What I Learned Series 4: Obesity

What I Learned Series 4: Obesity

Ok I haven’t been posting as often here in the What I Learned Series due to a caseload of work coming up but I will now try to post weekly to strengthen my knowledge on certain topics! I’ll explain What I Learned in my own words!

What is Obesity?

Obesity in the simplest definition is the abnormal accumulation of fat with a BMI of >30 however in some cases BMI is not an accurate indicator of obesity as the BMI scale does not apply to young children and men with very high levels of muscle mass like bodybuilders.

Obesity is a maladaption where energy intake remains high and energy utilisation remains low causing excessive adipose tissue to be deposited. Adipose tissue does provide the body the benefit of secreting hormones however too much release of hormones can lead to metabolic disorders such as metabolic syndrome.

Metabolic syndrome is a series of metabolic disorders which can lead to certain diseases like diabetes, hypertension, and hypercholesterolaemia to name a few.

An increase in adipose tissue may lead to hyperplasia which is the increase in number of a certain tissue.

Pear Shaped or Apple Shaped?

People with an apple-shaped body are at a higher risk of developing metabolic syndrome as the hormones released from adipose tissue can disrupt other hormones by the organs. People with a pear shaped body are at a lower risk of developing metabolic syndrome and may even be said to have a protective effect against metabolic syndrome. Bottom-line is the risk is much higher the more adipose tissue there is above the waist.

Main Triggers for Obesity

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  • Trans fatty acids

Trans fatty acids from foods such as cakes, donuts, and fried foods is a key factor for obesity which may change the absorption of nutrients and impair mitochondrial function.

  • Excessive energy intake
  • Sugar

Risk Factors for Obesity

  • Low dietary fibre
  • Low physical activity
  • Less than 6 hours sleep a day
  • Medications

What Contributes to Energy Expenditure?

Basal Metabolic rate (50-60%) + Physical Activity (30-40%) + Thermogenic Effect of Food (10%) = Energy Expenditure

When taking less energy, the body reduces its BMR to conserve energy. Your body cannot differentiate your situation whether you want to lose a muffin top or if you are in the Sahara desert with no food available so when you decrease calories in a diet, your body will slow its metabolic rate down so you won’t burn as much. Quick example: You require 2000 calories/day. You diet on 1500. You’ll lose weight initially then your body will adapt to running on 1500 calories/day which means no more weight loss making it difficult to lose more. This adaption usually takes 3 months which is the main culprit for yo-yo dieting where people gain weight again.

Standard Women BMR: 1500 kcal/day (1300 when dieting)

Standard Men BMR: 1800 kcal/day(1500 when dieting)

Wait, so why is Obesity Difficult to Treat then if It’s About Eating Less?


Obesity can be easy to treat if people can eat less than they burn but you never know what it’s like to be someone with obesity unless you have it. People with obesity usually have leptin sensitivity or hyperleptinaemia. Leptin is a hormone that tells us “You’ve eaten enough, I’ll make you feel full” – It regulates satiety. 

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In normal cases, the more adipose tissue we have (fat) then the more leptin will be released telling us to stop eating and to prevent us from having too much fat. If we consume too much and too often we are overworking the release of leptin (hyperleptinaemia) which can cause leptin resistance. (sounds similar to insulin resistance right?) With leptin resistance, our body will not receive as much leptin making us unable to feel satisfied making fat gain even faster. 

Certain foods such as trans fats and processed foods can mess with our hormones increasing the risk of leptin and metabolic syndrome.

Why is it Difficult to Find Genes that Trigger Obesity?

We have 25,000 genes in each of us and 99% of them are silent genes so it is difficult to find a relationship between obesity and genetics. – Like finding a needle in a haystack and to make it harder to find the needle, our diet can upregulate or activate the expression of silent genes through methylation.

It has been found that fruits and vegetables can upregulate the expression of genes that make us feel full and trans fats can upregulate the expression of genes related to obesity.

Only a small proportion (5%) of obese individuals have mutations in the leptin gene (LEP) and 3% of severely obese individuals have loss of function mutations in the gene expressing the leptin receptor (LEPR)

It has been suggested that the dysfunction of the MCR4 gene in humans accounts for 6% of obesity cases which leads to hyperphagia, hyperinsulinaemia, and hyperglycaemia.

