TOXIC ENVIRONMENTS AND DIABETES: WHAT THEY ARE, HOW THEY HAPPEN AND WHAT WE CAN DO ABOUT THEM

EXCELLENCE IN DIABETES: AN INTERNATIONAL CONFERENCE

TOXIC ENVIRONMENTS AND DIABETES:

WHAT THEY ARE, HOW THEY HAPPEN AND WHAT WE CAN DO ABOUT THEM

Stephen Leeder and Shauna Downs

Menzies Centre for Health Policy

The University of Sydney

Doha, Qatar, March 2014

When considering the effect of the environment on diabetes we want you to see it from two angles – the way the environment causes diabetes and the way in which the environment determines who receives adequate treatment for diabetes.

First, with regard to the effect of the environment on diabetes, we know that all human health and disease is ultimately a manifestation of the interplay between our genes and the environment in which we live.  For diabetes, we realise that the environment plays a major role in provoking insulin resistance leading to type 2 diabetes.  We speak of obesogenic environments where excessive supply of fat and carbohydrate and lack of exercise lead to the development of diabetes, most spectacularly apparent in Pacific nations such as Nauru and Tonga. There, indigenous diets rich in root crops, fish and seafood have been replaced by ones from the economically advanced nations including Australia and NZ that are high in fat and cheap processed foods including turkey tails and mutton flaps (1).

Second, with regard to how the environment affects how we treat patients with diabetes. The environment is critical to determining whether treatment will be adequate for patients suffering type 1 (10% of all diabetics worldwide) and type 2 diabetes.  With effective treatment theoretically available that can be applied to both forms of diabetes, most notably insulin for type 1 and for 40% of type 2 diabetes and complication surveillance for both, environmental forces including poverty, migration, politics that lack a concern for equity and war limit the availability to all who need it of this care. These environmental factors determine who shall live and who shall die, and who will suffer. 

The environment therefore plays an important role in both the natural history and what we might call the unnatural history, where we apply therapies, of diabetes, associated with the origin of the disease in the vast majority of cases (type 2) and the destiny of those who suffer from it in virtually all cases – type 1 and type 2 alike.

To return to our first concern – how the environment causes diabetes, ponder for a moment the broader relation of the environment to all biology, and consider how varied the environment can be and yet sustain life, often going beyond survival to exuberance.  If you have long enough – thousands or millions of years – evolution can lead to the emergence of life forms that can handle amazingly different environments.  

Thermophiles are organisms that thrive in temperatures of 50C with a range of 40C to 70C. The ones that live in the depths of the ocean near hydrothermal vents under pressures exceeding 200 atmospheres do not need sunlight. They generate energy by converting carbon dioxide to methane and they use the same carbon source in constructing proteins.  Their genomes are dramatically different from non-thermophiles. 

The genome of a thermophile named Methanococcus was sequenced by Craig Venter and his colleagues who found that only 44% of its genes ‘resembled anything that had been previously described’ (2). They remind us of how brilliant evolution is and how adaptable life can be. At the other end of the temperature scale are organisms that prosper in the frozen wastes of polar ice. Other organisms have self-repair mechanisms that allow them to survive exposure to huge amounts of radiation.

The Plutella xylostella caterpillars have been shown to adapt to an obesogenic environment over the course of eight generations (3).  Caterpillars reared on carbohydrate rich foods progressively developed the ability to eat excess carbohydrate without accumulating fat whereas those reared in carbohydrate-scarce environments were more likely to store ingested carbohydrate as fat (3).

What’s wrong with humans, we ask, that they apparently cannot adapt to changing diets?  Well, maybe they can – we don’t know, but if we are waiting for genetic adaptation we would need to wait for many generations, though with genetic engineering we might do it quickly.

So when considering the environment and diabetes, there are two points of interaction that deserve our attention.  These two points are:

1. The environment that encourages the development of type 2 diabetes in large populations of people including the environment that may create adverse epigenetic effects on the developing foetus and child.
2. The environment that limits access to care for both type 1 and type 2 diabetes

The Environment that leads to type 2 Diabetes

Obesity, unhealthy diets and a lack of physical activity all increase type 2 diabetes risk (4–8). The good news is that lifestyle modifications can be as effective as pharmaceuticals (e.g., metformin) in preventing diabetes (9). The bad news is that the environments in which we live are often not conducive to making healthy choices.

