Obesity News Bulletin

Covid-19: One of the many Obesity related co-morbidities?

Thousands of academic articles have been published on Covid-19 over recent weeks, reflecting the amount of data being generated and the importance of finding ways to fight the SARS-CoV-2 virus. The more we learn about the disease, the more complex it appears to be, with as many questions as answers arising (1). However, one aspect of the disease is now quite well established – the major risk factors that make individuals more susceptible to severe Covid-19 illness. After advanced age and male sex, the major risk factors are obesity and other, related underlying health conditions such as hypertension, cardiovascular disease (CVD), type 2 diabetes (T2D) and respiratory diseases (2).

Obesity is a major risk factor for CVD, T2D, hypertension and many other serious conditions, including a number of cancers, and its role in the development of these diseases is the reason it is such a major public health concern. However, Covid-19 has cruelly exposed another health issue associated with obesity – increased susceptibility to infections, particularly respiratory infections. Individuals with obesity often have respiratory dysfunction due to the presence of large fat deposits around the chest and upper abdomen. This is characterised by altered respiratory mechanisms, increased airway resistance, impaired gas exchange and low lung volume and muscle strength (3). As a result, obesity increases the risk of contracting respiratory tract infections including influenza and pneumonia (4, 5).

In the 2009 Influenza A H1N1 pandemic, patients with obesity were disproportionately affected by the virus, with more than twice the mortality rate of people with normal weight (6). Although this was an influenza virus, not a coronavirus, this should nevertheless have been a warning sign that people with obesity are likely to be at greater risk during viral respiratory pandemics. This warning was enhanced by a later study which looked at the response to the H1N1 vaccine. People with obesity initially produced high levels of antibodies, but within 12 months their antibody titres had dropped significantly, and they had double the risk of contracting the virus (7). This suggests that obesity compromises the immune system and its ability to fight viral respiratory infections.

In the case of Covid-19, it is most likely that the impact of obesity on the severity of the disease is due primarily to immune system dysfunction. A range of functional abnormalities have been identified in obesity, but in viral infections the dysfunction of Natural Killer (NK) cells is particularly relevant as they are important in both the initial stage of infection and then clearing the virally infected cells (8). The low-grade, chronic inflammation caused by excess visceral adipose tissue surrounding vital organs in the abdominal cavity, which is implicated in cardiometabolic complications of obesity, has also been highlighted as a possible cause of the over-exaggerated immune response seen in many Covid-19 fatalities (9).

It has also been suggested that visceral adipose tissue may act as a ‘reservoir’ for Covid-19. Adipose tissue expresses the protein ACE2 which is the entry point for SARS-CoV-2 into cells, so it is feasible the virus could infect visceral adipose tissue which then becomes a reservoir for more extensive viral spread, increased viral shedding, immune activation, cytokine amplification and systemic tissue damage (10).

Research into this disease will be ongoing for many years, and it is important to elucidate the mechanisms by which obesity contributes to the severity of Covid-19 illness, in order to identify potential targets for treatment. Two relatively simple areas for investigation would be zinc deficiency and vitamin D deficiency. Both these nutrients are essential for effective regulation of the immune system, and obesity increases the risk of deficiency of both (11, 12). Testing patients for zinc and vitamin D status would therefore be warranted, so that deficiencies could be corrected. In addition to playing a vital role in immune function, zinc also acts intracellularly to inhibit the RNA polymerase enzyme which replicates viral RNA (13), so any deficiency in circulating zinc could hinder the body’s attempts to fight the virus.

While it is vital we understand as much as possible about this new virus and learn how we might be able to minimise the impact of similar future outbreaks, it is arguably even more important to renew and re-invigorate our efforts to tackle obesity. We need to reduce obesity rates, not just to help limit the impact of future pandemics, but also to reduce the devastating effects of CVD, T2D and other obesity-related illnesses on the health and well-being of the millions of people with obesity, and ease the burden these diseases place on our healthcare systems. Unfortunately, healthcare professionals are not generally well trained to manage patients with obesity. A 2015 analysis of the NHS workforce estimated that fewer than 0.1% had received any specialised obesity training (14), which may be due to the fact obesity is not considered a disease in the UK. In the US, where obesity is recognised a disease, obesity is higher on the agenda but a very recent study revealed that U.S. medical schools “are not adequately preparing their students to manage patients with obesity” (15). It is vital that the curricula of medical and nursing courses are reviewed in relation to obesity, and that specialised training is provided to existing health professionals, to ensure they have the knowledge and skills to support and treat patients with obesity.


