The kids are not alright. Check out The Who, miming their 1965 hit on the banks of Regent’s Park boating lake in Swinging London (1). See how thin they were? That’s how everyone looked back in the day – and I know, because I was there. I wasn’t on the lake but way back behind the camera, a skinny teenager in a crowd of rubbernecking ectomorphs.
We didn’t all die before we got old but most of us got a lot heavier, and so did our children.
Globally, 40 million children under age 5 and at least 340 million adolescents aged 5-19 are classified as overweight (2). In the 5-19 age group the rate of overweight almost doubled in 8 years, growing from 10.3% in 2000 to 18.4% in 2018. This astonishing increase represents a near-future collapse in public health which the pharma-centric model has no answers for, and cannot deal with. Fat kids tend to become fat grown-ups, and it matters, a lot.
Overweight 5-year olds have a roughly tenfold increased risk of becoming obese adults (3), and this comes with greatly increased morbidity. This includes a doubling of the risk of gallstones (4), severe liver disease including hepatocellular carcinoma which is 4 times more prevalent in the heaviest groups (5), hypertension, metabolic syndrome and a hugely increased risk of diabetes.
In general, youths who are obese are more likely to have diseases we think of as adult conditions. They experience accelerated ageing, they have many more health crises – and they die earlier.
One large meta-analysis found that compared to healthy weight children, overweight children required 17% more acute hospital services, while obese children needed 36% more (6). This translated, in a large and well-controlled Swedish study, into an almost 3-fold increased risk of early death (7).
One important link between overweight / obesity and worse health is the inflammatory stress generated by excess abdominal adipose tissue (8), described in the previous post. But inflammatory stress not only leads to physical disease, it also damages brain function. It helps to explain why obese children and adolescents have a higher risk of anxiety and depression (9-12).
Fat shaming plays a role, but there is persuasive evidence that inflammatory stress down-grades neurogenesis, synaptic formation / pruning and neuromodulation (13-15). This has negative effects on mood, intelligence, educational attainment and even earning ability in later life (16, 17).
It is bad news indeed for the current generation of children, but the problems may affect future generations even more severely. This is where the Barker hypothesis and epigenetic shift come into play.
A Chinese research team recently showed (in mice) that a high-fat diet led to changes in gene expression, transmitted via a maternal microRNA, which increased the susceptibility to liver and colorectal cancer not just in their offspring but in subsequent generations as well (18).
Worryingly, the odds for developing liver cancer increased intergenerationally. The incidence in the offspring of an obese mother and grandmother was higher than the offspring of an obese mother but normal-weight grandmother.
The Chinese findings are supported by a Mexican group (also working with mice) who found that maternal obesity lead to mitochondrial dysfunction and metabolic disturbances in the offspring which increased their risk of becoming overweight and experiencing diabetes, heart disease and accelerated ageing (19, 20).
Taken together, these findings imply that if we do not find a way of bringing human populations back towards normal weight, the burden of degenerative disease at the public health level will continue to spiral out of control.
Fortunately, the Mexican researchers showed us a way forward. They and others discovered that many of the poor outcomes of maternal obesity in the next generation were improved by allowing the young mice to take physical exercise (19, 21, 22). The million $ question is, does this apply to humans too? Because heavy parents tend to have heavy children … (23).
Researchers have looked for genetic variations that might be implicated, but the hundred or so that have been found confer only a very slightly increased risk of obesity and cannot explain the current pandemic adequately; 150 years ago obesity was rare, and our genes have not changed since then.
However, genes may still play a role. Obesity changes the expression of 62 genes involved in the taste receptors on the tongue (24), showing a link between obesity and altered food preferences. Kids force-fed on junk foods start to like them, because their hippocampi and taste receptors are progressively degraded by their terrible diet (25-27).
Most obesity, therefore, is unlikely to be genetically inherited.
One very large meta-analysis suggested that around 20 percent of a child’s body mass index is inherited from their mother, and a further 20 percent is inherited from their father (23). It also found that the more overweight parents are, the more overweight their child is likely to be.
However, as the genetic links are weak, this points more towards environmental factors. The main two, diet and physical activity, are transmitted culturally between generations.
It seems likely that in the majority of homes, children’s food preferences are predominantly acquired from their mothers. Levels of physical activity, however, appear to be more closely related to those of fathers, if they are present (28, 29); and at least one of these studies (28) suggests that paternal obesity, which is generally co-present with paternal inactivity and thus inactivity in the children (29), is more important.
So there is a case for exercise programs directed at the child and ideally the father too. I doubt these would work well in the real world, but we should try.
In overweight and obese children, levels of some inflammatory markers are reduced by physical exercise (ie 30), and there is evidence that this leads to improved cognitive function (31). Physical activity is known to improve cognitive function and academic performance in normal weight children (ie 32-34), and it would be surprising if this were not to occur in overweight and obese children also.
Humans, however, are slightly more complicated than rodents. Roughly half of all parents do not see and therefore do not concede that their children have a weight problem (35, 36), even if the children themselves are aware of it (37). Which raises a series of moral and legal dilemmas …
The science that links childhood obesity to under-performance and an increased risk of illness and death is conclusive. These children are effectively being abused and harmed, even though the results of that abuse and harm are delayed. They will rack up more medical costs over time, and make a disproportionate contribution to national healthcare budgets.