Although modifying the environment to reduce smoking prevalence has been successful in high-income and several low and middle-income countries (LMICs) by increasing taxes, restricting advertising and banning smoking in restaurants and public spaces, there has been less success in terms of improving our surrounding obesogenic environment.

Intrauterine Environment

Perhaps one of the most critical environments in which to intervene to prevent diabetes is the intrauterine environment during foetal development. In 1989, David Barker and colleagues showed that lower birth weight was associated with an increased risk of heart disease later in life (10). This relationship has since been found to apply not only to heart disease but also to hypertension, stroke and type 2 diabetes. The first 1000 days from conception to two years is a key period for disease risk later in life - what women eat (or don’t eat) during this period has lasting and irreversible consequences for their offspring later in life (11). 

The developmental-origins hypothesis posits that the long-term risk of disease is initially induced through adaptive responses that the foetus or infant makes to cues from the mother about her health state (12). Both over and under eating during pregnancy can lead to accelerated weight gain in childhood and increase the offspring’s risk of diabetes later in life (12). Moreover, maternal hyperglycemia may lead to foetal hyperinsulinemia and fat deposition and maternal diabetes and obesity may increase the risk of metabolic disorders in their offspring, even during childhood (12). In fact, poor nutrition in utero and in early life, combined with overnutrition in later life, may play a role in the high prevalence of diabetes in many Asian countries (13). 

Food Environment

What people eat is inextricably linked to the food that is available, affordable and acceptable. The foods that typify the “western” diet, which has been linked to diabetes risk (4,14), tend to be high in salt, sugar and trans and saturated fat (15,16).

Although this dietary pattern is described as the “western” diet, given that it typifies consumption patterns in the United States and other high-income countries, it is now becoming more prominent in many LMICs worldwide. This nutrition transition has coincided with the influx of trans national food companies into emerging economies. As sales begin to stagnate in high-income countries, LMICs present a growth opportunity for these companies and a means of delivering profits to shareholders (16). This transition is leading to significant changes in the food environment and leading to an increase in the availability and affordability of ultra-processed and fast foods.

Although ultra-processed foods are widely available at a cheap price, their healthier counterparts are often less accessible by many pockets of the population, particularly those who are price conscious. Low-income communities are often characterised by food deserts – where fresh foods are virtually non-existent and energy dense foods of little nutritive value are abundant – making it more difficult for these populations to make healthy food choices.  A recent study in Sydney, Australia found that a healthy and sustainable food basket cost 30% more than a typical food basket in low-income areas in the city’s western suburbs (17).

Interventions to improve access to healthier foods are needed. In recognising the inequity in access to healthy foods, New York City provided vendor licenses for 1000 green carts that can only sell fresh fruits and vegetables in the city’s boroughs (18).

More recently, NYC doctors began providing prescriptions for fresh fruit and vegetables to low-income families at high risk of non-communicable diseases such as diabetes (19). However, in addition to ensuring that healthy foods are more affordable, disincentives for purchasing ultra-processed foods high in salt, sugar and unhealthy fat are needed. Taxing sugar-sweetened beverages and other ultra-processed foods, limiting advertising of these foods to children, and creating incentives for product reformulation such as front-of-pack traffic light labelling will all likely lead to a decrease in consumption of these foods (20–23).

The aforementioned interventions aimed at nudging consumers to make healthier choices are needed in order to improve the quality of the food environment but interventions are also needed more upstream in the food supply chain.

In order to make lasting and sustainable changes to the food environment, the food system as a whole must be targeted. Although reorienting the food supply to be less toxic and more conducive to a healthy diet will be difficult, small changes throughout the food supply to make healthier foods more available, affordable and acceptable are possible. Agricultural subsidies for cash crops such as corn and soybean oil in the United States have led to the distortion of prices of the “ingredients” of many ultra processed foods.

High-fructose corn syrup has become ubiquitous in the United States’ food supply thanks in part to large government subsidies.

Palm oil, which is high in saturated fat, has become the most consumed oil on the planet after huge investment in its production by Malaysia and Indonesia, as well as support from the World Bank (24).

It is now being imported by countries around the world as a cheap fat source for ultra processed foods. In order to ensure better access to healthy foods, food production must be realigned to support a healthier food environment.

A shift towards healthier agricultural production is beginning in the United States with corn farmers beginning to plant orchards and fruits and vegetables on parts of their land (25). 

Not only is this leading to increases in farmer incomes but also to an increased availability of fruits and vegetables.  This is no easy thing because corn has a spiritual significance in the farmland of the US.