Appetite and Satiety System

What I Learned Series 4: Obesity

Higher adipose mass can lead to higher leptin (inhibits hunger) levels (leptin resistance)

Obese people have been shown to have lower leptin levels in the brain. Obesity has been shown to lead to changes in the permeability of the blood-brain barrier.

In obese people, insulin release isn’t downregulated and the pancreas continues releasing insulin which can lead to T2D which leads to high levels of blood glucose levels

Peripheral hyperleptinaemia –Leptin binds to receptors in the Pancreas  to help downregulate insulin synthesis and release in the beta cells. Low insulin stimulates the release of leptin.

Leptin is synthesised in the adipose tissue

The greater the adipose tissue, the greater the leptin synthesis (positive association)

Central hypoleptinaemia – Reduces appetite

Food -> Rapid increase of insulin (stimulated by beta cells in pancreas) -> Stimulates glucose uptake in the adipose tissue -> Releases leptin

It takes 20 minutes after starting to eat for the body to insulin levels to peak (eating slowly can help treat obese people backed by evidence) as well as drinking 2 glasses of water can increase the production of leptin and reduce the production of ghrelin which is a hormone opposite to leptin which stimulates appetite

Endocrine Function of Adipose Tissue

Adipose tissue secretes a number of bioactive peptides called adipokines. These include:

  1. Adiponectin
  2. 2.Leptin
  3. 3.Resistin
  4. 4.IL-6
  5. 5.IL-1β
  6. 6.TNF-α
  7. 7.Visfatin
  8. 8.Retinol binding protein

What is adinopectin? Key regulator of Glucose homeostasis. When it is released, it enhances insulin binding to receptors in the pancreas, adipose tissue, and the muscle (Adinopectin increases insulin sensitivity)

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Leptin? Is produced in the adipose tissue and very well connected to insulin

All these proteins are pro-inflammatory cytokines (trigger inflammation) or upregulate the immune system. All are important at a low level for cell signalling but when they accumulate large quantities, they can lead to metabolic disruption, impair insulin signal, damage tissues like beta cells and endothelial cells. Diabetes, liver disease, atherosclerosis happens when these accumulate.

In obese individuals, adinopectin is lower, leptin is lower, and the rest are higher

Obesity linked Adipocyte Dysfunction

What I Learned Series 4: Obesity

The secretion of all these is disrupted in obesity due to the accumulation of fat in the adipocyte

For the same amount of oxygen, mitochondria produce less ATP than healthy individuals. Mitochondria are less efficient in obese individuals. The mass of mitochondria per cell is lower.

The ability to oxidise fat is lower than healthy individuals.

Mitochondria is the main source of free radicals.

Mitochondria produce large amounts of ROS which leads to insulin resistance and metabolic disruption compared to healthy individuals. ROS change the permeability of cell membranes. This may explain why obesity can increase the risk of some cancers.

So What is the Cure to the Obesity Crisis?

Sure eating well and exercising regularly may seem sensible but logistically it is difficult. You have to take into account sleep, smoking, culture differences, genetic factors, stress, and many more.

According to my lecturer which he shared from the book Saving Gotham:

What I Learned Series 4: Obesity

A key solution to obesity is changing the system by making healthy choices easier and more available

You may live near a McDonald’s but willpower can only go so far until the physiological drive to eat kicks in.

What I Learned Series 4: Obesity

Surgery Options for Obesity

What I Learned Series 4: Obesity

What I Learned Series 4: Obesity

Although the results may seem great the costs of bariatric surgery must be balanced against the cost of continuing medication if the patient were not to have bariatric surgery.

  • Examination of the cost per quality adjusted life year (QALY) for bariatric surgery has shown that bariatric surgery is more cost effective than conservative treatment.
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Jonathan Sumner

Who am I? Trainee Diet Police? Nope!

I want to improve peoples’ relationship with food; To fall in love with meal times rather than them focusing on numbers - For people to be healthy, be comfortable in their own skin, and to love themselves. 🙂
Jonathan Sumner
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