References

1. Bernstein L and Cha AE (2020) Doctors keep discovering new ways the coronavirus attacks the body. Washington Post. Published 10 May 2020. https://www.washingtonpost.com/health/2020/05/10/coronavirus-attacks-body-symptoms/?arc404=true

2. Centres for Disease Control and Prevention (2020) Coronavirus Disease 2019 (COVID-19). https://www.cdc.gov/coronavirus/2019-ncov/need-extra-precautions/groups-at-higher-risk.html

3. Murugan, A. T. & Sharma, G (2008) Obesity and respiratory diseases. Chron. Respir. Dis. 5: 233–242

4. Phung DT, Wang Z, Rutherford S, Huang C, Chu C (2013) Body mass index and risk of pneumonia: a systematic review and meta-analysis. Obes Rev. 14: 839e57.

5. Gounder AP, Boon ACM (2019) Influenza Pathogenesis: The Effect of Host Factors on Severity of Disease. J Immunol. 202: 341‐350.

6. Louie JK, Acosta M, Winter K, et al. (2009) Factors Associated With Death or Hospitalization Due to Pandemic 2009 Influenza A(H1N1) Infection in California. JAMA. 302: 1896–1902.

7. Green WD, Beck MA (2017) Obesity Impairs the Adaptive Immune Response to Influenza Virus. Ann Am Thorac Soc. 14: S406-S409

8. O’Shea D, Hogan AE (2019) Dysregulation of Natural Killer Cells in Obesity. Cancers (Basel). 11: 573. doi:10.3390/cancers11040573

9. Sattar N, McInnes IB, McMurray JJV (2020) Obesity a Risk Factor for Severe COVID-19 Infection: Multiple Potential Mechanisms. Circulation. https://doi.org/10.1161/CIRCULATIONAHA.120.047659

10. Ryan PD and Caplice NM (2020) Is Adipose Tissue a Reservoir for Viral Spread, Immune Activation and Cytokine Amplification in COVID‐19. Obesity. doi:10.1002/oby.22843

11. Vimaleswaran KS, Berry DJ, Lu C, et al. (2013) Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts. PLoS Med. 10: e1001383. doi:10.1371/journal.pmed.1001383

12. Gu K, Xiang W, Zhang Y, Sun K, Jiang X (2019) The association between serum zinc level and overweight/obesity: a meta-analysis. Eur J Nutr. 58: 2971-2982

13. te Velthuis AJ, van den Worm SH, Sims AC, Baric RS, Snijder EJ, van Hemert MJ(2010) Zn(2+) inhibits coronavirus and arterivirus RNA polymerase activity invitro and zinc ionophores block the replication of these viruses in cell culture. PLoS Pathog. 6: e1001176. doi:10.1371/journal.ppat.1001176

14. Candesic (2015) College of Contemporary Health: Training Market for Obesity.

15. Butsch WS, Kushner RF, Alford S et al. (2020) Low priority of obesity education leads to lack of medical students’ preparedness to effectively treat patients with obesity: results from the U.S. medical school obesity education curriculum benchmark study. BMC Med Educ 20: 23. https://doi.org/10.1186/s12909-020-1925-z

Covid-19, Obesity, BAME… and Vitamin D

Covid-19 and ethnicity

Over recent weeks, as the coronavirus pandemic has progressed, we have been inundated with data and statistics about the impact of the virus in a range of different countries, communities and demographic groups, but perhaps the most shocking are the numbers of people from black, Asian and minority ethnic (BAME) backgrounds who have died from Covid-19.

The numbers

In the UK, concern was first aired when it was reported that the first ten doctors to die from the virus were all from BAME groups (1), and that more than 60% of all healthcare workers to die from the coronavirus were BAME individuals (2). Early data on the ethnic breakdown of Covid-19 patients entering hospital revealed that 34% were of BAME heritage, compared to 14% of the population as a whole (3). A recent report from the Institute of Fiscal Studies (IFS) revealed that people of British Black African heritage are 3.5 times more likely to die from Covid-19 compared with the white population; people of Black Caribbean heritage 1.7 times more likely and British Pakistanis 2.7 times more likely (2).

On the other side of the Atlantic, a similar picture has emerged with regard to African-Americans, who have accounted for 27% of Covid-19 deaths (a mortality rate 2.6 times that of white Americans) according to a recent report (4). These disparities in death rates between ethnic groups are likely to be due to a complex interplay of a multitude of factors which influence health behaviours, immune profiles, infection risk and health outcomes (5).

Social, economic and health issues

In the US, attention has focused on the fact that African Americans are often socioeconomically disadvantaged, live in more densely populated areas and more crowded conditions. This potentially increases transmission of the virus. They are also more likely to be employed in key worker roles, and less likely to be able to work from home, so have greater risk of infection (6). In addition, African-Americans have higher incidence of obesity, type 2 diabetes mellitus (T2DM) and hypertension than their white counterparts (7, 8) – these have been identified as the three biggest risk factors for severe Covid-19 illness after age (9).

