. Superoxide anions, markers of oxidative damage and mediators of subclinical inflammation can be analyzed in the fetal, amniotic and/or maternal samples. If it is such mitochondrial inheritance as postulated, the affected female offspring would transmit the disease to all their children, and affected male offspring, however, would not transmit the disease to their children. The possibility of such pattern can be studied in the populations with high prevalence of type 2 diabetes in young age.

**Public health perspectives:** Examples of prevention and control programmes in the communicable diseases as a model for similar strategies required at individual and population levels for diabetes epidemic are summarized [78] in **Table 3**. Control programme to protect the other susceptible populations (**Table 3**) is the dire need today to control diabetes epidemic.


**Author details**

**References**

Madhur Dev Bhattarai

NEJMp068182

sheets/whatisph.ashx

Journal. 1981;**282**:1847-1851 6786649

WHO\_DCO\_WHD\_2013.2\_eng.pdf?ua=1

Address all correspondence to: mdb@ntc.net.np Nepal Diabetes Association, Kathmandu, Nepal

[1] International Diabetes Federation. Diabetes Atlas. Brussels: IDF; 2015. Available from:

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[2] WHO. Global Report on Diabetes. Geneva: WHO; 2016. Available from: http://apps.who.

[3] WHO. Preventing Chronic Disease: A Vital Investment. Geneva: WHO; 2005. Available

[4] Anderson GF, Chu E. Expanding priorities – confronting chronic disease in countries with low income. New England Journal of Medicine. 2007;**356**(3):209-211. DOI: 10.1056/

[5] Hornby AS. Oxford Advanced Learner's Dictionary of Current English. Oxford: Oxford

[6] American Public Health Association. Fact Sheet: What is Public Health? Washington: APHA, April 23 2015. Available from: https://www.apha.org/~/media/files/pdf/fact-

[7] Lloyd-Jones DM, Hong Y, Labarthe D, et al. American Heart Association special report: Defining and setting national goals of cardiovascular health promotion and disease reduction. Circulation. 2010;**121**:586-613. DOI: 10.1161/CIRCULATIONAHA.109.192703

[8] Greeenland P, Lloyd-Jones D. Time to end the mixed and often incorrect messages about prevention and treatment of atherosclerotic cardiovascular disease. Journal of the American College of Cardiology. 2007;**50**(22):2133-2135. DOI: 10.1016/j.jacc.2007.05.055

[9] Rose G. Strategy of prevention: Lessons from cardiovascular disease. British Medical

[10] WHO. World Health Report 2002: Reducing Risks, Promoting Healthy Life. Geneva: WHO; 2002. Available from: http://www.who.int/whr/2002/en/whr02\_en.pdf?ua=1 [11] WHO. A Global Brief on Hypertension: Silent Killer, Global Public Health Crisis. Geneva: WHO; 2013. Available from: http://apps.who.int/iris/bitstream/10665/79059/1/

from: http://apps.who.int/iris/bitstream/10665/43314/1/9241563001\_eng.pdf

https://www.idf.org/e-library/epidemiology-research/diabetes-atlas

int/iris/bitstream/10665/204871/1/9789241565257\_eng.pdf

University Press; 2010. ISBN 978-0-19-479910-2

\*The vulnerable populations to be protected by the control programme of diabetes include the offspring of malnourished or overweight mothers during their *in utero* life.

† National and international health and diabetes agencies should clearly spell out the control programmes, with appropriate budget allocation, for the control of diabetes epidemic.

**Table 3.** Examples of prevention and control programmes in the communicable diseases as a model for similar strategies for individuals and susceptible populations in diabetes epidemic (table published with minor modification) [78].