 

In addition to realigning agricultural production towards foods that promote good health rather than staple crops that are then used as cheap ingredients (e.g., high-fructose corn syrup) for ultra processed foods, food-processing practices must improve. Product reformulation can reduce the levels of salt and sugar and replace trans and saturated with healthier unsaturated fat but ensuring that a healthier replacement is available may also depend on upstream agricultural production. For example, product reformulation to reduce trans fat would have the greatest public health impact if replaced with polyunsaturated fat (5).

However, given that saturated fat rich palm oil is so widely available at a low cost, it is often the replacement oil of choice for manufacturers. Ensuring that supply chains for healthier oils are strengthened through increasing yields, reducing wastage, etc. could help to incentivise the use of healthier oils in product reformulation. In 2005, Dow Chemicals launched canola and sunflower seeds used in cooking oils that had a longer shelf life and were suitable for frying in response to the requirement for mandatory trans fat labelling in the United States (26).

This led to its uptake by manufacturers in produce reformulation and the removal of 600 million tons of trans and saturated fat from the US diet (26) over the interval 2005 to 2012, likely reducing the risk of diabetes in many individuals.

Physical Activity Environment

In addition to the toxic food environment, the cities we build are now less conducive to walking and engaging in physical activity than they once were. Convoluted cul-de-sac communities are replacing the easily walkable grid-based communities of the past.

 

Moreover, as people move from rural labour intensive work to urban sedentary employment, activity levels have declined. This is compounded by the massive amount of screen time that children and adults are exposed to which is problematic given that the relative risk of diabetes has been shown to increase by 20% per two hours of television viewing per day (6).

Although there have been innovations to increase physical activity (e.g., stand-up desks) structural changes are needed to make it easier to engage in incidental physical activity such as walking to work, school or to the grocery store. Much like the food environment, we need to think more upstream.

Creating more opportunities for physical activity needs to be a part of urban planning and design. Increasing access to bike lanes, sidewalks and public transportation systems will increases physical activity levels (27,28) and could help to prevent type 2 diabetes.  Industry may wish to make a profit here – take the Fitz bike that allows you to walk a bit and then coast!

The environment that limits diabetes care

In addition to our surrounding food and physical activity environments, the environment that limits diabetes care must be improved. Many children with diabetes, especially type 1, die of the disease in less economically advanced societies for a lack of insulin. They often have to buy their own insulin and its cost is too often prohibitive (29–31). A choice has to be made by families, as one commentator puts it, between insulin for one of their children and starvation for the others. It is, as has been said, as though insulin had not been discovered (29). 

In recognition of this problem, some countries have taken steps to try to improve insulin access. Tanzania has a network of diabetes clinics that aim to provide affordable treatment with free consultations and heavily subsidised, or free for the poorest patients, insulin and other medicine and laboratory tests (32). Although access to much needed medical services and medicines has undoubtedly improved, and recent investment in a mobile clinic might lead to further improvements in access, many lower socioeconomic populations with diabetes are still unable to access continuous treatment leading one patient seeking treatment to say: “this problem is something that happens to poor people. For someone who’s rich, it's not a problem” (33).

Cost as a barrier to accessing insulin and other diabetes treatment is not unique to low and middle-income countries.  A study in the US found that 19% of elderly survey respondents had to cut back on their use of diabetes medication in the previous year due to costs (34). A similar situation exists in other high-income countries worldwide.

Beside treatment with insulin, there is much that can be done to assist people with diabetes to live with their disorder and avoid the disabling complications of vascular disease, blindness and renal failure.  If the environment does not support such services, death and disability follow. To take the South East Asian Region, where 1.5 billion people live, 72 million have diabetes, most of whom live in India. Nearly 20,000 children under 15 develop diabetes each year.  More than half of the deaths occur from diabetes in people under the age of 60 and almost a third (27%) under the age of 50 (35). India is the largest contributor to regional mortality with nearly one million deaths each year (35).

  

To conclude, we do not have the luxury of waiting millions (or even hundreds) of years for evolution to modify our genome so that we live happily in what are currently toxic environments, whether they be toxic because of nutrition and urban design or toxic because of poverty and political inertia.  We assuredly do not know everything that needs to be known about diabetes and the environment but we know enough to act and to advocate for change – at all points in the agri-food chain, in the way we design our cities, in what we argue for by way of international justice to allow all people access to lifesaving diabetes therapies.  We have a huge agenda.  We have strong support form our communities.  Let’s get on with it!

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