These socioeconomic and health issues are similar for BAME communities in the UK. They often live in densely populated areas and sometimes live in extended, multi-generational cohabiting families, which could increase infection of vulnerable members of the community. People from BAME backgrounds also represent a disproportionate number of medical and support staff in the NHS, so may be more exposed to the SARS-CoV-2 virus (2). The Black African / Caribbean population has the highest rate of obesity of all ethnic groups in the UK (10), but the most significant health issue affecting BAME groups is T2DM, which is of course a significant risk factor for Covid-19 morbidity and mortality. Black and South Asian populations in the UK have 3-5 times the prevalence of T2DM compared to the white population, and are diagnosed on average 10-12 years younger (11). Clearly there are a number of social, economic and health factors which may be contributing to increased risk of infection and increased severity of Covid-19 in BAME populations, but there is one
further factor that should be considered – the possible role of vitamin D deficiency in vulnerability to Covid-19.

Vitamin D

Vitamin D is essential for regulation of immune function, and has been shown to reduce the production of pro-inflammatory cytokines that are associated with lung damage caused by acute viral respiratory infections such as influenza and Covid-19 (12). In fact, supplementation with vitamin D reduces the risk of respiratory infection, particularly in people with low vitamin D status (13). Vitamin D is synthesised under the skin following exposure to UVB radiation from sunlight, so individuals who get insufficient sunlight are at risk of vitamin D deficiency. This is a particular issue during winter in countries further from the equator, when sunlight has insufficient UVB for vitamin D synthesis. People with darker skin colour who live in these countries, which includes many BAME communities, are at even greater risk, as are those who rarely go outside or expose very little skin to the sun (14).

It is therefore very interesting to note that the current coronavirus pandemic took hold at the end of winter in the northern hemisphere (the time of year when vitamin D status is at its lowest) and the countries most affected by the virus are in the northern hemisphere, above 35 degrees latitude (15). At the same time, countries at the end of summer in the southern hemisphere, such as Australia and New Zealand, have fared very well. Furthermore, a cross-sectional analysis of countries in Europe has shown a statistically significant correlation between population vitamin D levels and Covid-19 cases and deaths (16).

Vitamin D deficiency could therefore be contributing to the disproportionate number of BAME individuals who are succumbing to Covid-19. It is also interesting to note that vitamin D status tends to fall with age, particularly for older people in care homes, and with rising BMI (17). Obesity is strongly associated with vitamin D deficiency, although why this is the case is not clear. The leading theory is that dysfunctional adipose tissue in obesity sequesters vitamin D and impairs its release so it is no longer bio-available (18). Vitamin D plays an essential role in glucose homeostasis, insulin sensitivity and regulation of adipokines such as leptin, as well as inflammatory cytokines (19). Vitamin D insufficiency may therefore be involved in mediating insulin resistance and inflammation associated with obesity.

Vitamin D deficiency could therefore be a part of the Covid-19 pandemic jigsaw, contributing to the vulnerability of people with obesity as well as those of BAME heritage. Routine vitamin D screening could be introduced for hospitalised Covid-19 patients, and BAME health and social care workers, especially those with excess weight, to establish whether there is a link and to provide the opportunity to correct any deficiencies as part of treatment and prevention measures.

Conclusion

Vitamin D is just one of many factors, as discussed here, which might contribute to the vulnerability of BAME individuals to Covid-19, but it could be contributing to a toxic combination of factors, including obesity and other comorbidities, that is putting our BAME communities, particularly those individuals working on the frontline of health and social care, at very high risk of severe Covid-19 illness. Unfortunately, the risk to BAME health workers could have been predicted, and measures to protect them put in place, as the mortality rate for the BAME population for the 2009 influenza A (H1N1) epidemic in England was nearly twice that of the white population (20). It is vital that research is undertaken to determine the underlying causes of the unacceptably high price BAME communities are paying in the current pandemic. In the meantime, health and social care workers of BAME heritage, especially those with excess weight, should be afforded the protection they merit as key workers at higher risk from Covid-19, including ensuring healthy vitamin D status.