So are parents who allow their children to become obese merely unaware, are they anti-social, or are they child-abusing criminals? (Cue howls of protest from the Fat Acceptance movement, whose advocacy of fat may provide short-term psychological benefits but does nothing to alleviate longer-term health costs.)
This idea was first mooted in 2010 in a BMJ report which suggested that medical staff encountering obese children should be ‘mindful of the potential role of neglect or abuse’ (38). The following year, a paper out of the Harvard School of Public Health stated that severe childhood obesity ‘could be regarded as abuse’, requiring medical or other intervention by the state (39).
Not long thereafter, some courts decided that child obesity could indeed be regarded as child abuse and constitute grounds for removal of an obese child from the family (40).
If we allow current trends to continue, and as political systems everywhere move towards increased state intervention and control, we may see more of such cases with all the shame, pain and disruption that would entail.
Would it not be better to bring Big Phood to heel, forcing them to cease and desist the marketing of toxic, calorie-laden and habit-forming junk foods to our children? And take a little more exercise too.
- UNICEF, multiple authors. The State of the World’s Children 2019. Children, food and nutrition. https://www.unicef.org/media/60806/file/SOWC-2019.pdf
- Freedman DS, Lawman HG, Galuska DA, Goodman AB, Berenson GS. Tracking and Variability in Childhood Levels of BMI: The Bogalusa Heart Study. Obesity (Silver Spring). 2018 Jul;26(7):1197-1202.
- Koebnick C, Smith N, Black MH, Porter AH, Richie BA, Hudson S, Gililland D, Jacobsen SJ, Longstreth GF. Pediatric obesity and gallstone disease. J Pediatr Gastroenterol Nutr. 2012 Sep;55(3):328-33.
- Andreasson A, Carlsson AC, Önnerhag K, Hagström H. Waist/Hip Ratio Better Predicts Development of Severe Liver Disease Within 20 Years Than Body Mass Index: A Population-based Cohort Study. Clin Gastroenterol Hepatol. 2017 Aug;15(8):1294-1301.e2.
- Kelly B, West J, Yang TC, Mason D, Hasan T, Wright J. The association between body mass index, primary healthcare use and morbidity in early childhood: findings from the Born In Bradford cohort study. Public Health. 2019 Feb;167:21-27.
- Lindberg L, Danielsson P, Persson M, Marcus C, Hagman E. Association of childhood obesity with risk of early all-cause and cause-specific mortality: A Swedish prospective cohort study. PLoS Med. 2020 Mar 18;17(3):e1003078.
- Choi J, Joseph L, Pilote L. Obesity and C-reactive protein in various populations: a systematic review and meta-analysis. Obes Rev. 2013 Mar;14((3)):232–44.
- Lindberg L, Hagman E, Danielsson P, Marcus C, Persson M. Anxiety and depression in children and adolescents with obesity: a nationwide study in Sweden. BMC Med. 2020 Feb 21;18(1):30.
- Kiecolt-Glaser JK, Derry HM, Fagundes CP. Inflammation: depression fans the flames and feasts on the heat. Am J Psychiatry. 2015 Nov 1;172(11):1075-91.
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- Michopoulos V, Powers A, Gillespie CF, Ressler KJ, Jovanovic T. Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond. Neuropsychopharmacology. 2017 Jan;42(1):254-270.
- Adelantado-Renau M, Beltran-Valls MR, Moliner-Urdiales D. Inflammation and Cognition in Children and Adolescents: A Call for Action. Front Pediatr. 2020 Sep 9;8:583.
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- Hagman E, Danielsson P, Brandt L, Svensson V, Ekbom A, Marcus C. Childhood Obesity, Obesity Treatment Outcome, and Achieved Education: A Prospective Cohort Study. J Adolesc Health. 2017 Oct;61(4):508-513.
- French SA, Wall M, Corbeil T, Sherwood NE, Berge JM, Neumark-Sztainer D. Obesity in Adolescence Predicts Lower Educational Attainment and Income in Adulthood: The Project EAT Longitudinal Study. Obesity (Silver Spring). 2018 Sep;26(9):1467-1473.
- Sun Y, Wang Q, Zhang Y, Geng M, Wei Y, Liu Y, Liu S, Petersen RB, Yue J, Huang K, Zheng L. Multigenerational maternal obesity increases the incidence of HCC in offspring via miR-27a-3p. J Hepatol. 2020 Sep;73(3):603-615.
- Rodríguez-González GL, Reyes-Castro LA, Bautista CJ, Beltrán AA, Ibáñez CA, Vega CC, Lomas-Soria C, Castro-Rodríguez DC, Elías-López AL, Nathanielsz PW, Zambrano E. Maternal obesity accelerates rat offspring metabolic ageing in a sex-dependent manner. J Physiol. 2019 Dec;597(23):5549-5563.
- Lomas-Soria C, Reyes-Castro LA, Rodríguez-González GL, Ibáñez CA, Bautista CJ, Cox LA, Nathanielsz PW, Zambrano E. Maternal obesity has sex-dependent effects on insulin, glucose and lipid metabolism and the liver transcriptome in young adult rat offspring. J Physiol. 2018 Oct;596(19):4611-4628.
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