References

1. Siddique H (2020) UK government urged to investigate coronavirus deaths of BAME doctors. The Guardian. Published 10 April 2020. https://www.theguardian.com/society/2020/apr/10/uk-coronavirus-deaths-bame-doctors-bma
2. Boyd C (2020) Death rate among black and Asian Brits is more than 2.5 TIMES higher than that of the white population, reveals stark analysis by Institute of Fiscal Studies. Mail Online. Published 1 May 2020. https://www.dailymail.co.uk/news/article-8276097/Clear-disparity-ethnic-groups-Covid-19-deaths-IFS-study.html
3. Intensive Care National Audit Research Centre (2020) ICNARC report on COVID-19 in critical care. Published 17 April 2020. https://www.icnarc.org/Our-Audit/Audits/Cmp/Reports
4. APM Research Lab (2020) The colour of coronavirus: Covid-19 deaths by race and ethnicity in the US. Published 1 May 2020. https://www.apmresearchlab.org/covid/deaths-by-race
5. Pareek M, Bangash MN, Pareek N, Pan D, Sze S, Minhas JS, Hanif W, Khunti K (2020) Ethnicity and Covid-19: an urgent public health research priority. The Lancet. 395(10234): 1421-1422.
6. Gupta S (2020) Why African-Americans may be especially vulnerable to COVID-19. Science News. Published 10 April 2020 https://www.sciencenews.org/article/coronavirus-why-african-americans-vulnerable-covid-19-health-race
7. Centers for Disease Control and Prevention (2020) National diabetes statistics report 2020. https://www.cdc.gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report.pdf
8. American Heart Association (2016) High blood pressure and African Americans. https://www.heart.org/en/health-topics/high-blood-pressure/why-high-blood-pressure-is-a-silent-killer/high-blood-pressure-and-african-americans
9. Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, and the Northwell COVID-19 Research Consortium (2020) Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. JAMA. Published online 22 April 2020. doi:10.1001/jama.2020.6775
10. UK Government (2019) Ethnicity facts and figures. https://www.ethnicity-facts-figures.service.gov.uk/health/diet-and-exercise/overweight-adults/latest
11. Goff LM (2019) Ethnicity and Type 2 diabetes in the UK. Diabetic Medicine. 36: 927-938 12
12. Greiller CL and Martineau AR (2015) Modulation of the Immune Response to Respiratory Viruses by Vitamin D. Nutrients. 7: 4240-4270
13. Martineau AR, Jolliffe DA, Hooper RL, et al. (2017) Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. 356: i6583. doi:10.1136/bmj.i6583
14. National Institute of Health and Care Excellence (2018) Vitamin D deficiency in adults – treatment and prevention. https://cks.nice.org.uk/vitamin-d-deficiency-in-adults-treatment-and-prevention#!backgroundSub:2
15. Rhodes JM, Subramanian S, Laird E, Kenny RA (2020) Editorial: low population mortality from COVID-19 in countries south of latitude 35 degrees North supports vitamin D as a factor determining severity. Aliment Pharmacol Ther. 00: 1–4. DOI: 10.1111/apt.15777
16. Ilie PC, Stefanescu S, Smith L et al. (2020) The role of Vitamin D in the prevention of Coronavirus Disease 2019 infection and mortality. PREPRINT (Version 1) available at Research Square https://doi.org/10.21203/rs.3.rs-21211/v1
17. Vimaleswaran KS, Berry DJ, Lu C, et al. (2013) Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization analysis of multiple cohorts. PLoS Med. 10: e1001383. doi:10.1371/journal.pmed.1001383
18. Pramono A, Jocken J, Blaak E (2019) Vitamin D deficiency in the etiology of obesity related insulin resistance. Diabetes Metab Res Rev. 35: e3146 https://doi.org/10.1002/dmrr.3146
19. Zakharova I, Klimov L, Kuryaninova V, Nikitina I, Malyavskaya S, Dolbnya S, Kasyanova A, Atanesyan R, Stoyan M, Todieva A, Kostrova G and Lebedev A (2019) Vitamin D Insufficiency in Overweight and Obese Children and Adolescents. Front. Endocrinol. 10: 103. doi: 10.3389/fendo.2019.00103
20. Zhao H Harris RJ Ellis J Pebody RG (2015) Ethnicity, deprivation and mortality due to 2009 pandemic influenza A(H1N1) in England during the 2009/2010 pandemic and the first post-pandemic season. Epidemiol Infect. 143: 3375-3383.

Covid-19 and Obesity

From the early days of the coronavirus epidemic in China, we have been aware that older adults and people with underlying health conditions, such as diabetes and cardiovascular disease, are at greatest risk of severe illness and mortality caused by the virus, SARS-COV-2.

But when the epidemic spread to Europe, it quickly became apparent that overweight and obesity are also major risk factors for becoming critically ill with Covid-19. This was first noted in Italy (1), then in the UK, where 73% of the first 5,500 critically ill patients had overweight or obesity (2), and then the US. A recent publication in the Journal of the American Medical Association showed that, of 5,700 patients hospitalised with Covid-19 in the New York City area, 42% had obesity (3). Another study showed that, once hospitalised, patients aged below 60 with BMI > 30 are twice as likely to need critical care compared with patients with a BMI < 30 (4).

Given that hypertension and type 2 diabetes are two of the common comorbidities of obesity, this revelation was not surprising, but it also raised the question of whether obesity is an independent risk factor for critical illness or death from Covid-19, or if it is due just to the comorbidities. Data from Arthur Simonnet and colleagues in France showed that, of the Covid-19 patients in ICU, the need for ventilation rose with BMI, and this was independent of age, diabetes and hypertension – indicating that excess body fat itself increases an individual’s vulnerability to Covid-19 (5). Simonnet’s findings are supported by reports from the US that significant numbers of younger people with obesity, but otherwise healthy, are being hospitalised (6).

So how can obesity result in a worsening of symptoms and greater risk of death from Covid-19? One way is simply the physical presence of fat stores in the upper abdomen, which causes compression of the diaphragm and lungs, compromising respiratory function. However, probably the key factor is the effect that obesity has on the immune system.

In individuals with obesity, visceral adipose tissue in the abdominal cavity produces inflammatory cytokines that cause a chronic low-grade inflammatory state throughout the body. It is unclear how this affects the response to the viral infection in the lungs, but one theory is that inflammation caused by obesity occupies the immune system’s resources, reducing its ability to mount an effective response against the virus.

On the other hand, it has also been proposed that this constant activation of the immune system means that it over-reacts to the virus, causing excess inflammation and damage in the lungs (7).

There is also evidence that leptin may play an important role. Leptin is a hormone produced by adipose tissue, which is best known for its effects on reducing appetite by binding to receptors in the brain. In people with obesity, the CNS becomes resistant to leptin, so blood levels of leptin are high but it is ineffective at reducing appetite. However, T-lymphocytes, which are involved in the cell-mediated response to viral infections, also have leptin receptors and leptin deficiency or resistance can lead to dysregulation of cytokine production and increased susceptibility toward infectious diseases and inflammatory responses (8).

Research into the relationship between obesity and influenza viruses has been ongoing since the H1N1 ‘swine ‘flu’ influenza pandemic in 2009, and has shown that not only are individuals with obesity at increased risk of severe illness from the influenza virus, but they also respond less well to vaccines (9), and they are potentially more infectious because they shed virus for longer when infected (10).

When we add all this evidence up, it is clear that people with obesity are very vulnerable, not only to the current coronavirus, but also to influenza viruses and future viral pandemics.

Rising global obesity rates could be contributing to the spread of infection and are certainly putting added strain on already-stretched health services, highlighting the urgent need to tackle obesity and reverse this trend – something which governments and health systems around the world have so far failed to do.

Sources

1. Mills J (2020) Obese people are ‘at higher risk from coronavirus’. Metro. Published online 23 March 2020. https://
   metro.co.uk/2020/03/23/obese-people-higher-risk-coronavirus-12444395/
2. Intensive Care National Audit Research Centre (2020) ICNARC report on COVID-19 in critical care. Published 17 April 2020. https://www.icnarc.org/Our-Audit/Audits/Cmp/Reports
3. Richardson S, Hirsch JS, Narasimhan M, Crawford JM, McGinn T, Davidson KW, and the Northwell COVID-19 Research
   Consortium (2020) Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With
   COVID-19 in the New York City Area. JAMA. Published online 22 April 2020. doi:10.1001/jama.2020.6775.
4. Lighter J, Phillips M, Hochman S, Sterling S, Johnson D, Francois F, Stachel A (2020) Obesity in patients younger than 60
   years is a risk factor for Covid-19 hospital admission. Clinical Infectious Diseases. https://doi.org/10.1093/cid/ciaa415
5. Simonnet A, Chetboun M, Poissy J, Raverdy V, Noulette J, Duhamel A, Labreuche J, Mathieu D, Pattou F, Jourdain M,
   Lille Intensive Care COVID-19 and Obesity study group (2020) High prevalence of obesity in severe acute respiratory
   syndrome coronavirus-2 (SARS-CoV-2) requiring invasive mechanical ventilation. Obesity (Silver Spring). Published 9
   April 2020. doi: 10.1002/oby.22831.
6. Rabin RC (2020) Obesity Linked to Severe Coronavirus Disease, Especially for Younger Patients. New York Times. Pub-
   lished 16 April 2020. https://www.nytimes.com/2020/04/16/health/coronavirus-obesity-higher-risk.html
7. Sattar N, McInnes IB, McMurray JJV (2020) Obesity a Risk Factor for Severe COVID-19 Infection: Multiple Potential
   Mechanisms. Circulation. Published 22 Apr 2020. https://doi.org/10.1161/CIRCULATIONAHA.120.047659
8. Maurya R, Bhattacharya P, Dey R and Nakhasi HL (2018) Leptin Functions in Infectious Diseases. Front. Immunol.
   9: 2741. doi: 10.3389/fimmu.2018.0274.
9. Green WD, Beck MA (2017) Obesity Impairs the Adaptive Immune Response to Influenza Virus. Ann Am Thorac Soc.
   14: S406-S409.
10. Maier HE, Lopez R, Sanchez N, Ng S, Gresh L, Ojeda S, Burger-Calderon R, Kuan G, Harris E, Balmaseda A, Gordon A
    (2018) Obesity Increases the Duration of Influenza A Virus Shedding in Adults. J Infect Dis. 218(9): 1378-1382.

How does birth weight affect adult obesity in a low resource context?

South Africa is experiencing rapid increases in weight gain across the entirety of its population. Obesity is rising in both males and females, across all ages and socioeconomic groups. Like many other low-middle-income countries, it is experiencing a double burden of malnutrition alongside these high obesity rates. Malnutrition is present in one quarter of children under the age of three, resulting in stunting.

This stunting has been reported to be associated with adulthood disease risk, including obesity. Researchers thus far have not been able to look at this relationship in a low-middle-income country in the same participants by following them from birth into early adulthood. The authors of this study were able to do this for the first time using the Birth to Twenty Cohort which is a longitudinal study of children born in 1990 in South Africa.

Authors found that relative weight gain from birth into adulthood was positively related to fat mass, including both visceral and subcutaneous fat in adulthood. Being stunted at age two was inversely associated with fat-free soft tissue mass (i.e. lean body mass) in adulthood. This finding is analogous to trends that have been shown across Brazil, Guatemala and India.

What is driving rates of obesity in Chinese boys?

Over recent decades, alongside economic development, China has undergone a rapid nutrition transition that has resulted in a dramatic acceleration of obesity. Unlike other countries across the world, like the USA and UK, where childhood obesity rates have stabilised, the prevalence in China continues to worsen.

This crisis in China is also unique in terms of how it presents between genders. Dissimilar to other countries, obesity is higher in boys than girls. Boys are almost twice as likely to have obesity. Up until now, there has been limited evidence explaining why these unique sex differences have emerged.

Using a cross-sectional national health survey, Wang and colleagues revealed, as would be expected, that adolescent boys were much more likely to have energy intakes exceeding expectations. Importantly however, it found significantly different self-perceptions by sex, with boys much more likely to underestimate their weight and be satisfied with their current health behaviours.

These weight perceptions were supported by mothers, who were more accurate in predicting their daughter’s weight vs those with a son. Clearly, weight-related beliefs in China have a role to play in the increasing – and widening – rates of obesity in children.

The lasting impact of where we live

The neighbourhoods we live in influence how we behave and ultimately shape our health outcomes. Regardless of how much money an individual earns, if they live in a less-affluent neighbourhood evidence would tell us that they will have poorer health outcomes than if they lived in a more affluent neighbourhood. This effect is particularly strong when looking at obesity and diabetes.

While this has been long understood, little is known about when risk factors emerge in childhood and adulthood in individuals living in socioeconomically different neighbourhoods, and the cumulative effect of disadvantage over childhood. Researchers from Finland set out to answer this question through a population cohort, where participants were measured at repeated intervals for adiposity and behavioural risk factors. By linking postal codes to neighbourhood deprivation scores, researchers assessed the impact of living conditions on diabetes outcomes.

They found that detrimental lifestyle factors by neighbourhood living conditions are present right from childhood and worsen into adulthood. These risk factors accumulate over time to accelerate increased rates of obesity, hypertension and fatty liver by middle age.

When do trends of inactivity begin?

Physical activity is important for both the current and future health of children. For a long time a belief has been held that children are adequately active with a dramatic decline in behaviour beginning from later adolescence into adulthood. This decline is much more significant in girls then in boys. Based on this understanding, for many years adolescent physical activity has been targeted by both national and international organisations. However, there has been a recent suggestion that declines in activity begin earlier than adolescence.

A group of researchers from Glasgow set out to determine when exactly changes in activity take place. They used a UK longitudinal cohort study from North-East England with data on participants across eight years. In physical activity research, questionnaires have shown to be highly unreliable and inaccurate, but they are often what is used in cohort studies as they are low cost. In this cohort, objective data using accelerometers (electronic monitors that record activity patterns across the day) were used at four separate years, making it a valuable resource to look at changes over time.

The researchers revealed that all trajectories of activity behaviour declined from seven years of age with no indication of a difference by gender. This analysis proves earlier understanding wrong and provides a strong case that policy and intervention efforts should begin well before adolescence.

Antibiotic consumption and childhood obesity

A growing base of evidence suggests antibiotic use results in microbial disturbances in the gut. These disturbances in the microbiome may contribute to weight gain. In comparisons between individuals, it has been shown that those with obesity have a lower diversity of microbes in their gut. This research is supported by studies in animal models. In infancy, a baby’s microbiome is rapidly developing. It is thus suggested by some researchers that any antibiotic exposure in infancy may impede the establishment of the healthy gut microbiome and have lifelong metabolic consequences.

In a systematic review and meta-analysis, Miller and colleagues showed that the antibiotic use in infancy is indeed related to overweight and obesity in childhood. There were notable differences however by gender with boys appearing to be more affected by antibiotic use than girls.

The authors looked at multiple drugs finding that macrolides were most strongly related to increased obesity risk while narrow-spectrum drugs were not significantly associated. These researchers suggest in the fight against childhood obesity we need to examine antibiotic prescriptions and use across populations.

Assessment of dietary patterns, physical activity and obesity among older US adults

Obesity in older adults results in premature declines in physical and mental health and cognitive functioning. Evidence shows that the incidence of obesity and chronic diseases are higher in rural areas than in urban areas. Furthermore, more older adults are concentrated in these rural areas. There is limited understanding of the behavioural factors driving increases in obesity in older adults in rural communities. Specifically, if differences in dietary behaviour between rural and urban settings contribute to elevated obesity rates. A study recently published in in PLOS One set out to firstly assess rural-urban differences in obesity rates in older adults, and secondly the relationship with dietary patterns.

Researchers used census data in a sample of respondents aged 65 years of age and above from the USA. Regression models were utilized to investigate if rural-urban disparities in obesity, and associations with risk factors of fruit consumption, green vegetable consumption and physical activity. The results revealed, consistent with earlier evidence, that obesity rates were highest in rural areas. In these rural areas, fruit consumption was the lowest. A negative association between obesity and fruit and green vegetable consumption was observed in urban but not rural settings. These findings illustrate the importance of considering urban-rural status when developing obesity prevention programs and strategies. Interventions need to address the unique barriers experienced between the two settings.

Predictors of weight gain in school children

Childhood obesity is a growing public health concern given the rising prevalence rates observed in both developed and developing countries. There are a multitude of health-related consequences that worsen into adulthood. Current estimates demonstrate that about 25% of children are overweight or obese. Given that obesity tracks into adulthood understanding why and how it emerges in early life is critical to developing effective preventative efforts.

In the European Journal of Clinical Nutrition, a recent analysis explored predictors of BMI change, overweight and obesity in school children. This was conducted in a prospective manner using a cohort of Irish school children 6-10 years of age. Height and weight were assessed objectively and lifestyle factors through a questionnaire with parents. These measurements were assessed five years apart at baseline and follow-up. Logistical regression models were then run by the researchers to understand the associations.

Initial BMI was the main predictor of subsequent overweight and obesity in schoolchildren, followed by the socioeconomic status of the school. Schools in disadvantaged areas had higher rates of obesity. Alongside this processed food consumption, lower levels of participation in sport clubs and low fruit intake was associated with higher levels of obesity. These findings illustrate the need for programmes aimed at preventing obesity with a focus on early years and disadvantaged communities.

Access to green space plays a role in the development of diabetes

Socioeconomic characteristics of the urban environments and neighbourhoods are associated with rates of obesity and type 2 diabetes. Access to green space within an individual’s residential area has been shown to be beneficial for health and well-being however, there is limited understanding of the relationship with type 2 diabetes. The aim of this study in the BMJ Open was to investigate the relationship between green space, body mass index (BMI) and type 2 diabetes.

The study examined this relationship in adults (25-74 years of age) in a large German city through the Dortmund Health Study. Researchers used geographical information systems to develop three indicators of green space: proportion of green space, available recreation area per person and distance to the next park or forest. Through regression analyses researchers demonstrated no association between green space and BMI. However, a lack of green space and further distance from parks or forests resulted in increased incidence of type 2 diabetes. The results suggest the availability of green space is an important part of the residential environment playing a role in the development of type 2 diabetes. It is essential to consider the built environment individuals live in when developing prevention plans and actions.

Childhood obesity inequalities in Britain are increasing over time

Across most high-income countries in the world socioeconomic inequalities in childhood obesity have been well documented. However, it is not clear how they have changed over time. Using Britain as an example, this study published in The Lancet, investigated how socioeconomic inequalities in childhood and adolescent weight, height, and BMI have changed over time.

The analyses demonstrated that from 1953 to 2015 socioeconomic associated inequalities in childhood obesity emerged and widened, while height differences became narrower. In 2001, at age 11 a there was a difference of 1.40 kg at the 50th weight percentile whereas a difference of 4.88 kg was observed at the 90th weight percentile. This finding that relative socioeconomic inequalities in obesity are worsening is consistent with other cross-sectional evidence including the UK’s national measurement program.

These significant changes show the impact of social changes on child and adolescent growth and development. The increasingly obesogenic environments in societies disproportionately affects disadvantaged children. These findings illustrate that the numerous policy initiatives implemented in Britain since 1991 have been insufficient and ineffective.

As these inequalities continue to widen there is clearly a need for new approaches to reduce differences in rates of childhood obesity between advantaged and disadvantaged populations. These trends are similar in many countries globally. Without effective interventions, inequalities seen in childhood and adolescence will continue to widen further throughout adulthood with significant health consequences.

Obesogenic factors and environments contributing to rising rates of obesity in Mexican children

Mexico has one of the highest youth obesity rates worldwide currently at 34% of all children and adolescents. This problem is rapidly worsening in Mexico with drastic consequences. There is limited understanding of the factors driving the rapidly increasing rates in Mexico. An understanding of determinants is critical to developing interventions, health programs and policies to effectively take on the crisis.

A recent review in Global Health Action set out to compile, describe, and analyse dietary conditions, physical activity, socioeconomic status, and cultural factors that create and exacerbate an obesogenic environment among Mexican youth. The authors approached this through a narrative review conducted across scientific databases and governmental reports.

The findings revealed a multitude of contributing factors including reduced healthy meal options at public schools, high rates of sedentary lifestyles among adolescents, lack of open spaces and playgrounds, socioeconomic deprivation, false or misunderstood sociocultural traditional beliefs, misconceptions about health, a high percentage of overweight or obese adults, and low rates of maternal breastfeeding. The factors identified are exacerbating the obesity problem in this population. From this evidence it is apparent that the average Mexican child is surrounded by a multitude of obesogenic factors driving rising rates of obesity. Measures to control these factors is drastically needed to stop continuation of the escalating rates.

Acute and Chronic Effects of Exercise on Appetite, Energy Intake, and Appetite-Related Hormones

The simple equation for obesity is Energy out < Energy in. The simplest way of increasing our ‘Energy out’, is to exercise more. However, the benefits of exercise extend beyond just calories, and in fact, it’s thought that exercise can improve subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. The degree to which this effect exists in an individual is highly variable and difficult to predict. This review, published in Nutrients, seeks to understand how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses.

The review found that changes in perceptions of appetite, energy intake, and macronutrient composition in response to acute and chronic exercise stimuli are not modulated by levels of body adiposity or sex. However, in individuals with higher levels of habitual physical activity, they may exhibit improved sensitivity of the appetite control system through better compensatory adjustments for the energy content and density of food.

Although not conclusive, this paper draws attention to the benefits of exercise and need for an improved understanding of the individual factors that modulate appetite, appetite-related hormones, and food intake. Responses to exercise may help to explain the individual variability in body weight changes, and to facilitate the development of more efficacious weight management interventions.

A long-term maternal diet intervention to avoid the obesogenic effect in the offspring

The American Heart Association states that obesity among girls and women has generated a vicious cycle that contributes to the obesity epidemic. Studies into maternal overnutrition have found that high-fat diets in humans (which reflects the western diet), whereby the baby is exposed to over-nutrition during gestation, have increased risks of obesity, diabetes and other complications. In this study, published in The Journal of Nutritional Biochemistry, the diets of pregnant mice are varied to see whether they can prevent obesity related disease in the offspring, regardless of the weight-management of the mother.

The researchers transitioned the mice to normal fat (NF) diet 1 week, 5 weeks and 9 weeks before conception and continued this throughout gestation and lactation. After this, the offspring were given a high-fat diet for 12 weeks then sacrificed. They found that the mice whose parent had the NF diet for 9 weeks had a reduced risk of obesity, diabetes and other complications, regardless of maternal weight, suggesting a metabolic memory in the offspring that can be improved. Although the metabolic profiles of mice and humans are vastly different, the ease of access and economy of lifestyle interventions mean that a strategy to improve maternal diet for a period before conception, may be able to help prevent multi-generational obesity.

Eating faster is associated with general and abdominal obesity among Chinese children

Eating faster results in an increased rate of energy intake. However, the relationship between children’s eating speed, food intake and general abdominal adiposity is unknown, and forms the basis of this paper. A total of 50,037 Chinese children aged 7-17 years were enrolled from 7 provinces in China in 2013. Objective measurements of anthropometrics were taken and food speed was assessed by questionnaire.

There was a significant increasing trend across the slow, medium, and fast eating speed groups observed, in the prevalence of general obesity (7.2%, 10.0% and 15.9%), abdominal obesity (16.1%, 21.8%, and 29.4%) and waist-to-height ratio (WHtR) ≥ 0.5 (11.1%, 14.8%, and 22.0%). Compared with medium eating speed, fast eating speed was positively associated with obesity, abdominal obesity, and WHtR ≥ 0.5, while slow eating speed was negatively associated with these outcomes. They also found increased speed was associated with increased consumption.

Although this paper doesn’t tell us anything of the mechanism of this phenomenon, there are several biologically plausible suggestions. Such as, fast-eating leads to lower satiety and higher calorie intake, while slow-eating leads to enhanced thermic effect of food and also influences the release of gastrointestinal satiety hormones. More research should be done to see if it’s possible to change eating speed in adults, and whether this has any effect on obesity, as this could provide a simple non-invasive therapeutic target.